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Guideline in Cardiology of Sport and Exercise of the Brazilian Society of Cardiology and the Brazilian Society of Sports Medicine

GUIDELINES

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Presentation

In the year of 1986 in Belo Horizonte during the XLII Brazilian Cardiology Congress it was formalized, by gathering the signatures of all members, the creation of the Study Group in Sports Cardiology, which was in the beginning directly linked to SBC board, and afterwards a component of DERC.

The scientific fulfillment of this true practice of Brazilian cardiology was concluded with the first Guideline in Sports Cardiology. In the same rhythm of Societies of Sports Medicine and Cardiology all over the world, no doubt, the number of researchers and interested professionals that have their practice in sports and in the physical exercises of sports professionals and population in general will grow. The interest, even governmental, in heart disease prevention starts by the dissemination of physical activities for all. The current reality is the growth of people of all ages practicing physical activities in various modalities of sports.

The need of having a queries base compatible with our habits and usages was fulfilled with this text. The members are cardiologists and sports physicians, which facilitated the necessary integration and a legacy, the guideline, elaborated and within the difficulties of being the first one, to be optimized and periodically changed. The Sports Cardiology, being a new area of cardiology, is based in experience, but seeks to create its evidences in a global level.

Each day new modalities with increasing sports difficulties and intensities are "invented" and immediately incorporated to fitness centers, thousands of new long street races participants turn to us for technical evaluations and questioning, it all demands that the doctor keeps its practice updated, on behalf of more safety to sportsmen. It must be clear that there is no zero risk, despite the specialized emergency apparatus and acquired knowledge.

The fundamental is described in this Guideline, which was further studied in many heart disease aspects to facilitate reader's comprehension. Difficulties and lack of more consistent evidences in certain clinical situations will remain, but throughout the text you can find more pertinent solutions. Consistency with other BSC Guidelines was also sought.

This Guideline sought to approach the pre-participation evaluation and recommendations to prevent fatal and non-fatal events for the athletes, for people in general who practice sports and for para-athletes.

To conclude we would like to remember that, for the first time in a Guideline from Brazilian Society of Cardiology a chapter was added for disabled individuals, the cheered PARA-ATHLETES.

To the collaborators our best regards and congratulations. To the colleagues to use it we hope it can be useful for the good practice of Medicine.

Nabil Ghorayeb

1. Introduction

The pre-participation clinical evaluation (APP, PPE) for physical/sports activities should be understood as a systematic medical examination, uniform, able to comprehend the ample population of sports practitioners and athletes before their release to physical training. Its goal is to identify, or at least improve, the suspicion over cardiovascular diseases that are incompatible with the practice of physical activities seeking efficiency.

This evaluation, performed previous to the physical activity and periodically in its maintenance, has as its mean goal to prevent the development of cardiovascular system diseases (CSD) and sudden death by means of temporary or definite prohibition to practice physical activities or of treatment of the conditions that may be potentially fatal and triggered by physical exercise. The American Heart Association, as well as European Cardiology Society and Brazilian Society of Sports Medicine1-3 agree on recommending the PPE for all professional athletes. There is also an indication to prescribe correctly exercises for non-professional sports practitioners that perform high intensity activities.

Currently, the main argument against PPE implementation is over the costs involved in this evaluation. Due to the low prevalence of conditions capable of triggering sudden death during sports activities and to the big population of sports practitioners in the country, , a lot has been discussed on which would be the evaluation model with best cost-effectiveness. While some societies as a American Heart Association defend the simple implementation of a questions form and physical examination, believing that the financial and psychological cost bounded to false positive results in the performance of complementary exams do not justify the benefits that might be found, others, like European Cardiology Society, reinforce the use of complementary diagnosis methods, as its use is capable of modifying the occurrence of sudden death in the athletes population3-7. Although we do not have randomized works comparing the two evaluation methods, we suggest, like Brazilian Society of Sports Medicine, that PPE should be associated to complementary methods for professional athletes, considering its indication is completely justifiable in the pursue of guaranteeing the athlete's physical integrity and all the costs involved in their training. Another controversial aspect concerns the PPE in children, over which until now there is no consensus about protocols to be followed6,8,9.

These aspects will be approached in this document, which intends to establish the regulations for PPE in Brazil. For didactic purposes, and also because of the differences concerning physiology, epidemiology and clinical aspects, we have chosen to divide the individuals to be evaluated in three groups: one formed by sports practitioners, other by professional athletes and a third contemplating children and adolescents and also para-athletes or disabled athletes. There will always be an intersection zone among them, when several aspects of the exercise, like intensity, frequency, training volume, etc. are considered. The common sense of medicine practice and the individual experience of the evaluation doctor will be essential in the choice of a path for PPE performance in these cases.

2. Sports group

It is characterized by adult individuals who practice regular physical and sport activities, which intensity may vary from moderate to high, eventually competing, but without professional approach to the sport.

2.1. Anamnesis and clinical examination

The ideal would be that every individual who is candidate to practice sports in moderate/high intensity level be submitted, necessarily, to a medical examination that will allow the detection of risk factors, signs and symptoms of cardiovascular, pulmonary, metabolic or locomotor system diseases1,10,11. The classical techniques of clinical anamnesis must be employed with some differences, especially those that favor aspects related to exercise and to the history of family diseases or cardiovascular events related to the practice of sports.

During the anamnesis the Physical Activity Readiness Questionnaire (PAR-Q) developed in Canada, coupled with basic questionings applied by a doctor (Table 1), can be systematically applied. We must pay attention to sudden death or congenital heart disease cases in the family; family history for sickle cell anemia or other hemonoglobinopathies; provenience from endemic areas for Chagas disease or regions in which there is a prevalence of congenital diseases, like descendants from immigrants from the region of Veneto, in Italy, where there is a prevalence arrhythmogenic right ventricular dysplasia3-12,13. Special care must be taken when obtaining information related to the use of licit or illicit drugs that may be considered as doping, even involuntary, or that are hazardous to health or can cause sudden death13,14.

Among the symptoms, we must pay attention to palpitations, syncope, precordial pain or thoracic discomfort; dyspnea on exertion; dizziness/lipothymy; asthenia; or any other symptom triggered by physical exercise. Accurate sensibility is required to evaluate whether the abovementioned symptoms are indicative of a pathological condition or are merely the consequence of a competition or of a more intense training. As for the syncope in athletes, a detail investigation is required, for until evidence to the contrary it should be treated as an episode of sudden death spontaneously aborted14.

In the physical examination some clinical conditions should be highlighted, as: anemia; postural changes; infectious focuses (e.g., dental); systemic or severe infectious diseases; bronchial asthma, obesity, diabetes mellitus; systemic arterial hypertension; changes in cardiac and pulmonary auscultation; and special situations as pregnancy.

One must prioritize the search for characteristic signs related to the possibility of a heart disease, as: the presence of heart murmur, splitting in the third or fourth heart sounds, valve disease, changes in the palpation of superior and inferior limbs, Marfan syndrome physical features, besides the adequate measuring of blood pressure (on both arms in the first evaluation)15,16.

Also, in the physical examination one must characterize the eventual muscle-tendon shortening, especially from some muscle groups: hamstrings, quadriceps, iliopsoas, calf, thigh adductors, iliotibial tract, back and shoulder muscles, as the adequate therapeutic guidance can help preventing and treating muscle injuries, improving the sport performance.

Recommendation Grade: I

Evidence level: C

2.2. Complementary exams (non-cardiovascular)

We highlight, among routine laboratory exams aiming health: complete hemogram, fasting glycaemia, urea and creatinine, complete lipidgram, uric acid, hepatogram (AST, ALT, gamma-GT, bilirrubines, PAT/INR), urine exam, feces parasitological exam.

Recommendation Grade: I

Evidence level: B

In individuals subject to practice exercises or compete in heights superior to 2.000 m, it is important the performance of hemoglobin electrophoresis to discharge the possibility of hemoglobinopathies (e.g., sickle cell anemia). In our environment, especially on those with compatible epidemiology, the serology for Chagas disease is recommended6,7 (IA). Thoracic teleradiography in PA (posteroanterior) and left profile must be routinely required, because of its low cost and by providing relevant information about cardiovascular diseases, pulmonary diseases and thoracic structure diseases.

2.2.1. Electrocardiogram

2.2.1.1. Introduction

It is known that there are controversies in the approach of younger athletes; the American guideline (AHA/ACC/ACSM) does not contemplate the ECG inclusion, but the Italian protocol, already followed by the European Society of Cardiology (ESC), justifies and recommends its performance.

As regards individuals classified as master or aged, the rest ECG is mandatory; add to that the method's wide availability and low cost. At this age there is a bigger prevalence of cardiovascular diseases, being coronary artery disease the main one. This indication applies even to asymptomatic individuals and/or individuals without knowledge of previous cardiovascular pathology.

2.2.1.2. Method

The conventional 12 lead ECG should be performed de 12 with the individual in supine position, registered in speed of 25 mm/s and obtained at least 24 hours after the last sport activity. Previous rest of at least 5 minutes is mandatory17,18.

2.2.1.3 Analysis

The exam must be evaluated by a professional physician, cardiologist and with experience in the sport area, so that physiologic changes in the athlete's heart are not mistaken by eventual heart diseases.

2.2.1.4. Changes

The 12 lead ECG has limited diagnosis value for detection of coronary artery disease in population of asymptomatic individuals, mainly because of electrocardiographic patterns variations associated to physical training17. It is more useful when performed as part of a pre-participation evaluation, when it can identify non-expected changes, as previous myocardial infarction (in high age brackets), arrhythmias, and conduction disorders, among others.

It can also help in the diagnosis of less prevalent diseases, as MHCM, long QT syndrome, short QT syndrome, Brugada syndrome, WPW syndrome and pre-excitement, besides arrhythmogenic right ventricular dysplasia.

The 12 lead ECG may help in the diagnosis evaluation of aortic and mitral valvopathies, ectopic beatings (ventricular and supraventricular extrasystoles), bradyarrhythmia and tachyarrhythmia, other ventricular and supraventricular arrhythmias, disorders in the conduction system (LBB, RBB, AVB of varying grades). It can also detect changes in the ST segment, as early repolarization, St segment depression or elevation ST, T wave inversion in precordial and/or peripheral leads, raise in the R/S waves voltage suggesting LVE2,19.

There may be variations in the prevalence of electrocardiography changes, those being greater in the female gender than in the male gender; regarding the age, in the population of masters or aged, we find a greater frequency of inverted T waves in precordial and/or peripheral leads, increased R/S waves suggesting LVE and stimulus conduction disorders.

The variations found in conventional 12 lead electrocardiograms are also statistically significant regarding the type of sport practiced and depending on the age bracket evaluated in table 2.

Recommendation grade: I

Evidence level: A

2.2.2. Exercise testing

The exercise testing (ET) may be indicated in the initial evaluation of a sport practitioner in the early identifying of cardiovascular disease, as well as contribute to prognosis analysis in asymptomatic individuals or when there is reference to some symptom potentially indicative of this condition. Its indication also stands with goal to cardiorespiratory aptness evaluation in training evolution in some sport modalities, notoriously the ones with predominance of aerobic component21-23.

The cardiovascular overload imposed by physical activity stress, performed as leisure, during the practice of some sport or in competition, requires a great metabolic demand and peripheral hemodynamic. To cover this demand, there is a progressive increase in oxygen consumption by the heart with the objective of making possible the elevation of cardiac debt. The identification of eventual limitations to cover this crescent demand of oxygen by the cardiac muscle can be evaluated by ET.

Although the ET should always be indicated in the PPE, in the specific condition of leisure activities of light and moderate intensities asymptomatic individuals can be released without the need of examination. In further conditions, the ET will always be recommended24.

In adults up to 65 years old the coronary artery disease is the main responsible by mortality and the ET indication to those individuals aims predominantly the identification of myocardial ischemia, reflecting probable coronary disease (CAD). Also in asymptomatic people and even in those who have a known CAD the indication of ET is sustained by the need of an adequate prescription of physical activity.

The presence of changes in the rest electrocardiogram, often recurring from the athlete's left ventricular hypertrophy, reduces the diagnosis capacity, in the electrocardiographic aspect, of myocardial ischemia in ET. The simultaneous analysis of other ET variables contributes to the evaluation25,26.

The response evaluation of arterial blood pressure in the ET enables the adoption of early preventive and therapeutic measures, besides contributing to the correct exercise prescription.

The occurrence of palpitation during physical activity shall be investigated by means of ET with the objective of reproducing under monitoring the patient's complaint. The cardiac arrhythmia diagnosis may then be performed, the adequate treatment being oriented.

2.2.2.1. Variables to be evaluated in the exercise testing

2.2.2.1.1. Exercise capacity

The low exercise capacity expresses a bad prognosis. Its identification will deserve investigation as to the reason of its existence27,28.

2.2.2.1.2. Thoracic pain

Reproduce by ET the complaint of pain or thoracic discomfort during the exercise will allow the probable myocardial ischemia diagnosis by coronary disease, with consequent investigation proceeding e withdrawal from physical activities. If during the ET completely non-ischemic characteristics of pain are identified and the pain is indicated by the athlete as similar to the one that motivated the ET and there isn't change in any testing variable, the coronary disease probability becomes insignificant, therefore the athlete can be released for competition29.

2.2.2.1.3. ST-T Segment

ST unlevelling

ST segment sub-unlevelling or supra-unlevelling in slow, horizontal or descendant ascension may characterize CVD, in special CAD, especially when there is concomitantly the reference to thoracic pain or other manifestation that contributes to myocardial ischemia diagnosis30.

In asymptomatic athletes, when there are ST changes during ET, even if they are not accompanied by thoracic pain and occur in high double product and in high exercise capacity, associated to frequent cardiac arrhythmias, the temporary withdrawal or the postponement of the physical activity start and the proceeding in the cardiovascular disease investigation are justifiable.

This approach may be based on the bigger cardiovascular demand and the bigger risk of cardiovascular events, including sudden death, during exercise or during the practice of sports, noticeably for those over 35 years old and when one or more risk factors for CAD are present.

The ST segment analysis should consider:

The morphologic characteristics, being descendent more serious than horizontal and this more serious than slow lenta31,32.

The earliness of its appearance during exertion and these changes persistence lately in the recovering phase are conditions that indicate bigger risk and more severe33,34.

The reason between the depression variation in the ST segment concerning the heart rate variation [(delta ST in mm x 100) / delta HR]. It is considered potentially ischemic when equal or bigger than 1,635,36.

The ST depression when it is bigger than 10% in relation to the previous R wave amplitude. This adjustment in the ST segment evaluation deserves to be considered mainly because of the habitual presence of high R waves, expressing left ventricular hypertrophy physiologically present in the athletes37.

Still related to the ventricular repolarization we must pay attention to the fact that, when starting from a variation in rest ECG, these variations normalization during exercise is an important sign of benignity and good prognosis. Inversely, variations that do not normalize or even get worse with the raise in HR and of double product are often a sign of the presence of subjacent coronariopathy or myocardiopathy38-40.

Ventricular depolarization

In the presence of a ST segment depression during exertion, an increase in R wave amplitude and simultaneously reduction or maintenance of Q wave amplitude in lateral leads (V4, V5, CM5, V6), increase the diagnosis efficacy for myocardial ischemia41,42.

2.2.2.2. Systemic arterial blood pressure

Excessive high arterial blood pressure values during the exercise test enable to infer that during the exercise or sport practice the arterial blood pressure shall be very high as well. Sports that require a bigger static component will possibly be accompanied by even higher systolic, diastolic, arterial blood pressure.

The arterial hypertension laboratorial investigation and treatment should begin in sequence, and the sport activities should be interrupted temporarily until better control is reached43. On the other hand, progressive fall or systolic arterial blood pressure during ET, especially when systolic arterial blood pressure values inferior to pre-exertion are reached should deserve proceeding in the investigation of presence of cardiac disease.

2.2.2.3. Heart rate

Chronotropic incompetence indicates a bad prognosis and has been associated to endothelial malfunction, change in the autonomic modulation, elevated values in the inflammatory markers and coronary disease.

The heart rate inadequate response may be considered by the inability of reaching 85% of the maximum estimated heart rate. The function 208 (age x 0.70) may be used to predict the maximum heart rate. Topic index under 80% is another method to identify chronotropic incompetency, and it has prognosis value. It is obtained by the reason [(Obtained HR Reserve /Estimated HR Reserve) x 100]44.

The heart rate reduction in the recovery first minute related to the heart rate in the peak of exertion enables to infer the cardiac vagal modulation. This observation was first identified in athletes comparatively to cardiac insufficiency patients45,46. Reductions equal or inferior to 12 beatings per minute have been associated to bigger mortality incidence47.

2.2.2.4. Cardiac Arrhythmias

Cardiac arrhythmias of a lesser level of complexity, as eventual ventricular extrasystoles on ET, often express increase in the sympathetic autonomic modulation imposed by graduated exercise. Such conditions taken isolated, without the presence of other variations do not justify greater restriction to physical activities in asymptomatic individuals.

Symptomatic or asymptomatic individuals, who develop complex ventricular arrhythmias, as ventricular tachycardia, sustained or not, will deserve investigation previous to release to physical activities.

The presence of seven or more ventricular extrasystoles exclusively in recovery phase, or in recovery and exertion, express a potentially bigger risk of future cardiac events48.

Recommendation Grade and Evidence Level

Physical activity as leisure, of light or moderate intensity, in asymptomatic individual without cardiovascular risk factor: perform exercise test when initiating physical activity program.

Recommendation Grade: IIa

Evidence level: A

Physical activity as leisure, of light or moderate intensity, in asymptomatic individual with cardiovascular risk factor: perform exercise test when initiating physical activity program.

Recommendation Grade: IIa

Evidence level: A

High intensity leisure activity, sport and competition: perform exercise test when initiating physical activity program.

Recommendation Grade: IIa

Evidence level: A

At any moment:

Reference to thoracic pain or discomfort, tiredness or dyspnea of non-defined cause, palpitation, identification of previously inexistent arrhythmias, pre-syncope or syncope related to exercise or arterial blood pressure elevation in rest, compromising or not target organ: perform exercise test.

Recommendation Grade: I

Evidence Level: A

Note: the exercise test requirement will depend on initial clinical evaluation and may be contraindicated or eventually anteceded or succeeded by other complementary exams, if necessary.

2.2.3. Echocardiogram with Doppler

It should be used in the cases of heart disease familiar/clinical history or suspect physical exam, as well as for cases of rest electrocardiogram with positive criteria for cardiomyopathy (Table 3)49. Also in known cases of congenital heart diseases, especially those of low complexity, in which the physical activity and even sports practice seeking efficacy are not contraindicated, the periodical echocardiogram performance helps in the evolutive evaluation and in the correct management of the condition in question. We should reinforce the importance of echocardiogram with Doppler associated to physical exertion in situations in which the cardiac function verification during exercise can help in diagnosis and conduct50.

Recommendation Grade: IIa

Evidence level: B

Table 3 - Criteria to consider a 12 lead electrocardiogram as suggestive of heart disease and of indication of echocardiogram European Cardiology Society (adapted from Pelliccia A)18.

Regarding athletes with age superior to 35 years old, the standard protocol associated with question form for coronary artery disease specific evaluation should be applied. In men >40 years old and women >55 years old and in individuals with more than 2 risk factors for coronary artery disease (besides gender and age) 51,52 the performance of functional test with exercise should be considered.

In case of positive in the initial evaluation for coronary artery disease the investigation must go deeper with more accurate exams, like echocardiogram at rest, stress echocardiography or myocardial tomographic scintigraphy, evaluating each case individually.

Recommendation Grade: IIa

Evidence level: B

2.2.4. Other complementary exams

The use of other diagnosis tools, be it laboratory, charts, graphics methods, invasive or not, should comprise to clinical criteria and scientific evidences established in literature, as function of those found along the PPE.

Specific details on the indication and interpretation of those complementary exams will be found on the topic about sudden death and cardiovascular events prevention in physical and sports activity in this guideline.

3. Athletes group

This group is characterized by individuals who practice physical and sports activities in a regular and professional basis, systematically competing, with professional attachment to sports through clubs and/or sponsors of any kind. This group works always in pursue of records and limits overcoming, often submitting themselves to high intensity training load which places them invariably under intense physical and psychological stress, with frequently hazardous consequences.

3.1. Anamnesis and physical examination

The athletes' pre-participation evaluation (PPE) demands a manageable strategy regarding economics, especially in a country in development such as Brazil, with continental dimensions, well-populated and with great social and economic diversity. The cardiologic approach deserves special attention, as the event of sudden death depends mainly on cardiovascular causes. In this context, it is fundamental a correct anamnesis and physical examination53,54.

It should be considered in the anamnesis, contributing to a correct interpretation of the physical examination, that the cardiac adaptations to physical exercise depend on its frequency, quantity and intensity, varying according to different demands observed in several sports modalities, different training systems and also individual responses55. This last aspect is what makes it possible that individuals submitted to similar physical activities have different cardiac characteristics. Therefore, there are HR and SAP variations that depend on the habitual physical activity and also on characteristics proper of each individual. It should be noted that the variations that produce the athlete's heart syndrome should, for starters, be considered as normal physiologic adaptations to physical exercise, transitory and with no negative results on health56,57.

Laboratory exams are not required at first; its requirement should come from the clinical data obtained, with emphasis on cardiovasculatory aspects. The laboratory exams listed in the first part of this document (sports group) should also be considered in the athletes' group.

Recommendation Grade: I

Evidence level: A

3.1.1. Considerations on overtraining syndrome (OTS)

Many times the magnitude and the clinical repercussions of cardiovascular variations configure a health problem as the overtraining syndrome should be considered. Because it is a profile that is difficult to ascertain and depends essentially on the clinical analysis for its presence to be suspected, we have chosen to include here its description and the recommendations to manage it. In the confirmation of diagnosis, the laboratory sometimes has a fundamental role.

There are two types of overtraining: the sympathetic, or Basedow type, and the parasympathetic, or Addison type.

The OTS of parasympathetic type is more common in veteran athletes. It is not always followed by decline in sports efficiency. Many times it manifests only by some lethargic state, consequence of great vagal predominance. The sympathetic reflex responses are inhibited, which can lead to orthostatic hypotension, dizziness, faintness and Stokes-Adams episodes in daily life situations.

The OTS of sympathetic type, which is more common, usually causes decline in sports efficiency, irritability, insomnia, loss of appetite, profuse sweating, persistent tachycardia and other tachyarrhythmias, slow return to basal heart rate after physical exertion and arterial hypertension. It may indicate an accentuated catabolic process, with loss of weight by loss of muscle mass, and even osteoporosis and stress fractures. Laboratory variations may occur, with increase in urinary nitrogen excretion, reduction of anabolic hormones, like testosterone and growth hormone, and defense factors depletion with less immune resistance. By configuring the catabolic process, the anabolic hormones reduction is accompanied by increase of catabolic hormones, like cortisol. Thus, the reason serum cortisol / serum testosterone usually presents values above normal. The decrease in efficiency and the related symptoms demand immediate reduction or even interruption of physical exercises, in long resting period. The recovery time is variegated, requiring monitoring to indicate the best time to return to activities.

3.2. Electrocardiogram

Sports practice promotes morphofunctional variations in the heart related to training time and intensity, which are demonstrated in ECG at rest, like ventricular overload, atrioventricular conduction and rhythm disturbances, imposed by the exercise's vagal exacerbation. Abnormalities that can put the athlete in risk during sports practice can be detected, representing the expression of a subjacent heart disease. When an athlete's ECG is analyzed, the main goal is to discern between physiological patterns and those that require action and/or additional tests to exclude (or confirm) the suspicion of subjacent cardiovascular disease leading to increased risk of sudden death in sport58.

Mistakes in the differentiation between physiologic and pathologic may have serious consequences. Athletes can be unnecessarily disqualified for competitions because of ECG variations which are inserted in the normal interval for athletes. On the other hand, they can be submitted to unnecessary exams, raising in much the evaluation costs. This is particular relevant for the professional, as the competitor disqualification generates psychological and eventually financial troubles. Alternatively, potentially fatal cardiovascular disease signs can be wrongly interpreted as variant from normal in an athlete's ECG.

The peculiarities of athletes' electrocardiogram in rest imply that the exam interpretation should be performed by cardiologist doctors with experience in the exercise physiology area or sports doctor with training in the cardiology area.

Currently available data enable to define the ECG usefulness and cost-effectiveness of use in pre-participation evaluation59,60. The Sociedade Brasileira de Cardiologia (Brazilian Cardiology Society) recommends it in every initial cardiologist appointment. The European Cardiology Society and the International Olympics Committee, the FIFA, indicate its performance in everyone who wishes to ingress in a leisure or competitive physical exercise program61. The American Heart Association does not indicate it as mandatory in pre-participation evaluation for the practice of exercise or sports62. In Brazil, in many institutions where athletes are evaluated its performance is mandatory.

3.2.1. Variations considered physiologic X suggesting heart diseases

The efforts concentrate on better understanding interpretation basis, defining ECG criteria to discern between athlete's heart and actual heart diseases. More studies are necessary to test if the accuracy, usefulness and cost-effectiveness of ECG presents criteria variations regarding gender, age, ethnics and different levels of training and/or type of sport63,64. The variations in athletes' ECG may be divided in two groups: commons and/or related to sports training (group1) or sporadic and/or suggestive of heart diseases (group2), as listed in table 4.

Athletes often (up to 80%) show electrocardiographic variations as sinus bradycardia/arrhythmia (13-69%), first-degree atrioventricular block (35%), early repolarization (50-80%), resulting from physiological adaptations recurring from the increase in vagal tone. They can also present voltage criteria (i. e., based only in QRS amplitude measurings) for physiological left ventricular hypertrophy that reflects the remodeling of this cavity, without the concomitant presence of pathologic Q waves, electrical axle deviation, atrial overload and repolarization variations65,66.

Those physiological variations in the ECG must be clearly separated from patterns suggestive of heart disease recognized by repolarization variations, pathological Q waves, electrical axle deviation, intraventricular conduction defect, pre-excitement, short/long QT interval and Brugada. Those findings are rare (5%), but may be the expression of heart diseases, genetic inheritance and canalopathies, which predispose to sudden death67.

Variations caused by cardiac adaptation to physical exertion (group 1) should not cause alarm and the athlete may be released to practice competitive sports without further evaluation, as should continue under investigation athletes with signs suggestive of heart diseases even though asymptomatic, in the absence of positive family history or abnormal findings in the physical exam68-70.

Recommendation Grade: I

Evidence level: A

3.3. Exercise test

The exercise test (ET) may be indicated in the initial evaluation of athletes in any age bracket as part of the strategy for early identification of cardiovascular disease, as well as to contribute in the prognosis analysis, in asymptomatic or when there is reference to any symptom potentially indicating this condition71,72.

Your requirement will depend on the initial clinical evaluation and may be contra-indicated or eventually anteceded or succeeded by other complementary exams, if necessary.

The considerations on method made in the chapter dedicated to sports practitioners are totally applicable for professional athletes. We suggest, therefore, that the text quoted in this document be read.

Recommendation Grade: I

Evidence level: A

3.4. Cardiopulmonary test

For a long time, including in Brazil, athletes and individuals who participate in high efficiency physical activities have been submitted to the maximum cardiopulmonary exercise test (MCET), aiming performance evaluation and aerobic training prescription73. As described in table 5, MCET differs from conventional exercise test primarily by the addition of measuring and analysis of exhaled gases74,75. According to its primary objectives, when performed in athletes apparently healthy, contrary to exercise tests aiming clinical diagnosis, many times the arterial blood pressure measurings and even electrocardiogram are not performed, and the heart rate measuring is in this case obtained by the use of frequency meters.

With hundreds of equipments available today (in laboratories, clinics, hospitals, sports clubs and centers) capable of performing these measurings, it actually makes little sense to perform athletes' aerobic condition evaluation by a conventional exertion test, in which there is approximately 20% error when estimates based on formulae developed for clinical protocols for treadmill or cycloergometers. It is apparently consensual among physicians and physical education professionals that work with athletes that when performing a MCET is impossible, the tendency is to choose field tests like the 2,400 m or even the traditional Cooper test instead of the conventional exercise test.

In the clinical context of pre-participation evaluation of athletes and individuals who wish to start practicing intense aerobic exercises, the MCET has many advantages over the conventional exercise test, as illustrated in table 5, besides the objective and validated measurement of aerobic condition or maximum VO2. In certain clinical circumstances and for determined differentiated groups of athletes, for example master athletes or those individuals with cardiovascular and/or pulmonary infirmities who are involved with recreational sports competition (e.g., half marathon races, marathon races, high mountain climbing, road cycling competitions, water circuits, etc.) or professionally, the inclusion of MCET in their pre-participation evaluation may be recommended or even fundamental for the individual risk stratification, because of aggregated information by measure and analysis of exhaled gases. In these circumstances and whenever possible, the use of closest ergometer for the sports activity practiced should be preferred.

With the crescent involvement of middle-aged individuals in mass sports events76, it is probable that MCET will be used to obtain objective and valid subsidies that orient the training more scientifically or to have more safety in the characterization of a low clinical risk for unfavorable cardiovascular events, especially those that have coronary risk factor.

Among the several possibilities of additional clinical information derived exclusively from a MCET in the physically active healthy athlete or individual, two stand out: a) more accurate and objective identification of limiting factor(s) for maximum exertion (cardiovascular, respiratory and muscular or metabolic) and b) evaluation of systolic volume behavior, obtained by the analysis of curves and of oxygen pulse maximum values (VO2/FC) and of ventilatory equivalents (VE/VO2 and VE/VCO2) when an incremental and maximum protocol is performed during at least 8 to 10 minutes (more commonly ramp protocol)77.

In many cases, especially when considering the high relative prevalence of electrocardiography abnormalities of male athletes with long years of predominantly aerobic training, compromising at least in part the diagnosis specificity and sensibility of tracings obtained in exertion, the behavior of cardiopulmonary variables obtained during the MCET may contribute to solve doubts and adequately stratify the individual risk of a given athlete. In other situations, a systolic arterial blood pressure reduction in the MCET last minutes in an apparently healthy athlete, when accompanied by normal ventilatory responses, probably reflects an accentuated reduction of peripheral vascular resistance resulting from metabolic acidosis with a preserved or even crescent cardiac debt and not an acute dysfunction of cardiac inotropism/lusitropism recurring from myocardial ischemia.

The MCET is already incorporated in the cardiologic practice to evaluate heart failure patients56 and to identify the etiology of exertional dyspnea57 and recently considered as capable of identifying myocardial ischemia58 or abnormal responses after cardiac surgeries59.

With athletes, it is the procedure of choice when one wishes to obtain a valid measure and needs the aerobic condition and the determination of threshold heart rate to prescribe the exercise.

Recommendation Grade: I

Evidence level: A

It is for a more accurate stratification of the exercise limiting factor.

Recommendation Grade: II.a

Evidence level: A

When there are changes in the rest electrocardiogram that may interfere in its interpretation to exercise or suspect hemodynamic responses.

Recommendation Grade: II.a

Evidence level: B

Its routine use in apparently healthy children and adolescents, just for the purpose of stratify the risk of sudden death to exercise do not seem particularly useful.

Recommendation Grade: II.b

Evidence level: B

3.5. Echocardiogram

The pre-participation evaluation's goal is to prevent occurrences that could risk the integrity of individuals who practice recreational or competitive physical activities, prioritizing the identification of structural and/or functional cardiovascular variations that could increase the risk of morbidity and mortality during this practice40,60,61.

The use of complementary methods in the routinely cardiovascular evaluation is controversial, and the most relevant aspect of this strategy is the cost-efectiveness39. In this scenery, echocardiography has an essential role, by the possibility of diagnosing the main diseases implied in athletes' sudden death (Table 6) and differentiating athlete's heart physiological variations from hypertrophic cardiomyopathy pathologic hypertrophy in an innocuous, fast and relatively low cost way.

The sudden death in young athletes (12-35 years old) affects, mostly, afro-descendants individuals (>50%) and of the masculine gender (1:9). However, the risk of sudden death do not depend on the competition level (school, amateur, professional)63-65.

3.6. Recommendations

Institutions internationally known as the European Cardiology Society (ECS), the International Olympic Committee (IOC) and the American Heart Association (AHA) differ as to the definition of screening diagnosis exams to establish the public health investigation protocols66-68. This question's complexity lies in the relative infrequency of sudden death in young athletes (between 1:100.000 and 1:300.000 per year), besides the questionable efficiency in preventing its occurrence, being a fact that this event invariably causes repercussion and commotion in the society3,5.

Considering this scenery, the European Cardiology Society (ECS) supported by the consistent Italian experience, which monitored athletes for 25 years, determines in its screening program for individuals between 12-35 years old an initial exam composed by family history, physical examination, 12-lead ECG, and additional exams will only be performed with positive findings during the initial evaluation. (figure 1)17,69.


This strategy was effective in reducing in almost 90% the annual incidence of sudden death in athletes in the Italian northeast40.

The use of echocardiography in population programs in young asymptomatic athletes (12-35 years old) proved to be a high cost strategy and to the moment there is no population study with adequate follow-up to prove its efficacy63-65.

Regarding athletes with age superior to 35 years old, the standard protocol associated to questionnaire for specific evaluation of coronary artery disease should be applied. In men >40 years old and women > 55 years old should be considered the performance of functional test with exercise and in individuals with more than two risk factors for coronary artery disease (besides gender and age)1,70.

In case of positivity in the initial evaluation for coronary artery disease the investigation should proceed with more accurate exams, and echocardiogram at rest or stress echocardiography may be used, evaluating each individual case40,41.

Several studies have suggested the introduction of limited echocardiographic modalities with restricted two dimensional examination being performed in 5 minutes. The results show a good sensibility and specificity for the diagnosis of several illnesses related to sudden death in athletes, especially the hypertrophic cardiomyopathy implied in more than 30% of the cases of sudden death in young athletes71.

The recommendations in table 7 take into consideration the formulation of a population screening investigative strategy for public health policies and cannot be fitted to take decisions in singular cases, based in studies result and population records founded in cost planning programs.

Currently, professional athletes' associations and executive boards have their own protocols, due to legal and economic issues involved in the professional aspect40.

The pre-participation evaluation based in initial medical appointment and 12-lead ECG enables the identification of athletes under greater risk of sudden death, however it is not a definite screening strategy in this segment. Other more accurate diagnosis methods will have more space as initial screening exam in the future72-74,78.

Currently, echocardiography represents the confirmatory diagnosis modality to be performed after suspicion during initial pre-participation evaluation.

Recommendation Grade: I

Evidence level: A

There is no evidence for its routinely use in population screening programs in asymptomatic individuals.

Recommendation Grade: III

4. Children and adolescents group

Characterized by individuals who practice sports and physical activities in a very variable way, engaging mostly in recreational sports that reach moderate and high intensity levels, being as competitive as the athletic levels, even without systematic training, in certain situations they even surpass athletic levels. It is, therefore, impossible to discern between athletes and non-athletes in terms of intensity and energetic expenditure. They are children and adolescents that may compete systematically, sometimes already professionally linked with sports through clubs and sponsors of any nature. Sometimes they are submitted to intense physical and psychological stress, including, in some situations, by the parents or carers questionable positioning, when they should always be oriented as to inherent risks of such practice in this age bracket12,75.

The main causes of sudden death more often related to physical activities in this age bracket3 are: hypertrophic cardiomyopathy, congenital coronary artery anomaly, arrhythmogenic right ventricular dysplasia, Marfan syndrome cardiologic variations Marfan (aortic rupture), pre-excitement syndrome (WPW), Brugada syndrome, long QT syndrome, hemodynamic and arrhythmic repercussions of congenital heart diseases, myocarditis, comottio cordis, Chagas disease, infections and others like conduction dysfunction, hydroelectrolytic variations, sickle cell anemia, besides undetermined causes. In Brazil we don't have statistics epidemiologic records of sudden deaths related to sports practice in this age bracket, being restricted only to report of cases in publications. The above-mentioned order is therefore selective, and its prevalence in the population studied is not characterized.

A competitive athlete is one which takes part on an organized team or individual sport that requires systematic training and regular competitions aiming a goal, be it a prize or excellence in the modality. In general they are federates and/or members of sports clubs. Especially at this age bracket, the differentiation between "competitive" athletes and non-athletes, as mentioned before, is almost impossible.

The sports pre-participation evaluation has been developed and has become more formal, being a legal attitude in some countries, like Italy. An already established global consensus is that of the performance of a well-conducted clinical history, focusing mainly on symptoms and personal background as well as heart disease family history, mainly the occurrence of sudden death. The best strategy to perform the PPE on this age bracket is still a matter under discussion in several countries3,75. Such data may be obtained through validated questionnaires like the one of the American Heart Association (AHA) and of the Recommendations on Sudden Death of the International Olympics Committee (Lausanne), adapted on table 1.

4.1. Specific evaluation: Tanner stages l 79,80

In the growth and development process, we have a sequence of pubertal events that culminate with the emergence of secondary sexual characters resulting from hormonal maturation, systematized by Tanner and classified in five stages, taking into account, in the feminine gender, the mammary development and the quantity and distribution of pubic hair, and, in the masculine gender, the genital organs aspects and also the quantity and distribution of pubic hair. The evaluation of these parameters is essential, as the increase in muscle mass, height, weight, besides motor specialization are related to them. Although there is constancy in the Tanner stages sequence, the time to pass from one stage to another is much variable, and thus the sexual maturation may last from 2 to 5 years.

The great increment in physical growth that occurs in puberty, the known growth spurt, is the phase in which the individual grows most. Usually, the growth acceleration in the feminine gender occurs in the beginning of puberty, between stages 2 and 3, and always antecedes the menarche, which usually coincides with the phase of growth deceleration, and with stage 4. In the masculine gender, the acceleration usually happens in stage 3 and its peak is in stage 4.

Electrocardiogram at rest in this group follows the same controversy already described as routine examination. Because of the extreme regional differences in the country79,81 and taking into account the scientific evidences available, we recommend the ECG as follows:

Children and adolescents who are healthy and asymptomatic and have no important clinical fact observed in the initial medical evaluation with detailed clinical history and detailed physical examination, who meet the above-mentioned questionings.

Recommendation Grade: IIa

Evidence level: C

In the PPE of children and adolescents of 5 to 18 years old starting organized and competitive training in sports schools, fitness centers and clubs.

Recommendation Grade: I

Evidence level: A

In all children and adolescents with some suspicion of heart disease, detected with the data obtained during medical evaluation.

Recommendation Grade: I

Evidence level: A

4.2. Laboratory exams

Regarding the performance of laboratory exams, in the age bracket in question they assume some importance for the control of situations that are frequent in this population like parasitosis, anemia, alimentary mistakes and even some cases of malnutrition. We consider the exams listed below as passible of indication, always depending on previous clinical evaluation76,77:

Hemogram: hemoglobin analysis, associated to anemia and leukopenia, very common mainly in young people in training, and can cause an increase in the risk of superior aerial ways infection.

Iron and ferritin: it helps in the diagnosis of iron deficiency anemia and is also useful to detect overtraining syndrome, in which we find low levels of ferritin.

Sodium, potassium and chloride: detection of hydroelectrolytic disorders.

Lipid profile and glycemia: nowadays, due to constant mistakes in the nutrition of children and adolescents, it is becoming important in the primary prevention of hypercholesterolemia in adult age.

Chagas Disease Serology: it is still an endemic disease in Brazil and South America, cause of myocardiopathy, frequently sub-diagnosed, mainly individuals of a lower socioeconomic level.

Coprologic: identification of parasitosis.

Hemoglobin electrophoresis: evaluation of hemoglobinopathies like sickle cell anemia, important in the eligibility of competitive individuals.

Recommendation Grade: II

Evidence level: C

In selected cases with personal or family heart disease background, if variations in physical exam or electrocardiogram arouse, a deeper cardiologic evaluation is required before release for sports activity. This evaluation may include the performance of transthoracic echocardiogram, maximum exercise test and 24 hour holter77.

In official statement, the Sociedade Brasileira de Medicina do Esporte (Brazilian Society of Sports Medicine) recommends that, from the public health point of view, children and adolescents may take part in recreational physical activities of low or moderate intensity without the need of a formal pre-participation examination. When the goal is competitive sport or high intensity physical activity, the youngster needs a medical and functional evaluation, including body composition and aerobic and anaerobic capacity76.

Recommendation Grade: IIa

Evidence level: B

The American Heart Association, in document published in 2006 about exercise test in children and adolescents, describes among the main indications in this age bracket: 1- the specific evaluation of symptoms or signs induced or aggravated by exercise; 2- evaluate or identify abnormal response to exercise in children with heart diseases, pulmonary diseases or diseases in other systems, including the presence of myocardial ischemia and arrhythmias; 3- evaluation of the functional capacity for recreational or athletic activities77.

Recommendation Grade: IIa

Evidence level: B

The 36th Bethesda conference and the Recommendations for competitive sports participation in athletes with cardiovascular disease refers that the exercise test performance is indicated in the pre-participation evaluation of individuals with congenital heart diseases, valve diseases, myocardiopathies, arterial hypertension, arrhythmias and other conditions of suspected or diagnosed disease with the goal of evaluating functional capacity, symptoms, arrhythmias and orientate the allowed intensity for exercise81.

Recommendation Grade: I

Evidence level: A

4.2.1. Echocardiogram

Echocardiography represents a confirmatory diagnosis modality to be performed after suspicion during initial pre-participation evaluation. In children and adolescents it becomes a extremely useful exam in the presence of abnormalities in the physical exam that induce to suspicion of structural heart disease, especially when heart murmur is detected.

In cases in which ECG variations are detected, its performance is part of the arsenal for differential diagnosis of severe heart diseases that could potentially trigger sudden death during physical activity, as hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia1,12,79,80.

Recommendation Grade: I

Evidence level: A

To the moment there is no evidence to justify its routinely use in population screen programs in asymptomatic individuals.

Recommendation Grade: III

5. Group of carriers of cardiomyopathies and myocarditis

5.1. Hypertrophic cardiomyopathy (HCM)

Hypertrophic cardiomyopathy is an autosomal dominant disease characterized by myocytes myofibrillar disarray, followed by hypercontractility, hypodyastoly, asymmetric septal hypertrophy with or without obstruction of left ventricle outlet. This disease is the main cause of sudden death related to exercise and sports in individuals under 30-35 years old in North America, while in Europe arrhythmogenic right ventricular dysplasia prevails as main cause of sudden death in this age bracket3,82.

To the moment 12 genes are known which are implied in the genesis of this disease with more than 400 genetic mutations related to myocardial contractile proteins83. HCM carriers can be completely asymptomatic or present dizziness, syncope, especially related to exercise, dyspnea, palpitations and angina. Sudden death may occur to this patients due to ventricular and supraventricular arrhythmias (with pre-excitement or not), complete AV block, asystole and myocardial infarction3.

5.2. HCM complementary exams

5.2.1. Electrocardiogram

About 95% of the patients with HCM present electrocardiographic variations, the ST segment and the T wave being commonly affected. Around 50% of the electrocardiograms present signs of left ventricular overload84 and the pathologic Q waves are present in 30% of the cases. It should be noted that such finding may precede the pathologic hypertrophy that will be found lately in the echocardiogram85. The HCM Q waves arise by increase of the electrical forces generated in the hypertrophy areas. Its direction and magnitude are related to the vector that results from the areas with greater ventricular hypertrophy84. McKenna et al86 proposed a series of five echocardiographic, electrocardiographic and clinical criteria for the diagnosis of this disease, especially when its origin is in the family. Table 8 synthetizes the main electrocardiographic variations in patients with HCM.

5.2.2. Echocardiography

The differentiation between hypertrophy recurring from MHCM and that secondary to physical training (ventricular hypertrophy of the athlete's heart) requires the integration of several information with the pattern and distribution of the hypertrophy, parietal thickness, the size of the cavities, the evaluation of diastolic function by tissular Doppler and yet the family history. Furthermore, it is important to evaluate the echocardiographic response of athletes under suspicion to a sports untraining87. Regarding the prognosis, the identification of a septum bigger than 30 mm is a bigger risk factor for sudden death, especially among adolescents and young adults88. The echocardiogram enables the characterization of the type and extension of the compromising of the hypertrophic ventricle in an expressive number of cases, but magnetic resonance may be useful in those in which the echocardiography was not enough to reach diagnosis89,90.

5.2.3. Transthoracic Doppler echocardiogram

Class: I

Evidence level: B

Confirm the clinical suspicion of MHCM, determining the parietal thickness and the presence of dynamic gradient.

Investigate the presence of MHCM in first-degree family members.

Re-evaluation of clinical evolution and therapeutic interventions.

Myocardial contrast echo post-septal ablation to evaluate the size of the infarcted area.

Class II

Evidence level C

IIa: annual re-evaluation of family members of patients with MHCM between 12 and 18 years old. In individuals who are more than 21 years old the re-evaluation should be performed every 5 years;

IIa: tissular Doppler to differentiate MHCM from athlete's physiologic ventricular hypertrophy or hypertension pathologic hypertrophy;

IIb: stress echo with exercise in patients symptomatic to habitual routine exertion that do not put in evidence significant gradients at rest or with Valsalva's maneuver.

5.2.4. Transesophageal Doppler echocardiogram

Class: I

Evidence level: B

Patients with inadequate transthoracic window;

To evaluate valve compromising, mechanism and magnitude of mitral regurgitation when it is not clear in the transthoracic echocardiography;

Intraoperative evaluation in myomectomy and in septal ablation by alcoholization.

Class: IIa

Evidence level: B

Clarify the mechanism of an atypical mitral insufficiency.

5.2.5. Exercise tests and (HCM)

The exercise test (ET) presents independent value for the identification of patients under increased risk of sudden death. The presence of marked variations of the ST segment in patients with HCM may indicate ischemia without necessarily representing coronary infirmity. In this case the ET presents little diagnosis value, but could be a prognostic marker that should be taken into consideration84.

5.2.5.1. Indication of ET in patients with HCM

Class: I

Evidence level: B

Asymptomatic patients that do not present high risk criteria as associated element in prognostic stratification;

Asymptomatic patients that do not present high risk criteria and that wish to perform recreational physical activity;

ET as associated element in differential diagnosis between athlete's heart syndrome and HCM.

Class: IIa

Evidence level: C

Patients with doubtful symptoms not associated with other high risk criteria;

Sub-maximum ET in patients with implanted defibrillator that wish to perform low intensity physical activity aiming to evaluate functional capacity;

Sub-maximum ET in patients with implanted defibrillator that wish to perform low intensity physical activity aiming to evaluate heart rate response to exercise.

Class: III

Patients with high risk criteria without defibrillator;

Conventional ET aiming differential diagnosis between HCM and sports practitioner physiologic hypertrophy.

5.2.5.2. Role of exercise cardiopulmonary test in HCM

In athletes that are in the so-called gray zone the athlete's heart physiologic and the MHCM pathologic hypertrophy, the oxygen consumption and peak oxygen pulse measuring through the exercise cardiopulmonary test (MCET) may be of great help. Sports practitioners highly trained generally present values between 55-70 mL.Kg-1min-1. Sharma et al89 demonstrate that those athletes with no factual disease had a peak oxygen consumption significantly more elevated than athletes with HCM (66.2 mL.Kg-1min-1 versus 34.3 mL.Kg-1min-1). It is important to highlight that there wasn't superposition among the groups. Therefore, the investigators established as cut-off the cypher of 50 mL.Kg-1min-1 to distinguish HCM pathologic hypertrophy from that secondary to the athlete's heart.

5.3. Sport and HCM

Why is there low prevalence of HCM in high level athletes? The answer seems to be related to a natural selection process that excludes individuals with functional and structural variations secondary to HCM from the high intensity regular training required for someone to be an athlete89. Being a competitive athlete who has HCM is synonymous of sudden death? The answer is no. We all know cases of athletes who received a diagnosis for this infirmity when they already had quit their professional competitive activity or even while they were still on it. The problem is that intense exercise may be a trigger to launch severe arrhythmias, increase in the obstruction of left ventricle outlet and/or ischemia by compression of small vessels (possible fibrosis by repetitive ischemias), during the training and competition periods. As a matter of fact, there are no clinical or genetic studies to ensure a good prognosis.

When this infirmity is diagnosed, the rule to be followed has been the exclusion from competitive sports91. However, it is possible that some exceptions be made for asymptomatic athletes without high risk criteria that compete in sports like golf, cricket, bowling and shooting.

The recommendation for exclusion from competitive sports remains for athletes with positive genotype, but with negative phenotype for HCM, although currently we do not have enough evidences available, as they do not have clinical diagnosis nor present risk criteria for HCM. However, some mutations in the troponin gene (chromosome 1) may not express themselves as macroscopic ventricular hypertrophy, but express histopathologic variations in the myocardial muscle fibers, being of bigger risk for sudden death88.

In athletes with positive genotype and negative phenotype that practice acyclic sports (drastic variations in speed with unexpected accelerations and decelerations, e. g. soccer, basketball, tennis), there seems to be more risk than for those who compete in cyclic sports (jogging, swimming, cycling)88.

5.4. SD risk stratification in hypertrophic cardiomyopathy

There are criteria suggested by Rickers et al90 and Colin Lizalde92 to establish risk factors for SD in HCM carriers. Those criteria are found in table 9.

5.5. Recommendations for athletes with HCM diagnosis

Athletes with probable or unequivocal HCM diagnosis should be excluded from most competitive sports, with possible exception to those sports of low dynamic and static component (IA). This recommendation does not depend on age, gender, phenotypic appearance of the athlete, presence or not of symptoms, obstruction of left ventricle outlet, treatment with drugs, septal ablation, use of pacemaker or implanted defibrillator86.

Class: I

Evidence level: C

Patients with HCM diagnosis should be excluded from sports competitions of competitive feature. Those classified as low risk may participate on golf, pool, bowling and shooting;

Recreational sports that require high intensity or drastic variations in intensity are not recommended;

Individuals with positive genotype and negative phenotype (without clinical evidence of disease) may participate in sports as long as they are periodically evaluated;

Patients without high risk criteria and with normal exercise test may perform cyclic recreational physical activity of low intensity;

Patients with implanted defibrillator should be excluded from contact sports.

Class: IIa

Patients without high risk criteria and with normal exercise test may participate on recreational contact sports of low intensity and low volume.

Class III

Asymptomatic patients with HCM, even if of low clinical and genetic risk, high functional capacity and without family history of sudden death may participate in high intensity competitive sports.

6. Group of carriers of arrhythmogenic right ventricular dysplasia (ARVD) or left ventricular cardiomyopathy

It is a variation in the heart muscle of genetic cause by variation in the desmosome formation that is characterized by pathologic fibro-fatty replacement of right ventricular myocardium, and it may manifest also in the left ventricle92-94. This infirmity is an important cause of sudden death in youngsters, including competitive athletes. This disease has been described as the main cause of sudden death in athletes in the region of Veneto, Italy93,94. As highly trained athletes may have right ventricular hypertrophy besides a variety of variations in depolarization, repolarization and conduction of nervous stimulus, the differential diagnosis between athlete's heart syndrome and ARVD must always be performed. The echocardiogram may present technical limitations to access right ventricle images, and its structural and functional analysis may be damaged95,96. The cardiac magnetic resonance is a non-invasive image technique that has shown itself to be promising96. The demonstration of global or segmental dysfunction of right ventricle or the substantial increase of this cardiac chamber cavity associated to myocardial tampering and presence of fibrosis (MR delayed equilibrium) gives support to the ARVD diagnosis83,97-100.

6.1. SD risk stratification in arrhythmogenic left ventricular dysplasia

Some aspects must be considered in the SD risk stratification in arrhythmogenic right ventricular dysplasia.

Age Class: IIb, Evidence level: C

Age - There are divergent opinions on whether the appearance of symptoms in age to 20 years old would be of more risk.

Syncope Class: IIb, Evidence level: A

Syncope - great studies could not demonstrate a relation with increase in mortality.

ECG AR Class: IIA, Evidence level: C

High resolution electrocardiography - the presence of late potentials seems to positively co-relate with the seriousness of the disease and the occurrence of sustained ventricular tachycardia and ventricular fibrillation, when right ventricular dysfunction is present. However, new studies will be required to predict the development of ventricular arrhythmias.

Echocardiography Class: I, Evidence level: C

Echocardiography - sudden death is more frequent in patients with right ventricular diffuse dilatation and in those in who the left ventricle is involved, because its dysfunction seems to be a marker of risk of ventricular fibrillation and sudden death.

Programmed electrical stimulation Class: III, Evidence level: C

Programmed electrical stimulation - the induction of sustained ventricular tachycardia varies from 57% to 94% in patients with monomorphic sustained ventricular tachycardia, but is low in patients who present ventricular fibrillation or left ventricle involved. When the induction occurs in the presence of right ventricular dysfunction, the predictive value for sudden death is bigger.

Magnetic Resonance Class: I, Evidence level C

The MR identifies the right ventricular dysfunction, walls tapering and presence of delayed equilibrium (myocardial fibrosis) and the presence of microaneurysms.

Biopsy: little used in our milieu

24 hour Holter, exercise test and QT dispersion Class: III, Evidence level: C

24 hour Holter, exercise test and QT dispersion do not present value to identify patients in risk of sudden death as well as the type of ventricular arrhythmia.

Exercise - there are evidences that the exercise can be a triggering factor of potentially serious symptoms and arrhythmias, suggesting that these consequences depend on the sympathetic tone, especially in athletes99,100.

Finally, it is important to highlight that the most efficient way of detecting silent cardiac pathologies that sometimes may be the cause of sudden death related to exercise and sports is a careful pre-participation evaluation and that many variations found in routine exams and that may be confused with heart diseases are physiological adaptations resulting from intensive and regular training, composing the characteristics known as athlete's heart syndrome, cardiomegaly, conduction and rhythm disturbances and variations of ventricular repolarization in the electrocardiogram97,98,100,101.

Recommendations for athletes with arrhythmogenic right ventricular dysplasia diagnosis

Patients/athletes with unequivocal diagnosis of right ventricular dysplasia should be excluded from the practice of competitive activities92,93.

7. Group of myocarditis carriers

It is an infirmity associated to a heterogeneous clinical profile, being the probable cause of sudden death in some athletes73,102,103. Usually, myocarditis is result of an infection, but it can be associated to alcohol or drugs abuse103. Sudden death may occur in its active phase or even when there is already a scar in the myocardium, consequence of complex arrhythmias deflagrated from an instability electric substrate. In the athlete we can have left ventricular increase by the disease per se, by hypertrophy secondary to physical training or by a mix of both. The differential diagnosis in this cases is made by the athlete's clinic (presence of arrhythmias, palpitations, pre-syncope or syncope or yet by systolic dysfunction). The cardiac magnetic resonance and the performance of endomyocardial biopsy in certain circumstances can help in the diagnosis. It is important to highlight that several studies have shown H1N1 flu as responsible for a kind of serious myocarditis, almost always accompanied by cardiogenic shock. Recently, the organizing committees of the Singapore Asian Games and of the Winter Olympics in Canada recommended that all athletes participating in these events came to these countries vaccinated against swine flu. We also remind here of the possibility of myocarditis by dengue virus in our country because of the constant outbreaks of this disease in Brazil.

7.1. Recommendations for athletes carriers of myocarditis

Athletes diagnosed with myocarditis should be removed from all competitive sports and undergo a recovery period of at least 6 months after the onset of clinical manifestations. These athletes may be released for training and competition after 6 months if:

Left ventricular function, ventricular wall motility and cardiac dimensions return to normal (based on echocardiographic and radionuclide studies at rest and with exertion);

Frequent or complex forms of ventricular and supraventricular arrhythmias and clinically relevant arrhythmias are absent;

Inflammatory markers and heart failure are standardized;

The ECG at rest is standard, although the persistence of ST alterations criterion alone is not impediment to return to training and competitions.

8. Group of carriers of coronary artery disease

The ischemic heart disease has declined over the decades, in Brazil. In 1980, the standardized death rate from coronary artery disease (CAD) was 65/100,000 inhabitants, and in 2005 the data showed 46/100,000 inhabitants104. Coronary artery disease accounts for the majority of the events of sudden death associated with exercise in people aged over 35 years old105. The mechanisms responsible for triggering coronary events during vigorous physical activity result from increased sympathetic activity and increased release of catecholamines, platelet adhesion and activation (leading to risk of thromboembolic events), electrolyte abnormalities by elevated potassium (serving as a trigger for ventricular tachyarrhythmias) and complications as subendocardial ischemia, leading to plaque rupture106, 107 or possible plaque erosion108, 109, facts implicated as immediate causes of exercise-related events in adults. In the young individual, the leading cause of sudden death during sports is hypertrophic cardiomyopathy110.

In the last decade, the practice of physical activity has been recommended as part of intervention in primary and secondary prevention of coronary artery disease by providing a steady improvement in functional capacity (Class I) alleviating angina at rest (Class I), with improvement in the severity of exercise-induced ischemia (Class IIa) and the reduction of some cardiovascular risk factors (Class IIa). Proposed mechanisms and described the benefits of physical exercise in CAD ​​are: increment of endothelial function, regression of atherosclerotic plaque formation and increased flow of collateral circulation, vasculogenesis, remodeling and decreased apoptose108. However, for this population start a physical practice is needed as to the stratification chance of having an event cardiovascular 109, 111. The algorithm for the stratification of the patient begins with history taking and physical examination and the subsequent application of a progressive exercise test and maximum for the induction of cardiac arrhythmias, ischemic stress induced ventricular dysfunction and atrioventricular conduction disturbances. Data provided by exercise testing will guide the prescription of physical practice, you must follow some basic principles, such as frequency, duration, intensity and type of exercise112, 113.

Type of exercise: aerobic exercise program are those that yield better benefits for the cardiovascular system and control of risk factors. This type of program is characterized by cyclical exercises of large muscle groups, such as walking, jogging, swimming, cycling, dancing, aerobics, among others.

Frequency of exercise: the recommended exercise frequency is 3-5 times a week, and in some groups (hypertensive and obese) the frequency can be up to 7 times a week.

Exercise intensity: the best way to measure the intensity of physical exercise is through heart rate, determined by maximum exercise testing (ET). The training heart rate should be between 70 and 85% of maximal HR obtained in ET and can be used to Karvonen formula (HR training = (HR maximum - HR at rest) x% of HR reserve recommended + HR at rest) or the corresponding heart rate between the anaerobic threshold and respiratory compensation point, assessed by spirometry. In beginners patients the range 50-60% HR reserve and 60-80% HR reserve for contingent should be used. Patients on beta-blockers should associate with HR training determined by functional testing to feel exertion by the Borg scale.

In muscular endurance exercises for the major muscle groups, you should use 40-60% of maximum voluntary contraction (low to moderate intensity) with 8-15 repetitions, three sets to one, or empirically, starting with low loads and evolving until the sense of effort is low to moderate.

Duration of aerobic exercise: 30-60 continuous minutes

8.1. Anamnesis and physical examination

Data supplied by anamnesis and physical examination are essential for the evaluation of coronary artery disease, whether it is stable course or not, helping to stratify the individual and exercise schedule (Class IIa, Evidence level B).

8.1.1. Clinical history

The clinical history is extremely important in the stratification of candidate patient with physical practice supervised or not, guiding the physician regarding the evolution and the current stage of the disease. You can identify the presence or absence of symptoms (pain, fatigue, shortness of breath) and with what degree of effort they are triggered. One should make an inventory regarding medications, as they may influence the dynamics of programming and practice exercises, must abide by certain characteristics of the symptoms that drive the probability of the presence of angina as:

Location: chest, retrosternal shoulder, epigastrium, cervical, hemithorax, back;

Type: constrictive, tightness, heaviness, tightness, discomfort, burning, stabbing;

Irradiation: upper (right, left, both), shoulder, jaw, neck, back, epigastrium;

Trigger factors: physical exertion, sexual activity, position, power, breathing, emotional component, spontaneous;

Factors relief, rest, sublingual nitrate, analgesic, food, antacid, position and apnea;

Associated symptoms: sweating, nausea, vomiting, pallor, dyspnea, hemoptysis, cough, pre-syncope and syncope.

The classification of chest pain becomes fundamental, and divide this into three groups: typical, atypical and not cardiac114, 115.

Typical angina (definite)

Triggered by exercise or emotional stress;

Retrosternal discomfort or pain;

Relieved by rest or nitroglycerin

Atypical angina (probable)

Presence of only two factors above

Non-cardiac chest pain

Presence of only one or none of the above factors

Besides clinical history of chest pain risk factors for CAD should be considered in the stratification of individuals, such as diabetes, hypertension, dyslipidemia, smoking, family history of premature CAD (<55 years for men and <65 years for women), inactivity and stress.

8.1.2. Physical examination

Physical examination may be normal or show some changes identified by ectoscopy, palpation and auscultation, such as a stroke deflected to the left, the presence of an accessory heart sound (and B3 or B4), identifying a blow that may give clues about " status "of the heart. A blood pressure measurement should be performed in both arms, and in orthostatic, sitting and lying and at least one lower limb, with the goal of postural hypotension or identify certain problems that can cause there is a significant difference in blood pressure among members. The physical examination is usually normal in patients with stable angina27. Presence of atherosclerosis at other sites can provide data for an investigation of CAD in some individuals with lower limb pulses decreased, arterial stiffening and abdominal aortic aneurysm. Despite the physical examination in subjects with CAD be little instructive, complete workup, particularly the cardiovascular system should be performed carefully, because it can provide important information on other associated conditions such as valvular disease, hypertrophic cardiomyopathy and other.

8.2. Echocardiography in chronic CAD:

The transthoracic echocardiography has been used as an important diagnostic tool in coronary artery disease as well as a method for the evaluation of prognosis in these pacientes30. In patients clinical history and electrocardiogram are inconclusive, echocardiography can demonstrate reversible abnormalities of wall motion or not, identifying areas of hypokinesia, acnesia, dyskinesia and aneurysms (Class I) and extent of these changes, providing also an important variable in assessing left ventricular function, ejection fraction (Class I) 116.

8.3. Benefits of exercise on coronary disease

There are several physiological benefits elicited by exercise in patients with stable CAD. Table 10 summarizes the benefits for level of evidence.

8.4. Risk stratification for inclusion of patients in exercise and cardiac rehabilitation programs

The risk of patients in exercises and cardiac rehabilitation programs can be categorized according to table 11117.

8.5. Computed tomography, magnetic resonance and athlete's heart

Despite the great usefulness and practical applicability of Doppler echocardiography in the evaluation of different heart diseases, there are situations where it is necessary to use other imaging modalities for the diagnosis and also for risk stratification. In particular in the evaluation of athletes with suspected heart disease using these methodologies can be important, such as the distinction between mild hypertrophic cardiomyopathy and myocardial hypertrophy secondary to sport activity118, 119.

The complexity of the cardiac movements requires that equipment intended to produce image be sophisticated enough to reproduce the anatomy of the heart without artifacts resulting from the mobility of the heart itself 118. The magnetic resonance equipment equal or greater than 1.5 Tesla can be used for this end118.

Tomography data available in the literature are based on studies of equipment of 64 rows of detectors. Systems with at least 32 rows of detectors can be used effectively, there is only a need for more adequate preparation of the patient, to improve the quality of images obtained118.

The professionals involved should have received appropriate training in specialized centers, to ensure greater safety and better quality of examinations performed118.

The use of magnetic resonance imaging and computed tomography for the risk stratification of asymptomatic individuals and release for sports is still limited. There are no jobs available in the literature assessing the potential contribution that the resonance could have that effect. In addition, CT is at least in part, its limited application because it uses ionizing radiation, which restricts its indiscriminate use, especially in the younger population. However, this technology has definite role in some conditions that may be present in the evaluation of asymptomatic wanting to do sports activities118, 120,121.

The presence of signs suggestive of myocardial ischemia in young people may be related to the existence of anomalous origin of a coronary artery. This is a condition in which the use of CT or MRI is fundamental and well defined122.

In older individuals who wish to practice physical activities, CT can also help, especially if there is conflict between the results of other noninvasive tests with regard to the existence of silent myocardial ischemia. The most common situation is when there is stress test compatible with the presence of ischemia and myocardial scintigraphy normal or doubtful. In this condition, the high negative predictive power of the test may have a fundamental role to exclude the presence of obstructive coronary disease or to indicate the need for if further invasive diagnostic investigation.

The high spatial resolution of CT also enables it to be used for diagnosis of other conditions such as congenital heart disease, cardiomyopathies, and vascular anomalies, but also those ends are achieved with MRI, which has the added advantage of not using ionizing radiation118 .

Other medical conditions that may involve the use of MRI for release for sports involve the existence of underlying heart disease that has not presented clinical manifestation previously. In these cases, the clinical recommendations for the use of resonance are within the regulations established in habitual cardiology118.

For evaluation of heart disease in athletes who compete in categories aimed for people over 40 years and with conflicting non-invasive tests118, tomography can be a useful test, because it has a negative predictive value greater than 97% and may be useful for rule out obstructive disease. Other clinical conditions may need further investigation, such as arrhythmias or the development of changes to electrocardiogram120.

The heart of the professional athlete or amateur elite to resonance is characterized by having larger dimensions mass, end-diastolic volume and end-systolic volume. Such changes, however, occur without altering ejection fraction, regional contractility or contraction pattern of the ventricles. This aspect should always be considered as cases of hypertrophic cardiomyopathy usually show changes in the pattern of cardiac contractility, even if there is slight increase in thickness of the ventricular myocardium. Thus, the shape of ventricular twist in both the longitudinal and in the transverse plane, is preserved in athletes, even elite, which does not occur in cases of hypertrophic cardiomyopathy119.

In cases of heart adaptation to stress found in elite athletes the degree of hypertrophy that affects the left ventricle differs from that which interests the right ventricle, being more pronounced in the cavity systemic. Furthermore, when there is a relationship between physiological hypertrophy volumes, dimensions and ejection fraction of the left ventricle compared to the right ventricle are comparable in athletes and sedentary individuals without structural heart disease119, 120.

A major cause of death in young athletes is hypertrophic cardiomyopathy condition that should always be remembered and researched evidence of abnormalities that arise for this subgroup. The literature reports cases there are up to 13 mm thickness in the left ventricular myocardium as an adaptive response, especially in the case of elite athletes male. It is important to remember that in different sports among them weightlifting, rowing, cycling, swimming, marathons and professional football athletes may also have significant increases of cardiac dimensions, without presenting heart disease121.

Hypertrophic cardiomyopathy resonance can also understand the presence of delayed enhancement, which may indicate the existence of fibrosis and be present in varying degrees, regardless of the clinical manifestation of heart disease. Some studies have associated this image pattern to the occurrence of arrhythmias and changes to the dilated form of the disease, a finding that should raise caution in case driving118, 119.

The arrhythmogenic also shows up as a challenge in athletes, especially due to the wide variety of image patterns that it can present. It must be remembered that the simple presence of fat tissue in the myocardium is not pathognomonic of that entity, since the presence of fat in heart muscle may be a consequence of other inflammatory conditions, degenerative and ischemic besides being a usual finding in patients over 65. The diagnosis of dysplasia is made from the existence of regional abnormalities in the ventricles, and the existence of areas of delayed enhancement in the ventricular walls, reflecting the presence of inflammation and / or myocardial fibrosis. The combination of these findings, with or without the presence of fat associated, allows for the identification of dysplasia. Important data such cases arises from the fact that due to the evolving nature of this entity, the diagnosis involves the removal of sports activities121, 122.

Another condition that has clinical importance is myocarditis. This entity can have your event facilitated by the existence of conditions that lead to decreased immune activity, such as occurs when there is excessive training for a long period, habitual condition of elite athletes. The resonance has been shown to be an effective evaluation of these patients revealed the presence of late enhancement, even in cases where there is no change in ventricular contractility, which allow defining the presence of these changes. Some authors mention that the image pattern may even allow them to infer the causative agent of entidade121. Changes in the presence, extent and intensity of delayed enhancement in these conditions are important prognosis121, 122.

Resonance and computed tomography can be important allies in risk stratification and evaluation of structural heart disease in athletes. Although its routine use is to essentially complement evaluation by clinical examination, ECG and echocardiography may, under some conditions such as anomalous origin of the coronary arteries, in search of arrhythmogenic dysplasia and myocarditis, they can compose the line front and are arguably important stages of the diagnostic evaluation table 12.

9. Risk stratification of SD-related exercise / sport in arrhythmogenic genetic syndromes.

9.1. Canalopathies

The canalopathies are inherited arrhythmogenic heart disease, no structural, caused by genetic alterations that result in dysfunction of cardiac ion channels, exposing their patients to a risk of sudden death123. Canalopathies The best known are the long QT syndrome (LQTS), short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia TVPC. The sinus node disease and disease Lenegre or conduction system disease are also examples of canalopathies.

The ion channels, ion currents passing through these channels, proteins that bind to cell membrane structure myocardial and the junctions between these structures are part of electrical impulse formation and transmission of these impulses throughout the heart muscle so synchronous generating the potential cardiac action124, 125. The performance of each of these functions is determined by different genes. Mutations that occur in these genes cause specific dysfunctions and diseases known to cause canalopathies126, 127. The ion channels present on the cell membrane allow entry and exit of ions, following a voltage gradient. The change caused by genetic mutation in each of these channels may generate a gain or loss of function. There are ion channels responsible for depolarization and repolarization of the cell membrane. The first channel from right to left, called electrogenic channel, allows entry of three sodium ions (Na +) to each output of calcium ion (Ca2 +) across the membrane. The depolarization channels are: 1) INa, sodium channel carried by SCN5A gene whose mutations that cause gain of function resulting in LQTS 3, while the loss of function causes Brugada syndrome and congenital sinus node disease, 2) channel iCal L-type calcium; 3) INa / Ca channel sodium and calcium channel called electrogenic. The channels involved in myocardial repolarization of the cell are: 1) IK1 potassium channel KCNJ2. This channel is responsible for the output of potassium at the end of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 3. while the loss of the function of this channel results in long QT syndrome type 7 and Andersen syndrome. 2) ITo1 and ITo2 responsible for early repolarization - phase 1 of the action potential, 3) IKr - Potassium Channel - Gene KCNH2/KCNE2. This channel is responsible for the output of potassium in the beginning of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 1. 4) IKs potassium channel gene KCNQ1/KCNE1. This channel is responsible for the output of potassium in the middle of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 2. The loss of function of the KCNQ1 gene (the alpha subunit which forms pores in the cell membrane) and the KCNE1 gene (which encodes the protein which forms the slow component of the IKs channel) causes long QT syndrome type 1.

9.2. Long QT syndrome

The long QT syndrome is the prototype of canalopathies. Reported for more than 50 years, initially as autosomal recessive syndrome of Jervell and Lange-Nielsen128 (congenital deafness, increased QTc interval and syncope or sudden death) and subsequently autosomal dominant Romano-Ward syndrome (deafness without prolonged QTc ), the LQTS showed an inherited trait of sudden death in patients without structural heart disease. Currently, there are several types of known LQTS, mutations in certain genes that cause distinct changes in ventricular depolarization and repolarization (Table 13).

Different mutations in the same gene may result in loss or gain of function and, consequently, different syndromes. LQTS: long QT syndrome, AD: autosomal dominant, AR: autosomal recessive.

The typical clinical features of LQTS include syncope or sudden death associated with QTc interval prolongation and ventricular tachyarrhythmia presence and torsades de pointes. Classically, there are triggers of syncope in LQTS, adrenergic activity in LQTS 1 and sudden awakening or auditory stimulus in LQTS 2. However, there is a wide variety of presentations, the carrier of the mutation may be asymptomatic since, with no increase in QTc, even have syncope or sudden death in the first days of life. Therefore, we developed diagnostic criteria for scoring changes on 3 main criteria: clinical history, family history and electrocardiographic variation129 (table 14).

9.2.1. Genetic alterations of the long QT syndrome (LQTS)

The genetic alterations are known in approximately 60% of clinical cases of LQTS. They are currently 7 known genes responsible for these syndromes. However, hundreds of mutations have been described, which is the cardiac canalopathy with the highest number of mutations described130.

The most common mutation occurs in the gene KCNQ1, responsible for LQTS 1 (40-50%) and the syndrome of Jervell-Lange-Nielsen type 1. This mutation causes a loss of function of the potassium current IKs, which plays an important role in cellular repolarization and QT interval adaptation to heart rate. The KCNE1 gene, whose mutation causes LQTS5, is much less frequent (2-3%) and is also responsible for the function IKs 123, 131, 132.

The KCNH2 gene (HERG) encoding the alpha subunit of potassium channels rapid and KCNE2, which encodes the beta subunit are responsible for the rapid entry of potassium during the third potential action131, 133. The loss of function of the alpha subunit represents 40% of the genotyped LQTS and is responsible for LQTS 2134.

The LQTS 3 represents approximately 10% of all diagnosed mutations in LQTS occurs by changes in the SCN5A gene, which produces a gain of function sodium continuous input during the plateau phase, facilitating premature depolarizations of the cardiac cell. Hundreds of other mutations have been described. However, clinical applications of these mutations to identify treatment and monitoring of patients and relatives of LQTS are restricted to known forms125.

9.2.2. Risk Stratification in LQTS

Genetic analysis has been widely used in risk stratification and specific therapeutic interventions in patients with prolonged QT interval, as well as their families, to identify patients with normal QT interval.

The recommendation of strategies for risk stratification and treatment for medical conditions are infrequent, and therefore the data obtained on the disease cohort studies, some with large number of participants, with follow along, others with more limited or Following narrower limits the level Evidence for the recommendations to B.

The most robust risk marker identified is a previous episode of aborted sudden cardiac death and its most common cause, are episodes of polymorphic ventricular tachycardia, or not degenerating into ventricular fibrillation. Patients who experience this condition are 12.9 times greater risk of new episodes of sudden death. Prior Syncope is also a risk marker extremely disadvantageous135.

For asymptomatic patients were identified as risk factors: QTc> 500 ms for patients with LQTS 1 and 2 male patients in LQTS 3, regardless of the QT interval. Mutations involving a gene segment encoding the pore of the channel are also linked with poor prognosis. So once again it is clear the value of genotyping in patients with this syndrome. The presence of sudden death in the family was not a marker of increased risk of events136.

9.2.3. Recommendations

Restriction of physical activity: although in LQTS 2:03 episodes of ventricular arrhythmia are not related to effort, it is recommended that all affected patients avoid physical exertion competitive. This recommendation is particularly important in the case of swimming for LQTS1. In 2 patients with LQTS should avoid acoustic stimuli especially during sleep, such as alarm clock and telephone. Obviously, drugs known to prolong the QT interval should not be used, as well as drugs which reduce the plasma levels of potassium and magnesium (interventions Class I).

All patients with prolonged QT interval should receive beta-blockers, although the protection is incomplete for patients with LQTS 2 and 3 (intervention Class I). For patients with mutation, but with normal QT interval, also recommended the prophylactic use of beta-blockers (IIa)137, 138.

The pacemaker has been considered an adjuvant therapy, always in conjunction with beta-blocker 139, 140. It is effective in preventing recurrence of torsades de pointes, although its role is not well defined. The mechanisms involved are suppression of pauses preceding and the precipitate torsades de pointes, and by shortening of the QT interval. In general, is indicated for the prevention of severe bradycardia or pauses resulting from the use of beta-blockers in patients who cannot tolerate adequate doses, who remain symptomatic despite its correct usage or when there is evidence of pause-dependent arrhythmias. Certain genotypes of LQTS may benefit more than others with pacemaker implantation. The effect of bradycardia on transmural dispersion of repolarization was more pronounced in LQTS3 and LQTS2 and inexpressive in LQTS1. The correct programming of the pacemaker is important in preventing arrhythmias in LQTS. The stimulation at higher frequencies shorten the QT interval and reduces the dispersion of ventricular repolarization. The minimum frequency limit should be set to 70 to 80 bpm and can be increased in situations of higher risk, such as in surgical procedures and post-partum period. The occurrence of atrioventricular functional in some patients (especially children with very prolonged QT) immediately before the start of torsades de pointes causes the DDD pacing mode most widely used. There is no consensus on the best programming on the frequency response and time delay atrioventricular. Some of the programming features that enable drops low heart rate should be turned off, as hysteresis and sleep function.

The implantable cardioverter-defibrillator is recommended for all survivors of sudden death with good functional status and life expectancy of greater than 1 year (Class I recommendation). Patients may present syncope despite beta-blocker therapy may also benefit from defibrillator (IIa). The defibrillator may be considered in patients at high risk for sudden death, such as LQTS 2 and 3, even asymptomatic (Class IIb recommendation)141, 142.

The sympathetic denervation may be considered for patients with syncope or polymorphic ventricular tachycardia that are already on beta-blockers (IIb)143, 144.

9.3. Short QT syndrome

In this disease there is a shortening of repolarization, favoring the genesis of ventricular arrhythmias by reentry. Characterized by a short QT interval QTc <320 ms with peaked T waves, which can have increased amplitude, with its ascending phase and normal phase descending rapidly125, 127,145,146. As clinical parameters for diagnosis are still unclear, genetic analysis is useful to confirm the diagnosis in suspected cases. Mutations in three genes were described KCNH2, KCNQ1 and KCNJ2 all resulting in a gain of function channel IKr, IKs and IK1, respectively, and determining the short QT syndrome type 1, 2 and 3. As the number of patients with a confirmed diagnosis is low, is not yet determined whether any specific type of mutation determines a worse prognosis. Risk factors for the occurrence of arrhythmias are not known.

Treatment for this condition is still a matter of controversy. In patients with mutations in the KCNH2 gene, showed the use of quinidine prolong refractoriness and suppress arrhythmia induction during electrophysiological study 146 for the other mutations, their utility has not been established. The disease seems to have high lethality, however, there may be a diagnostic bias only in serious cases. The use of the defibrillator may be considered, however, one must keep in mind the downside of the possibility of inappropriate shocks for the phenomenon of double counting (QRS complexes and T waves)147, 148.

9.4. Brugada Syndrome

This syndrome is characterized by the occurrence of syncope or sudden death caused by polymorphic ventricular tachycardia in structurally normal hearts. His most peculiar aspect is the occurrence of ST-J point in right precordial leads V1 to V3, although this phenomenon has already been described in inferior leads149. Perhaps influenced by gender 90% of cases occur in men. Until now, only been identified in the SCN5A gene mutations that are present in about123 1/3 of affected123, 150. Clinically, the disease manifests with syncope or sudden death, mainly in the third or fourth decades of life. Fever is a trigger for arrhythmias.

Risk stratification in individuals with ST-J point that occurs spontaneously have a worse prognosis compared to those in the typical pattern was only observed after infusion of flecainide, procainamide or ajmaline. The occurrence of syncope associated with the occurrence of spontaneous elevation, increased risk of sudden death six times. The presence of sudden death in the family has not proved useful for risk stratification as well as the detection of gene mutation SCN5A.151, 152

The use of programmed ventricular stimulation for risk stratification is controversial. In the series of Brugada et al 152, the absence of inducible arrhythmias during electrophysiological study had a negative predictive value of 93% at 3 years for clinical events. However, the number of patients and cols.136 Priori, electrophysiological studies had low accuracy for predicting events. Currently, the use of programmed ventricular stimulation is Class IIb indication for risk stratification in asymptomatic patients.153, 154

As therapeutic recommendations, the use of defibrillator is indicated for Class I patients recovered from sudden death. It is Class IIa indication for patients with ST spontaneous point that J expressed or syncope who had previously documented ventricular tachycardia.

The infusion of isoproterenol can be useful in the treatment of thunderstorm (Class IIa) as well as the use of quinidine for that situation (Class IIb)

9.5. Catecholaminergic polymorphic ventricular tachycardia

The disease is characterized by episodes of polymorphic ventricular tachycardia, triggered during stress or emotions in children and young adults who have hearts structurally normal155, 156. The ECG at rest is normal, except for a relative bradycardia for age and frequent presence of wave U. It manifests clinically as syncope triggered by physical or emotional stressful situations155, 156. Two mutations were described in RyR2 and CASQ2 genes that encode the ryanodine receptor, protein responsible for calcium release from the sarcoplasmic reticulum, and calsequestrin protein which binds to calcium in the sarcoplasmic reticulum. The genetic analysis does not contribute to risk stratification, but it is important to identify carriers of the mutation that has not yet manifested symptoms.

The typical manifestation is the occurrence of arrhythmias during exercise, most often when they reach 120-130 beats per minute, starting with isolated ventricular premature beats, progressing to episodes of non-sustained ventricular tachycardia and sustained, if effort is maintained (Figure 3 ).

The use of beta-blockers is very effective in reducing symptoms, and indication Class I to patients with clinical manifestations, IIa Child carriers of the mutation, but that did not exhibit symptoms, and Class IIb for adults in the same situation157, 158.

The defibrillator use in Class I indication is retrieved from Class IIa and sudden death in patients who remain with sustained ventricular tachycardia or syncope despite beta-blocker therapy.

It has been recently suggested treatment with cardiac denervation friendly left as a therapeutic alternative for patients who cannot make use of beta-blockers. The mechanism of action of this therapy seems very attractive for these patients, since it reduces cardiac catecholaminergic stimulation, which in theory would reduce the triggering stimulus arrhythmia. Some authors have reported promising initial experiments, but there is little evidence that this alternative is incorporated routine, currently only recommended in cases of failure or contraindication of beta-blockers.

The recommendations regarding the release for sports activities take into account the type of activity and the diagnosis established from the pre-participation evaluation and any additional tests that may be necessary. Sports are categorized into static and dynamic according to table 15. The recommendations are summarized in Tables 16, 17 and 18.

10. Basic life support in the athlete

10.1. Sudden death in athletes

Although rare, sudden death (SD) in sports is an event that causes public outcry, especially when it involves high-performance athletes. Statistics from different countries show that its prevalence varies from 0.28 to 1 per 100,000 athletes159, 160. Different structural and arrhythmogenic variations are responsible for cases of sudden cardiac arrest in athletes, however, the most common is hypertrophic cardiomyopathy, accounting for 25-36% of cases159, 160. Vigorous exercise linked to heart disease seems to be the hidden trigger that triggers the arrhythmia responsible for cardiopulmonary arrest (CPA).

Guidelines nacionais3 internacionais161 and advise the pre-participation cardiovascular screening, which is, in general, in a detailed history, physical examination and 12-lead electrocardiogram. Such a screening would be able to detect approximately 90% of athletes who had a fatal event, although there are reports of the sportsmen SD victims who did not have any structural or condução162 isolation, screening is not able to significantly decrease the number of deaths from sudden cardiac arrest in this risk group, mainly by not performing this evaluation by athletes and the possible false-negative results, necessitating the establishment and strengthening of a second pillar, basic life support.

10.2. Initial care to the athlete

Care for better emergency care are summarized as a set of actions taken in the first minutes that follow after a sudden event. These actions can be summarized in two pillars: the organization and planning of the emergency care team, at the places where physical activity is performed, and training of first responders in CPR and handling of automated external defibrillator (AED). Sites where physical activities, such as training centers, schools, colleges, gyms, etc.. must have an emergency response plan well organized, with professionals trained in basic life support (BLS) and communication services with fast and effective prepared to perform advanced life support in cardiology (ACLS).

Effective treatment of an athlete who suffers a sudden PCR depends on a sequence of interdependent actions, so that, when linked together, form a chain effect, increasing the survival rate of victims, named by the American Heart Association, the "current survival, "comprised of the following links: fast access, early CPR, early defibrillation and early ACLS.

Most sudden PCR in athletes occurs due to a tachiarrhythmia163 (ventricular fibrillation) and therefore can be treated with defibrillation. The reduction in mortality in athletes surprised by such an event requires CPR training programs and handling the DEA, and rescuers equipped and trained to recognize emergencies, activate the emergency system, providing quality CPR and use the AED. There are current guidelines for sports facilities that have more than 2,500 patrons or develop physical activity programs for individuals belonging to certain risk groups, such as heart disease and the elderly, have defibrillators strategically allocated131.

It is already well established that for each minute without cardiopulmonary resuscitation (CPR) survival of a victim PCR witnessed decreases from 7 to 10%. However, in the context of ventricular arrhythmias structural diseases appear to be more susceptible to small delays compared to a defibrillation129 context a structurally sound heart, which possibly brings to athletes victims of a sudden PCR a more significant decline in survival while waiting for an AED, stressing the utmost importance of the third link in the chain, early defibrillation.

The consequent increase in survival programs of public access to defibrillation has been well documented in numerous studies, including leases as casinos164, and airplanes165 airports 132 however, little is known about the impact of this initiative on the specific risk group of athletes, mainly by that this is a rare event.

Important risk marker, the pre-participation medical evaluation should be mandatory for practitioners of physical and sports activities, as it is able to detect cardiovascular abnormalities that predispose to sudden death. Despite different recommendations, there is a consensus that every athlete should do, necessarily, a medical history, physical examination and 12-lead ECG, complementing the research with other tests according to the degree of suspicion.

Sportsmen victims of SD should be handled promptly and need immediate CPR quality, providing a vital amount of blood flow to the brain and heart. The local emergency team should be able to accomplish an ideal time between collapse and defibrillation of 3-5 minutes, thus increasing the chances of success of shock. As in most cases the post-pace defibrillation is not capable of a perfusion effective CPR should be resumed immediately after the shock.

Finally, periodic medical evaluation, an effective local protocol for emergency responders and trained in BLS and able to provide quality CPR, early defibrillation and quick contact centers with qualified ACLS are the pillars of support for a common goal: reducing the number cases of sudden death in athletes and increased survival of victims.

10.3. Special aspects of prevention of SD related to exercise and sport

10.3.1. Doping: illicit substances in sport (www.wada-ama.org)

Some used as doping substances are able to cause deleterious effects, particularly cardiovascular system, including sudden death. Among the most commonly used substances include anabolic steroids themselves, ephedrine and amphetamine. Among the most used social drugs are cocaine, marijuana and 3,4-methylenedioxymethamphetamine MDMA, known as ecstasy.

10.3.1.1. Anabolic steroids (AS)

These substances cause various side effects, including unwanted cardiovascular effects. The EA may induce arterial hypertension (AH) and secondary nephrosclerosis. Testosterone may cause increased vascular response to norepinephrine and, as a consequence, promote fluid retention and increased peripheral vascular resistance leading to HA3.

Another important effect is described by Tagarakis et al166, which demonstrated for the first time at the microscopic level, an adaptation of cardiac capillaries myocytes and with concomitant use of anabolic steroids and physical training. That would cause a disproportionate increase in myocardial mass in relation to cardiac capillaries. The results of this study suggest that the use of EA could develop an imbalance between supply and O2 consumption, especially during exercise.

10.3.1.2. Ephedra

Stimulants in general cause tachycardia and increased myocardial oxygen consumption, which may cause arrhythmias and myocardial infarction in susceptible individuals.

Ephedrine can cause symptomatic ventricular tachycardia, ventricular extrassísstoles frequent atrial fibrillation and sudden death. Importantly, many so-called natural products and "derived from flora" have substances like ephedrine in its formula without being part of the bull.

10.3.1.3. Cocaine

Cocaine use causes widespread vasoconstriction, and its main consequence, hypertension. Although cocaine use cause intense vasoconstriction in the central nervous system, this may also impact on other organs such as the kidneys causing failure renal1. Cocaine use can cause, yet, MI, cardiac arrhythmias, congestive cardiomyopathy, myocarditis, subarachnoid hemorrhage, rupture of the aorta, hypertension, myocardial ischemia or induced by exercise and sudden cardiac death.

10.3.1.4. Amphetamines

It is the prototype of CNS stimulants. Have wide variety of salts and mixtures under various forms of presentation, the most used dextroamphetamine sulfate. This substance has a direct action by stimulation of adrenergic receptors in cortical level and ascending reticular activating system and an indirect action, displacing the endogenous sites of their nerve endings. Its side effects are more pronounced: general insomnia, dizziness, profuse sweating, shivering and euphoria; Cardiovascular palpitations, tachycardia, chest discomfort: neurological brain hemorrhage.

10.3.1.5. MDMA (3,4 - methylenedioxymethamphetamine) (ecstasy)

It is a hallucinogen similar to amphetamine. Due to its low cost and availability in tablets, its popularity and consumption have increased significantly. The ingestion of MDMA increases the release of serotonin, dopamine and norepinephrine by presynaptic neurons. Furthermore, prevents the metabolism of neurotransmitters by inhibiting monoamine oxidase. Its major cardiovascular effects are hypertension, tachycardia and arrhythmia, which can lead to SD167, 168.

10.4. Evaluation of the athlete, organization and planning of care

Sudden death related to exercise and sport is a dramatic event and the doctors and some measures can and should be taken to try to prevent this rare but dreaded complication of sports / exercise.

We describe some preventive measures related to SD related to exercise and sport.

10.4.1 Aspects related to the athlete

10.4.1.1 - Pre-participation evaluation

Considering that in most cases the SD associated with the sport are caused by known or undiagnosed heart, every candidate for physical activity should undergo clinical examination prior, regardless of age. This clinical examination should be preceded by a good history with particular attention to the family history of cardiovascular disease and sudden death. The pre-participation evaluation in an attempt to detect these pathologies is the most efficient way to prevent one cardiovascular event fatal3. In a recent document, the International Olympic Committee ratifies the importance of periodic medical evaluations for athletes elite2.

While acknowledging that clinical examination alone can not fail to detect all heart diseases with potential to cause SD, this procedure with emphasis on the cardiovascular examination, preceded by a thorough history and past medical history and family history, is the first step to proper evaluation of the athlete.

Clinical examination should be accompanied ideally by a 12-lead electrocardiogram. Although there is a disagreement between the American school (this only recommends medical history and physical examination) and European School (this recommends adding the 12-lead electrocardiogram to anamnesis and clinical examination) 52, we remember that in the SBC guideline criteria for diagnostic test ordering Cardiovascular entity considers that the 12-lead electrocardiogram as a compulsory examination first visit cardiology (ECG-1-1096) 169. Moreover, it is known that numerous electrical heart diseases that can lead to SD are likely to be diagnosed by ECG at rest, including the long QT syndrome, Brugada syndrome, syndrome Lenegre-Lev syndrome and Wolf -Parkinson-White170. The European protocol that includes history, physical examination and electrocardiogram is adopted currently by the International Olympic Committee, the Italian Olympic Committee, FIFA and Football Union (UEFA) 171. Clinical examination should include a personal and family history and a specific screening for the syndrome Marfan172.

A more detailed evaluation before participation in physical activities and sports available in another section of this guideline.

10.4.1.2 For the preparation of the athlete

Tracking the athlete has to be done holistically. Therefore, to prevent cardiovascular clinical events, preventive measures are also important basic, adequate nutrition and hydration, respecting rest periods and avoiding training and competition in the hottest times of the day. Furthermore, it is important to monitoring and observation of athletes in training and competition for qualified medical staff, preferably with experience in sports medicine and basic first aid in cases of emergency clinical situations.

10.4.2 Issues related to training and competition venues

10.4.2.1 Emergency service and medical contingency plan

In addition to all the material needed to care for cardiac arrest should be prepared a contingency plan in medical training and competition venues, with staff trained in cardiopulmonary resuscitation, in the event of an emergency or clinical cardiovascular, optimizing the transport of athletes hospital for more complex, as the case173, 174.

10.4.2.2 Automated External Defibrillator

The automated external defibrillator (AED) should be available for use in less than 5 minutes in training and competition venues, clubs, arenas, stadiums, gyms and rehabilitation clinics with staff trained in cardiopulmonary resuscitation 174, 175.

Among young athletes cardiac arrest occur, usually after intense training sessions or during a competition. Although these events are rare (corresponding to 1% of those that occur in middle-aged or elderly), the value of a prompt service and successful resuscitation improves survival in long term176.

11. Para-athletes or athletes with special needs.

11.1. Cardiologic evaluations: pre-participation and re-evaluations

All Paralympic athletes must undergo independent evaluation of age, sex and disability associated with, the pre-participation evaluation should include children, adolescents, adults, master / seniors, men and women, under the sole responsibility of the attending physician (Recommendation Grade: I , Evidence level: C).

The evaluation should be comprehensive, taking into account the organism as a whole, emphasizing the physical and somatic; should keep in mind the interactions between physical, comorbidities, and their sequelae in physical training and sports performance (Recommendation Grade: I, Evidence level: C) (Figure 4).


The frequency of re-evaluations should be at the discretion of the attending physician, according to the characteristics of each case, however, the frequency should have the primary aim of the sport safe (Recommendation Grade: I, Evidence level C).

The evaluation of Paralympians obeys defined protocol, summarized in Table 21

After the initial evaluation, according to the findings must be given specialized tests at the discretion of the attending physician, such as cardiopulmonary exercise testing (CPET), echocardiogram (ECHO), vectorcardiogram (VCG), computed tomography, magnetic resonance, ultrasound, hemoglobin electrophoresis ( research SCD) and cardiac evaluations, ophthalmic (Marfan research, glaucoma, retinal detachment) and orthopedic177, 178 (Recommendation Grade: I, Evidence level C).

In athletes with cerebral palsy can use the evaluation score of spasticity (QSFC Quantitative sports and functional classification), based on the condition of muscles of upper and lower limbs and trunk, for use in clinical research, clinical and physical training179.

Athletes in wheelchairs and people with dentures should be thoroughly and then examined for pressure sores or scabs on the stump of the prosthesis implantation. The presence of ulceration in these places becomes temporarily ineligible athlete until they are restored local conditions of integument (Recommendation Grade: I, Evidence level C). The practice of urinary retention in wheelchairs should be ruled out, given the risk of large elevations of blood pressure and stroke. In cases of neurogenic bladder should be alert to the presence of subclinical urinary infections.

11.2. Cardiopulmonary exercise testing

The basics of cardiopulmonary exercise testing protocols include: 1) reproducibility of sports act according to the principle of specificity, 2) the adequacy sport and means of locomotion athlete, 3) perform the tests with stability and security, ensuring accuracy and reproducibility of measures11 (Grade Recommendation: I, Evidence level: B).

Special care should be taken in relation to the type and degree of disability, the athlete's posture, at room temperature, prior to emptying, prevention of hypotension, the risk of seizures and accidents, the blood pressure measurements and the proper veiling masks. Several factors may limit performance in evaluations: 1) Clinical: intellectual and sensory disabilities (visual, tactile, auditory, epilepsy, autonomic dysreflexia, neurogenic bladder, deprivation friendly, post-polio syndrome, tachypnoea stress, malnutrition, 2) locomotion: reduced mass, muscle strength and flexibility, increased muscle tone, decreased joint mobility, motor incoordination, osteoarticular lesions secondary to sports, injuries from amputation stumps, 3) cardiovascular: any associated disorders, 4) physiological: reduction of VO2 PICO, anaerobic threshold, respiratory compensation point, early fatigue, physical inactivity, and 4) socioeconomic and cultural: social exclusion, lack of patrocínio177.

According to the principle of specificity, has been used to arm ergometers players, throwers, weightlifters, swimmers and fencers, bike cycling and treadmill to other modalidades177; cyclists can use your own equipment coupled to the system 850 Mag Minoura180 (Recommendation Grade: I, Evidence level: C).

The cardiopulmonary tests can be performed by several specific protocols, citing the example summarized in Table 22.

The protocol Knechtle and Köplif (Institute of Sports Medicine Swiss Paraplegic Centre) for treadmill test in wheelchairs, starts at speed of 8 km / h and slope of 1%, with 0.5% increments every 2 minutes and speed constant until exaustão181, 182.

Field tests can also be performed with vantagens183, 184. Variations between 48-80% have been described in the regression equations for determining the physical capacity in paraplegics and quadriplegics. These variations can be explained by the level and degree of spinal cord injury, age, gender, physical activity and weight corporal183. In our environment, the values ​​for the aerobic power of Paralympic athletes have been similar (Table 23)180,185.

The pre-participation evaluation for leisure activities is similar, depending on the physical and mental stress. On many occasions, given the emotional burden involved and the lowest level of training, physical and psychological stress can be of great intensity, similar to the relative degree of competitions.

12. Prevention of events / sudden death in sports

The event prevention should include prevention of accidents, injuries and aggravation of preexisting comorbidities and sudden death.

The goals of a protocol event prevention in sports based on pre-participation screening:

Identifying predisposing conditions, ie cardiovascular diseases that can potentially cause sudden death;

Set if there are steps that can be taken to reduce the risk of sudden death: What? How should they be developed?

Standardize the approach to be adopted in every heart and discuss the possible disqualification of the athlete's exercise of his profession.

Prevention of events and sudden death in sports and leisure is performed taking into account the early diagnosis and treatment of cardiovascular diseases, as well as the application of existing criteria and unenforceability specific to the various conditions described in Parts I and II of this document and properly applied to Paralympic athletes187. It is imperative that the resources exist venues doctors and paramedics, appropriately equipped for emergency care.

In many institutions, the clinical director and / or the physician responsible for the care answerable to the respective Regional Council of Medicine compliance with those standards.

Individuals newly hospitalized or sedentary longstanding need progressive training with gradual increments in the frequency and duration of sessions and the intensity of the exercises, besides the risk of injuries and physical sequelae, the appearance of these can be discouraging factor training, damaging self-image, and predisposing to cessation program (Recommendation Grade I, Evidence level C).

12.1. Ethical Aspects

The medical evaluation should include experts from various fields, highlighting the sport and exercise medicine, cardiology, orthopedics and physiatry.

When it comes to athletes with disabilities, it is important to emphasize that it is the exclusive competence of the physician directing the training, diagnose any diseases and sequelae, order tests, prescribe treatment and athletes away from sports, being forbidden to assign medical functions or delegate its exclusive competence for professionals not qualified to practice medicine. (Federal Medical Council, Resolution No. 1236/87). Moreover, the implementation of the training will be conducted by physical education teachers and therapists. The interaction between physicians, physical education teachers, physiotherapists, physiologists, nutritionists and psychologists is critical to the success of the program. The training prescription should be made in prescription doctor, aiming mode, frequency and duration of sessions, training intensity and other observations, at the discretion of the attending physician. This conduct is ratified by the Federal Medical Opinion 4141/2003: "For all the above, it is for the doctor, after diagnosing the disease, prescribe the appropriate treatment to the patient and even the prescription of physical activity in the face of pathology diagnosis or prevention of various pathologies."

In many institutions, the clinical director and / or the physician responsible for the care of these standards by responding to the respective Regional Council of Medicine.

The relationship between doctor and other professionals practicing in health care should be based on mutual respect, freedom and independence of each professional, always seeking the interest and welfare of the patient (Code of Medical Ethics 08/01 / 1988 Article 18). The interaction between doctors and para-medical physical education teachers, physical therapists, nutritionists, psychologists and coaches is critical to the success of the training program and should be encouraged at every moment.

12.2. Recommendations

Nowadays, given the paucity of reports in the literature, the criteria for answering Paralympians are based generally on expert consensus (Evidence level C).

The determination of eligibility sports must follow the protocol of the International Paralympic Committee Classification Code and International Olympic Committee and Standards188 Brasileiro189. Thus, the para-athlete may be eligible and ineligible to a modality to another. The eligibility criteria are defined for each sport Paralympic sport by federations internacional190.

The recommendations for the care of Para-athletes are listed in Table 24.

13. Appendix

13.1. Elaboration of aptness or release reports to exercise and practice sports173

The medical report to release for amateur and competitive physical activities is a part of the medical act and a patient right. It should be objective, clarifying as to the kind of physical activity allowed and preferably suggesting the physical training intensity. In cases in which there are restrictions to the practice of a modality, those should be clearly mentioned in the document. Any and every information concerning the clinical profile, physical examination and complementary exams should be in the medical report when required and authorized by the patient.

With basis in evidence-based medicine the individual risk stratification is more appropriate, considering clinical condition and physical aptness, gender, age and conditions under which this practice will be performed. For most situations it is possible to compare the risk of a given individual with that expected for their fellows of same age and thus characterize the risk as much smaller, smaller, similar, bigger or much bigger. Specifically, it may also be convenient to characterize the practice as therapeutic, recreational or competitive. In addition, environmental factors, notably climatic, may be relevant.

As to the issuing of the report, this should characterize or specify any clinical restriction, be it of locomotor or cardiorespiratory nature. Ideally, the conclusive statement should attain to the limits of what was actually examined or evaluated, avoiding generic and poorly funded sentences as "apt to sports practice", being probably more adequate to use something like "formal clinical contraindications to the practice of recreational or competitive physical exercise were not found".

When the decision is for the professional disqualification, the part most interested in the information should be the athlete or their legal representative (when under 18), even when the athlete is part of a team and his/her evaluation was offered by the club or association to which they are associated. In these cases it would be prudent that the report be signed by the physician responsible and at least two other physicians that follow the decision, besides the athlete himself/herself, in at least two copies, one of them filed in the athlete's medical records. Special care must be taken to keep the athlete's integrity, keeping the secret required in each case.

14. References

  • 1. Corrado D, Pelliccia A, Bjornstad HH, Vanhees L, Biffi A, Borjesson M, et al; Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26(5):516-24.
  • 2. Maron BJ, Araujo CG, Thompson PD, Fletcher GF, de Luna AB, Fleg JL, et al; World Heart Federation; International Federation of Sports Medicine; American Heart Association Committee on Exercise, Cardiac Rehabilitation, and Prevention. Recommendations for preparticipation screening and the assessment of cardiovascular disease in masters athletes: an advisory for healthcare professionals from the working groups of the World Heart Federation, the International Federation of Sports Medicine, and the American Heart Association Committee on Exercise, Cardiac Rehabilitation, and Prevention. Circulation. 2001;103(2):327-34.
  • 3. Oliveira MAB, Leitão MB. Diretriz da Sociedade Brasileira de Medicina do Esporte: morte súbita no exercício e no esporte. Rev Bras Med Esporte. 2005;11(1):s1-8.
  • 4. Corrado D, Basso C, Pavei A, Michieli P, Schiavon M, Thiene G. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA. 2006;296(13):1593-601.
  • 5. Corrado D, Basso C, Schiavon M, Thiene G. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med. 1998;339(6):364-9.
  • 6. Marcus FI. Electrocardiographic features of inherited diseases that predispose to the development of cardiac arrhythmias, long QT syndrome, arrhythmogenic right ventricular cardiomyopathy/dysplasia, and Brugada syndrome. J Electrocardiol. 2000;33 Suppl:1-10.
  • 7. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA Study. Coronary Artery Risk Development in (Young) Adults. Circulation. 1995;92(4):785-9.
  • 8. Corrado D, Basso C, Schiavon M, Pelliccia A, Thiene G. Pre-participation screening of young competitive athletes for prevention of sudden cardiac death. J Am Coll Cardiol. 2008;52(24):1981-9.
  • 9. Franklin B. ACSM's guidelines for exercise testing and prescription: Lippincott Williams & Wilkins; 2000.
  • 10. Lazzoli JK, Oliveira MAB, Leitão MB, da Nóbrega ACL, Nahas RM, Rezende L, et al. I Consenso de Petrópolis - Posicionamento oficial da Sociedade Brasileira de Medicina do Esporte sobre esporte competitivo em indivíduos acima de 35 anos. Rev Bras Med Esporte. 2001;7(3):83-92.
  • 11. Lazzoli JK, Leitao MB. Avaliação pré-participação. In: Manual de medicina do esporte:do problema ao diagnóstico. São Paulo: Sociedade Brasileira de Medicina do Exercício e do Esporte; 2009.
  • 12. Maron BJ, Zipes DP. Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol. 2005;45(8):1318-21.
  • 13. Pelliccia A, Fagard R, Bjornstad HH, Anastassakis A, Arbustini E, Assanelli D, et al. Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26(14):1422-45.
  • 14. Bille K, Figueiras D, Schamasch P, Kappenberger L, Brenner JI, Meijboom FJ, et al. Sudden cardiac death in athletes: the Lausanne Recommendations. Eur J Cardiovasc Prev Rehabil. 2006;13(6):859-75.
  • 15. Pelliccia A, Di Paolo FM, Quattrini FM, Basso C, Culasso F, Popoli G, et al. Outcomes in athletes with marked ECG repolarization abnormalities. N Engl J Med. 2008;358(2):152-61.
  • 16. Thompson PD. Preparticipation screening of competitive athletes: seeking simple solutions to a complex problem. Circulation. 2009;119(8):1072-4.
  • 17. Pelliccia A, Culasso F, Di Paolo FM, Accettura D, Cantore R, Castagna W, et al. Prevalence of abnormal electrocardiograms in a large, unselected population undergoing pre-participation cardiovascular screening. Eur Heart J. 2007;28(16):2006-10.
  • 18. Pelliccia A, Maron BJ, Culasso F, Di Paolo FM, Spataro A, Biffi A, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation. 2000;102(3):278-84.
  • 19. Batlouni M, Schwartz HJ, Ghorayeb N. Eletrocardiograma. In: Ghorayeb N, Dioguardi GS (orgs). Tratado de cardiologia do exercício e esporte. São Paulo: Atheneu; 2007.
  • 20. Andrade J, Brito FS, Vilas-Boas F, Castro I, Oliveira JA, Guimarães JI, et al; Sociedade Brasileira de Cardiologia. II Diretrizes da Sociedade Brasileira de Cardiologia sobre teste ergométrico. Arq Bras Cardiol. 2002;78(supl.2):1-18.
  • 21. Gibbons RJ, Balady GJ, Beasley JW, Bricker JT, Duvernoy WF, Froelicher VF, et al. ACC/AHA guidelines for exercise testing: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Circulation. 1997;96(1):345-54.
  • 22. Fletcher GF. Current status of cardiac rehabilitation. Am Fam Physician. 1998;58(8):1778-82.
  • 23. Daher DJ, Ghorayeb N, Guiseline M, Dioguardi G. Avaliação pré-participação na academia. In : Ghorayeb N, Dioguardi GS. (orgs). Tratado de medicina no exercício e do esporte. São Paulo: Atheneu; 2007.
  • 24. Giagnoni E, Secchi MB, Wu SC, Morabito A, Oltrona L, Mancarella S, et al. Prognostic value of exercise EKG testing in asymptomatic normotensive subjects: a prospective matched study. N Engl J Med. 1983;309(18):1085-9.
  • 25. Myers J, Prakash M, Froelicher V, Do D, Partington S, Atwood JE. Exercise capacity and mortality among men referred for exercise testing. N Engl J Med. 2002;346(11):793-801.
  • 26. Weiner DA, Ryan TJ, McCabe CH, Chaitman BR, Sheffield LT, Ferguson JC, et al. Prognostic importance of a clinical profile and exercise test in medically treated patients with coronary artery disease. J Am Coll Cardiol. 1984;3(3):772-9.
  • 27. Vivacqua RC, Costa MA, Carreira MQ. Ergometria, ergoespirometria, cintilografia e ecocardiografia de esforço. São Paulo: Atheneu; 2009.
  • 28. Tavel ME. Stress testing in cardiac evaluation: current concepts with emphasis on the ECG. Chest. 2001;119(3):907-25.
  • 29. Polizos G, Ghamsary M, Ellestad MH. The severity of myocardial ischemia can be predicted by the exercise electrocardiogram. Cardiology. 2005;104(4):215-20.
  • 30. Watanabe M, Yokota M, Miyahara T, Saito F, Matsunami T, Kodama Y, et al. Clinical significance of simple heart rate-adjusted ST segment depression in supine leg exercise in the diagnosis of coronary artery disease. Am Heart J. 1990;120(5):1102-10.
  • 31. Hsu TS, Lee CP, Chern MS, Cheng NJ. Critical appraisal of exercise variables: a treadmill study. Coron Artery Dis. 1999;10(1):15-22.
  • 32. Ellestad MH, Crump R, Surber M. The significance of lead strength on ST changes during treadmill stress tests. J Electrocardiol. 1992;25 Suppl:31-4.
  • 33. Michaelides AP, Aigyprladou MN, Andrikopoulos GK, Richter DJ, Kartalis A, Tapanlis E, et al. The prognostic value of a QRS score during exercise testing. Clin Cardiol. 2005;28(8):375-80.
  • 34. van Campen CM, Visser FC, Visser CA. The QRS score: a promising new exercise score for detecting coronary artery disease based on exercise-induced changes of Q-, R- and S-waves: a relationship with myocardial ischaemia. Eur Heart J. 1996;17(5):699-708.
  • 35. Koide Y, Yotsukura M, Tajino K, Yoshino H, Ishikawa K. Use of QT dispersion measured on treadmill exercise electrocardiograms for detecting restenosis after percutaneous transluminal coronary angioplasty. Clin Cardiol. 1999;22(10):639-48.
  • 36. Lauer MS, Francis GS, Okin PM, Pashkow FJ, Snader CE, Marwick TH. Impaired chronotropic response to exercise stress testing as a predictor of mortality. JAMA. 1999;281(6):524-9.
  • 37. Azarbal B, Hayes SW, Lewin HC, Hachamovitch R, Cohen I, Berman DS. The incremental prognostic value of percentage of heart rate reserve achieved over myocardial perfusion single-photon emission computed tomography in the prediction of cardiac death and all-cause mortality: superiority over 85% of maximal age-predicted heart rate. J Am Coll Cardiol. 2004;44(2):423-30.
  • 38. Imai K, Sato H, Hori M, Kusuoka H, Ozaki H, Yokoyama H, et al. Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure. J Am Coll Cardiol. 1994;24(6):1529-35.
  • 39. Cole CR, Foody JM, Blackstone EH, Lauer MS. Heart rate recovery after submaximal exercise testing as a predictor of mortality in a cardiovascularly healthy cohort. Ann Intern Med. 2000;132(7):552-5.
  • 40. Frolkis JP, Pothier CE, Blackstone EH, Lauer MS. Frequent ventricular ectopy after exercise as a predictor of death. N Engl J Med. 2003;348(9):781-90.
  • 41. Maron BJ, Thompson PD, Ackerman MJ, Balady G, Berger S, Cohen D, et al.; American Heart Association Council on Nutrition, Physical Activity, and Metabolism. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 update: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation. 2007;115(12):1643-55.
  • 42. Ghorayeb N, Batlouni M. Hipertrofia ventricular: mecanismos envolvidos na indução e possibilidades de regressão. Rev Soc Cardiol Estado de São Paulo. 1998;8(2):298-301.
  • 43. Elhendy A, Modesto KM, Mahoney DW, Khandheria BK, Seward JB, Pellikka PA. Prediction of mortality in patients with left ventricular hypertrophy by clinical, exercise stress, and echocardiographic data. J Am Coll Cardiol. 2003;41(1):129-35.
  • 44. Lotufo PA. [Premature mortality from heart diseases in Brazil: a comparison with other countries]. Arq Bras Cardiol. 1998;70(5):321-5.
  • 45. Lessa I. Medical care and deaths due to coronary artery disease in Brazil, 1980-1999. Arq Bras Cardiol. 2003;81(4):336-42, 29-35.
  • 46. Huston TP, Puffer JC, Rodney WM. The athletic heart syndrome. N Engl J Med. 1985;313(1):24-32.
  • 47. Pelliccia A, Maron BJ. Athlete's heart electrocardiogram mimicking hypertrophic cardiomyopathy. Curr Cardiol Rep. 2001;3(2):147-51.
  • 48. Ghorayeb N, Cruz FE, Dioguardi G. Sudden death of athletes--a new fact? Arq Bras Cardiol. 2007;89(6):169-70.
  • 49. Myerburg RJ, Vetter VL. Electrocardiograms should be included in preparticipation screening of athletes. Circulation. 2007;116(22):2616-26.
  • 50. Corrado D, Pelliccia A, Heidbuchel H, Sharma S, Link M, Basso C, et al; Section of Sports Cardiology, European Association of Cardiovascular Prevention and Rehabilitation. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31(2):243-59.
  • 51. Mitten MJ, Maron BJ, Zipes DP. Task Force 12: legal aspects of the 36th Bethesda Conference recommendations. J Am Coll Cardiol. 2005;45(8):1373-5.
  • 52. Ljungqvist A, Jenoure PJ, Engebretsen L, Alonso JM, Bahr R, Clough AF, et al. The International Olympic Committee (IOC) consensus statement on periodic health evaluation of elite athletes, March 2009. Clin J Sport Med. 2009;19(5):347-65.
  • 53. Vivacqua RC. Ergoespirometria em atletas, sempre recomendada. [Acesso em 2011 ago 10]. Disponível em: http://departamento.cardiol.br/sbc-derc/revista 2008/44/pdf/Rev44-p25.pdf
  • 54. Ribeiro JP, Araújo CGS. Espirometria no diagnóstico diferencial da dispnéia. Rev Soc Cardiol RS. 1998;7(3):85-90.
  • 55. Corrà U, Giannuzzi P. Role of cardiopulmonary exercise testing in today's cardiovascular prevention and rehabilitation. Eur J Cardiovasc Prev Rehabil. 2006;13(4):473-4.
  • 56. Ribeiro JP, Stein R, Chiappa GR. Beyond peak oxygen uptake: new prognostic markers from gas exchange exercise tests in chronic heart failure. J Cardiopulm Rehabil. 2006;26(2):63-71.
  • 57. Oliveira RB, Myers J, Araujo CG, Abella J, Mandic S, Froelicher V. Maximal exercise oxygen pulse as a predictor of mortality among male veterans referred for exercise testing. Eur J Cardiovasc Prev Rehabil. 2009;16(3):358-64.
  • 58. Mezzani A, Agostoni P, Cohen-Solal A, Corrà U, Jegier A, Kouidi E, et al. Standards for the use of cardiopulmonary exercise testing for the functional evaluation of cardiac patients: a report from the Exercise Physiology Section of the European Association for Cardiovascular Prevention and Rehabilitation. Eur J Cardiovasc Prev Rehabil. 2009;16(3):249-67.
  • 59. Chaudhry S, Arena R, Wasserman K, Hansen JE, Lewis GD, Myers J, et al. Exercise-induced myocardial ischemia detected by cardiopulmonary exercise testing. Am J Cardiol. 2009;103(5):615-9.
  • 60. Herdy AH, Moritz P, Assis AV, Ribeiro F, Collaco J, Ribeiro JP. Abnormal response of left ventricular systolic function to submaximal exercise in post-partial left ventriculotomy patients. Braz J Med Biol Res. 2007;40(2):159-65.
  • 61. Maron BJ. Hypertrophic cardiomyopathy and other causes of sudden cardic death in young competitive athletes, with considerations for preparticipation screening and criteria for disqualification cardiol. Cardiol Clin. 2007;25(3):399-414.
  • 62. Ghorayeb N, Batlouni M, Pinto IM, Dioguardi GS. [Left ventricular hypertrophy of athletes: adaptative physiologic response of the heart]. Arq Bras Cardiol. 2005;85(3):191-7.
  • 63. Corrado D, Migliore F, Bevilacqua M, Basso C, Thiene G. Sudden cardiac death in athletes: can it be prevented by screening? Herz. 2009;34(4):259-66.
  • 64. Corrado D, Basso C, Thiene G. Essay: Sudden death in young athletes. Lancet. 2005;366 Suppl 1:S47-8.
  • 65. Maron BJ. Sudden death in young athletes. N Engl J Med. 2003;349(11):1064-75.
  • 66. Corrado D, Basso C, Rizzoli G, Schiavon M, Thiene G. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol. 2003;42(11):1959-63.
  • 67. O'Connor FG, Johnson JD, Chapin M, Oriscello RG, Taylor DC. A pilot study of clinical agreement in cardiovascular preparticipation examinations: how good is the standard of care? Clin J Sport Med. 2005;15(3):177-9.
  • 68. Beckerman J, Wang P, Hlatky M. Cardiovascular screening of athletes. Clin J Sport Med. 2004;14(3):127-33.
  • 69. Pelliccia A, Di Paolo FM, Corrado D, Buccolieri C, Quattrini FM, Pisicchio C, et al. Evidence for efficacy of the Italian national pre-participation screening programme for identification of hypertrophic cardiomyopathy in competitive athletes. Eur Heart J. 2006;27(18):2196-200.
  • 70. Thiene G, Corrado D, Basso C. Revisiting definition and classification of cardiomyopathies in the era of molecular medicine. Eur Heart J. 2008;29(2):144-6.
  • 71. Thompson PD, Franklin BA, Balady GJ, Blair SN, Corrado D, Estes NA 3rd, et al; American Heart Association Council on Nutrition, Physical Activity, and Metabolism; American Heart Association Council on Clinical Cardiology; American College of Sports Medicine. Exercise and acute cardiovascular events placing the risks into perspective: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology. Circulation. 2007;115(17):2358-68.
  • 72. Wyman RA, Chiu RY, Rahko PS. The 5-minute screening echocardiogram for athletes. J Am Soc Echocardiogr. 2008;21(7):786-8.
  • 73. Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. Sudden death in young athletes. Circulation. 1980;62(2):218-29.
  • 74. Corrado D, Thiene G, Nava A, Rossi L, Pennelli N. Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases. Am J Med. 1990;89(5):588-96.
  • 75. Wilsson JM, Jungner G. Principles and practice of screening for diseases. Geneva: World Health Organization;1968. (Public Health Papers, n.34).
  • 76. Barry J, Maron BJ, Pamela S. 36th Bethesda Conference: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol. 2005;45(8):1-53.
  • 77. Lazzoli JK, Nóbrega ACL, Carvalho T, Oliveira MAB, Teixeira JAC, Leitão MB, et al. Position statement of the Brazilian Society of Sports Medicine: physical activity and health in children and adolescents. Rev Bras Med Esporte. 2000;6(4):116-8.
  • 78. Thomas S, Reading J, Shephard RJ. Revision of the Physical Activity Readiness Questionnaire (PAR-Q). Can J Sport Sci. 1992;17(4):338-45.
  • 79. Tanner JM. Growth at adolescensce. 2nd ed. Oxford: Blackwell Scientific Publications; 1962.
  • 80. Maron BJ, Douglas PS, Graham TP, Nishimura RA, Thompson PD. Task Force 1: preparticipation screening and diagnosis of cardiovascular disease in athletes. J Am Coll Cardiol. 2005;45(8):1322-6.
  • 81. Baptista CA, Foronda A, Baptista L de P. Esporte competitivo na criança e no adolescente - exame pré-participação: eletrocardiograma obrigatório? Arq Bras Cardiol. 2009;93(2):188-95.
  • 82. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE. Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J. 1991;121(2 Pt 1):568-75.
  • 83. Richard P, Charron P, Carrier L, Ledeuil C, Cheav T, Pichereau C, et al; EUROGENE Heart Failure Project. Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy. Circulation. 2003;107(17):2227-32.
  • 84. Oliveira MA. Cardiomiopatia hipertrófica, atividade física e morte súbita. Rev Bras Med Esporte. 2002;8(1):20-5.
  • 85. Acunzo RS. Manifestaciones clínicas y electrocardiográficas, la estratificación del riesgo y el tratamiento de la miocardiopatía hipertrófica. In: Elizari M, Chiale P. (eds). Arritmias cardíacas: bases celulares y moleculares, diagnóstico y tratamiento. 2Ş ed. Barcelona: Editorial Medica Panamericana; 2003. p. 753-74.
  • 86. McKenna WJ, Spirito P, Desnos M, Dubourg O, Komajda M. Experience from clinical genetics in hypertrophic cardiomyopathy: proposal for new diagnostic criteria in adult members of affected families. Heart. 1997;77(2):130-2.
  • 87. Konno T, Shimizu M, Ino H, Yamaguchi M, Terai H, Uchiyama K, et al. Diagnostic value of abnormal Q waves for identification of preclinical carriers of hypertrophic cardiomyopathy based on a molecular genetic diagnosis. Eur Heart J. 2004;25(3):246-51.
  • 88. Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ, Seidman CE, et al. Task Force on Clinical Expert Consensus Documents. American College of Cardiology; Committee for Practice Guidelines. European Society of Cardiology. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol. 2003;42(9):1687-713.
  • 89. Sharma S, Elliott PM, Whyte G, Mahon N, Virdee MS, Mist B, et al. Utility of metabolic exercise testing in distinguishing hypertrophic cardiomyopathy from physiologic left ventricular hypertrophy in athletes. J Am Coll Cardiol. 2000;36(3):864-70.
  • 90. Rickers C, Wilke NM, Jerosch-Herold M, Casey SA, Panse P, Panse N, et al. Utility of cardiac magnetic resonance imaging in the diagnosis of hypertrophic cardiomyopathy. Circulation. 2005;112(6):855-61.
  • 91. Maron BJ, Ackerman MJ, Nishimura RA, Pyeritz RE, Towbin JA, Udelson JE. Task Force 4: HCM and other cardiomyopathies, mitral valve prolapse, myocarditis, and Marfan syndrome. J Am Coll Cardiol. 2005;45(8):1340-5.
  • 92. Colin Lizalde L de J. [Hypertrophic cardiomyopathy. Arrhythmia in hypertrophic cardiomyopathy]. Arch Cardiol Mex. 2003;73 Suppl. 1:S26-30.
  • 93. McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstrom-Lundqvist C, Fontaine G, et al. Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Task Force of the Working Group Myocardial and Pericardial Disease of the European Society of Cardiology and of the Scientific Council on Cardiomyopathies of the International Society and Federation of Cardiology. Br Heart J. 1994;71(3):215-8.
  • 94. Thiene G, Nava A, Corrado D, Rossi L, Pennelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med. 1988;318(3):129-33.
  • 95. Anderson EL. Arrhythmogenic right ventricular dysplasia. Am Fam Physician. 2006;73(8):1391-8.
  • 96. Hauser AM, Dressendorfer RH, Vos M, Hashimoto T, Gordon S, Timmis GC. Symmetric cardiac enlargement in highly trained endurance athletes: a two-dimensional echocardiographic study. Am Heart J. 1985;109(5 Pt 1):1038-44.
  • 97. Ghorayeb N, Dioguardi GS, Daher DJ, Baptista CA, Batlouni M. Avaliação cardiológica pré-participação do atleta. Rev Soc Cardiol Estado de São Paulo. 2005;15(2):97-104.
  • 98. Ricci C, Longo R, Pagnan L, Dalla Palma L, Pinamonti B, Camerini F, et al. Magnetic resonance imaging in right ventricular dysplasia. Am J Cardiol. 1992;70(20):1589-95.
  • 99. Maron BJ. Sudden death in young athletes. Lessons from the Hank Gathers affair. N Engl J Med. 1993;329(1):55-7.
  • 100. Maron BJ, Garson A. Arrhythmias and sudden cardiac death in elite athletes. Cardiol Rev. 1994;2(1):26-32.
  • 101. Maron BA, Haas TS, Maron BJ. Sudden death from collapsing sand holes. N Engl J Med. 2007;356(25):2655-6.
  • 102. Zehender M, Meinertz T, Keul J, Just H. ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. Am Heart J. 1990;119(6):1378-91.
  • 103. Isner JM, Estes NA 3rd, Thompson PD, Costanzo-Nordin MR, Subramanian R, Miller G, et al. Acute cardiac events temporally related to cocaine abuse. N Engl J Med. 1986;315(23):1438-43.
  • 104. Kloner RA, Hale S, Alker K, Rezkalla S. The effects of acute and chronic cocaine use on the heart. Circulation. 1992;85(2):407-19.
  • 105. Souza MF, Rocha MF, Malta DC, Neto OL, Silva Jr JB. Epidemiologia das doenças do aparelho circulatório no Brasil: uma análise da tendência da mortalidade. Rev Soc Cardiol Estado de São Paulo. 2006;16(1):48-62.
  • 106. Haskell WL, Lee IM, Pate RR, Powell KE, Blair SN, Franklin BA, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc. 2007;39(8):1423-34.
  • 107. Holmes DR Jr, Davis K, Gersh BJ, Mock MB, Pettinger MB. Risk factor profiles of patients with sudden cardiac death and death from other cardiac causes: a report from the Coronary Artery Surgery Study (CASS). J Am Coll Cardiol. 1989;13(3):524-30.
  • 108. Thompson PD. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Arterioscler Thromb Vasc Biol. 2003;23(8):1319-21.
  • 109. Hambrecht R, Wolf A, Gielen S, Linke A, Hofer J, Erbs S, et al. Effect of exercise on coronary endothelial function in patients with coronary artery disease. N Engl J Med. 2000;342(7):454-60.
  • 110. Maron BJ. Sudden death in hypertrophic cardiomyopathy. J Cardiovasc Transl Res. 2009;2(4):368-80.
  • 111. Leon AS, Connett J, Jacobs DR Jr, Rauramaa R. Leisure-time physical activity levels and risk of coronary heart disease and death. The Multiple Risk Factor Intervention Trial. JAMA. 1987;258(17):2388-95.
  • 112. Rodgers GP, Ayanian JZ, Balady G, Beasley JW, Brown KA, Gervino EV, et al. American College of Cardiology/American Heart Association Clinical Competence statement on stress testing: a report of the American College of Cardiology/American Heart Association/American College of Physicians--American Society of Internal Medicine Task Force on Clinical Competence. J Am Coll Cardiol. 2000;36(4):1441-53.
  • 113. Merz CN, Paul-Labrador M, Vongvanich P. Time to reevaluate risk stratification guidelines for medically supervised exercise training in patients with coronary artery disease. JAMA. 2000;283(11):1476-8.
  • 114. Diamond GA. A clinically relevant classification of chest discomfort. J Am Coll Cardiol. 1983;1(2 Pt 1):574-5.
  • 115. Vivacqua RC, Carreira MA (eds). Teste ergométrico na estratificação de pacientes com dor torácica. Rio de Janeiro: Editora DOC; 2009.
  • 116. Barbosa MM, Nunes MCP, Campos Filho O, Camarozano A, Rabischoffsky A, Maciel BC, et al. Sociedade Brasileira de Cardiologia. Diretrizes das indicações da ecocardiografia. Arq Bras Cardiol. 2009;93(6 supl.3):e265-e302.
  • 117. Moraes RS, Nobrega AC, Castro BR, Negrão CE, Stein R, Serra SM, et al. Sociedade Brasileira de Cardiologia. Diretriz de reabilitação cardíaca. Arq Bras Cardiol. 2005;84(5):431-40.
  • 118. Petersen SE, Hudsmith LE, Robson MD, Doll HA, Francis JM, Wiesmann F, et al. Sex-specific characteristics of cardiac function, geometry, and mass in young adult elite athletes. J Magn Reson Imaging. 2006;24(2):297-303.
  • 119. Maron BJ. Distinguishing hypertrophic cardiomyopathy from athlete's heart physiological remodelling: clinical significance, diagnostic strategies and implications for preparticipation screening. Br J Sports Med. 2009;43(9):649-56.
  • 120. Petersen SE, Wiesmann F, Hudsmith LE, Robson MD, Francis JM, Selvanayagam JB, et al. Functional and structural vascular remodeling in elite rowers assessed by cardiovascular magnetic resonance. J Am Coll Cardiol. 2006;48(4):790-7.
  • 121. Prakken NH, Velthuis BK, Cramer MJ, Mosterd A. Advances in cardiac imaging: the role of magnetic resonance imaging and computed tomography in identifying athletes at risk. Br J Sports Med. 2009;43(9):677-84.
  • 122. Midiri M, Finazzo M. MR imaging of arrhythmogenic right ventricular dysplasia. Int J Cardiovasc Imaging. 2001;17(4):297-304.
  • 123. Lehnart SE, Ackerman MJ, Benson DW Jr, Brugada R, Clancy CE, Donahue JK, et al. Inherited arrhythmias: a National Heart, Lung, and Blood Institute and Office of Rare Diseases workshop consensus report about the diagnosis, phenotyping, molecular mechanisms, and therapeutic approaches for primary cardiomyopathies of gene mutations affecting ion channel function. Circulation. 2007;116(20):2325-45.
  • 124. Berecki G, Zegers JG, Wilders R, Van Ginneken AC. Cardiac channelopathies studied with the dynamic action potential-clamp technique. Methods Mol Biol. 2007;403:233-50.
  • 125. Zimmer T, Surber R. SCN5A channelopathies--an update on mutations and mechanisms. Prog Biophys Mol Biol. 2008;98(2-3):120-36.
  • 126. Brugada R, Hong K, Cordeiro JM, Dumaine R. Short QT syndrome. CMAJ. 2005;173(11):1349-54.
  • 127. Sarkozy A, Brugada P. Sudden cardiac death and inherited arrhythmia syndromes. J Cardiovasc Electrophysiol. 2005;16 Suppl 1:S8-20.
  • 128. Jervell A, Lange-Nielsen F. Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval and sudden death. Am Heart J. 1957;54(1):59-68.
  • 129. Schwartz PJ, Moss AJ, Vincent GM, Crampton RS. Diagnostic criteria for the long QT syndrome: an update. Circulation. 1993;88(2):782-4.
  • 130. Hofman N, Wilde AA, Kaab S, van Langen IM, Tanck MW, Mannens MM, et al. Diagnostic criteria for congenital long QT syndrome in the era of molecular genetics: do we need a scoring system? Eur Heart J. 2007;28(5):575-80.
  • 131. Splawski I, Shen J, Timothy KW, Lehmann MH, Priori S, Robinson JL, et al. Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation. 2000;102(10):1178-85.
  • 132. Brink PA, Crotti L, Corfield V, Goosen A, Durrheim G, Hedley P, et al. Phenotypic variability and unusual clinical severity of congenital long-QT syndrome in a founder population. Circulation. 2005;112(17):2602-10.
  • 133. Bowlby MR, Peri R, Zhang H, Dunlop J. hERG (KCNH2 or Kv11.1) K+ channels: screening for cardiac arrhythmia risk. Curr Drug Metab. 2008;9(9):965-70.
  • 134. Jackson HA, Accili EA. Evolutionary analyses of KCNQ1 and HERG voltage-gated potassium channel sequences reveal location-specific susceptibility and augmented chemical severities of arrhythmogenic mutations. BMC Evol Biol. 2008;8:188.
  • 135. Goldenberg I, Mathew J, Moss AJ, McNitt S, Peterson DR, Zareba W, et al. Corrected QT variability in serial electrocardiograms in long QT syndrome: the importance of the maximum corrected QT for risk stratification. J Am Coll Cardiol. 2006;48(5):1047-52.
  • 136. Priori SG, Schwartz PJ, Napolitano C, Bloise R, Ronchetti E, Grillo M, et al. Risk stratification in the long-QT syndrome. N Engl J Med. 2003;348(19):1866-74.
  • 137. Vincent GM, Schwartz PJ, Denjoy I, Swan H, Bithell C, Spazzolini C, et al. High efficacy of beta-blockers in long-QT syndrome type 1: contribution of noncompliance and QT-prolonging drugs to the occurrence of beta-blocker treatment "failures". Circulation. 2009;119(2):215-21.
  • 138. Villain E, Denjoy I, Lupoglazoff JM, Guicheney P, Hainque B, Lucet V, et al. Low incidence of cardiac events with beta-blocking therapy in children with long QT syndrome. Eur Heart J. 2004;25(16):1405-11.
  • 139. van den Berg MP, Wilde AA, Viersma TJW, Brouwer J, Haaksma J, van der Hout AH, et al. Possible bradycardic mode of death and successful pacemaker treatment in a large family with features of long QT syndrome type 3 and Brugada syndrome. J Cardiovasc Electrophysiol. 2001;12(6):630-6.
  • 140. Chien WW, Foster E, Phillips B, Schiller N, Griffin JC. Pacemaker syndrome in a patient with DDD pacemaker for long QT syndrome. Pacing Clin Electrophysiol. 1991;14(8):1209-12.
  • 141. Daubert JP, Zareba W, Rosero SZ, Budzikowski A, Robinson JL, Moss AJ. Role of implantable cardioverter defibrillator therapy in patients with long QT syndrome. Am Heart J. 2007;153(4 Suppl):53-8.
  • 142. Zareba W, Moss AJ, Daubert JP, Hall WJ, Robinson JL, Andrews M. Implantable cardioverter defibrillator in high-risk long QT syndrome patients. J Cardiovasc Electrophysiol. 2003;14(4):337-41.
  • 143. Schwartz PJ, Priori SG, Cerrone M, Spazzolini C, Odero A, Napolitano C, et al. Left cardiac sympathetic denervation in the management of high-risk patients affected by the long-QT syndrome. Circulation. 2004;109(15):1826-33.
  • 144. Collura CA, Johnson JN, Moir C, Ackerman MJ. Left cardiac sympathetic denervation for the treatment of long QT syndrome and catecholaminergic polymorphic ventricular tachycardia using video-assisted thoracic surgery. Heart Rhythm. 2009;6(6):752-9.
  • 145. Maury P, Extramiana F, Sbragia P, Giustetto C, Schimpf R, Duparc A, et al. Short QT syndrome: update on a recent entity. Arch Cardiovasc Dis. 2008;101(11-12):779-86.
  • 146. Gaita F, Giustetto C, Bianchi F, Schimpf R, Haissaguerre M, Calò L, et al. Short QT syndrome: pharmacological treatment. J Am Coll Cardiol. 2004;43(8):1494-9.
  • 147. Schimpf R, Wolpert C, Bianchi F, Giustetto C, Gaita F, Bauersfeld U, et al. Congenital short QT syndrome and implantable cardioverter defibrillator treatment: inherent risk for inappropriate shock delivery. J Cardiovasc Electrophysiol. 2003;14(12):1273-7.
  • 148. Schimpf R, Bauersfeld U, Gaita F, Wolpert C. Short QT syndrome: successful prevention of sudden cardiac death in an adolescent by implantable cardioverter-defibrillator treatment for primary prophylaxis. Heart Rhythm. 2005;2(4):416-7.
  • 149. Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease. Circulation. 1998;97(5):457-60.
  • 150. Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation. 2005;111(5):659-70.
  • 151. Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, et al. Brugada syndrome: report of the second consensus conference. Heart Rhythm. 2005;2(4):429-40.
  • 152. Brugada J, Brugada R, Brugada P. Determinants of sudden cardiac death in individuals with the electrocardiographic pattern of Brugada syndrome and no previous cardiac arrest. Circulation. 2003;108(25):3092-6.
  • 153. Veltmann C, Schimpf R, Echternach C, Eckardt L, Kuschyk J, Streitner F, et al. A prospective study on spontaneous fluctuations between diagnostic and non-diagnostic ECGs in Brugada syndrome: implications for correct phenotyping and risk stratification. Eur Heart J. 2006;27(21):2544-52.
  • 154. Tatsumi H, Takagi M, Nakagawa E, Yamashita H, Yoshiyama M. Risk stratification in patients with Brugada syndrome: analysis of daily fluctuations in 12-lead electrocardiogram (ECG) and signal-averaged electrocardiogram (SAECG). J Cardiovasc Electrophysiol. 2006;17(7):705-11.
  • 155. Leite LR, Ponzi Pereira KR, Alessi SR, de Paola AA. Catecholaminergic polymorphic ventricular tachycardia. An important diagnosis in children with syncope and normal heart. Arq Bras Cardiol. 2001;76(1):63-74.
  • 156. Leenhardt A, Lucet V, Denjoy I, Grau F, Ngoc DD, Coumel P. Catecholaminergic polymorphic ventricular tachycardia in children: a 7-year follow-up of 21 patients. Circulation. 1995;91(5):1512-9.
  • 157. Napolitano C, Priori SG. Diagnosis and treatment of catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm. 2007;4(5):675-8.
  • 158. Leite LR, Henz BD, Macedo PG, Santos SN, Barreto JR, Zanatta A, et al. Catecholaminergic polymorphic ventricular tachycardia: a current overview. Future Cardiol. 2009;5(2):191-9.
  • 159. Maron BJ, Gohman TE, Aeppli D. Prevalence of sudden cardiac death during competitive sports activities in Minnesota high school athletes. J Am Coll Cardiol. 1998;32(7):1881-4.
  • 160. Luckstead EF, Patel DR. Catastrophic pediatric sports injuries. Pediatr Clin North Am. 2002;49(3):581-91.
  • 161. Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, et al; American College of Cardiology/American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114(10):e385-484.
  • 162. Drezner JA, Rogers KJ. Sudden cardiac arrest in intercollegiate athletes: detailed analysis and outcomes of resuscitation in nine cases. Heart Rhythm. 2006;3(7):755-9.
  • 163. Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA. 1996;276(3):199-204.
  • 164. Wang DW, Desai RR, Crotti L, Arnestad M, Insolia R, Pedrazzini M, et al. Cardiac sodium channel dysfunction in sudden infant death syndrome. Circulation. 2007;115(3):368-76.
  • 165. Goldenberg I, Moss AJ, Bradley J, Polonsky S, Peterson DR, McNitt S, et al. Long-QT syndrome after age 40. Circulation. 2008;117(17): 2192-201.
  • 166. Tagarakis CV, Bloch W, Hartmann G, Hollmann W, Addicks K. Anabolic steroids impair the exercise-induced growth of the cardiac capillary bed. Int J Sports Med. 2000;21(6):412-8.
  • 167. Olson KR. Poisoning and drug overdose (Lange Clinical Manual). United States of America: McGraw-Hill; 2007.
  • 168. Gahlinger PM. Club drugs: MDMA, gamma-hydroxybutyrate (GHB), Rohypnol, and ketamine. Am Fam Physician. 2004;69(11):2619-26.
  • 169. Barbosa ET. Criterios para solicitação de exames complementares do aparelho cardiovascular. Arq Bras Cardiol. 1997;68(3):I-IX.
  • 170. Panhuyzen-Goedkoop NM. Preparticipation cardiovascular screening in young athletes. Br J Sports Med. 2009;43(9):629-30.
  • 171. Papadakis M, Whyte G, Sharma S. Preparticipation screening for cardiovascular abnormalities in young competitive athletes. BMJ 2008;337:a1596.
  • 172. Maron BJ, Thompson PD, Puffer JC, McGrew CA, Strong WB, Douglas PS, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation. 1996;94(4):850-6.
  • 173. Conselho Regional de Medicina do Estado do Rio de Janeiro. (CREMERJ). Resolução do Cremerj 158/2000 sobre teste ergométrico [01ş/07/2010]. [Acesso em 2011 jun 18]. Disponível em: http://www.cremerj.org.br/legislacao/detalhes.php?id=283&item=1
  • 174. Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med. 2000;343(19):1355-61.
  • 175. Marenco JP, Wang PJ, Link MS, Homoud MK, Estes NA 3rd. Improving survival from sudden cardiac arrest: the role of the automated external defibrillator. JAMA. 2001;285(9):1193-200.
  • 176. Myerburg RJ, Estes NA 3rd, Fontaine JM, Link MS, Zipes DP. Task Force 10: automated external defibrillators. J Am Coll Cardiol 2005;45(8):1369-71.
  • 177. Oliveira Filho JA. O Atleta paraolímpico. In: Ghorayeb N, Dioguardi GS. Tratado de cardiologia do exercício e do esporte. São Paulo: Atheneu; 2007.
  • 178. Vital R, Silva Hesojy GPV. As lesões traumato-ortopédicas. In: Mello MT (ed). Avaliação clínica e da aptidão física dos atletas paraolimpícos brasileiros: conceitos, métodos, resultados. São Paulo: Atheneu; 2004.
  • 179. Khalili MA. Quantitative sports and functional classification (QSFC) for disabled people with spasticity. Br J Sports Med. 2004;38(3):310-3.
  • 180. Ackel CR, Lira CAB, Silva AC. A avaliação ergoespirométrica. In: Mello MT (editor). Avaliação clínica e da aptidão física dos atletas paraolímpicos brasileiros: conceitos, métodos e resultados. São Paulo: Atheneu; 2004.
  • 181. Knechtle B, Hardegger K, Muller G, Odermatt P, Eser P, Knecht H. Evaluation of sprint exercise testing protocols in wheelchair athletes. Spinal Cord. 2003;41(3):182-6.
  • 182. Knechtle B, Kopfli W. Treadmill exercise testing with increasing inclination as exercise protocol for wheelchair athletes. Spinal Cord. 2001;39(12):633-6.
  • 183. Oliveira Filho JA, Luna Filho B, Covre SH, Lira Filho E, Regazzini M, Greco J, et al. Signal averaged electrocardiogram in top deficient athletes. Arq Bras Cardiol. 1999;72(6):687-92.
  • 184. Janssen PM, Hasenfuss G, Zeitz O, Lehnart SE, Prestle J, Darmer D, et al. Load-dependent induction of apoptosis in multicellular myocardial preparations. Am J Physiol Heart Circ Physiol. 2002;282(1):H349-56.
  • 185. Oliveira JA, Salvetti XM, Lira EB, Mello MT, Silva AC, Luna B. Athlete's heart, oxygen uptake and morphologic findings in paralympic athletes. Int J Cardiol. 2007;121(1):100-1.
  • 186. Silva AC, Oliveira Fş JA. Avaliação dos paraolímpicos de Atlanta. São Paulo: UNIFESP-EPM; 2006.
  • 187. Ferrara MS, Buckley WE, McCann BC, Limbird TJ, Powell JW, Robl R. The injury experience of the competitive athlete with a disability: prevention implications. Med Sci Sports Exerc. 1992;24(2):184-8.
  • 188. IPC Classification Code and International Standards. [Acessed in 2011 Sep 10]. Available from: http://oldwebsite:palympic.org/Sport?Classification/Classification_Code.html
  • 189
    Comitê Olímpico Brasileiro. [Acesso em 2011 dez 07]. Disponível em: http://www.cob.org.br
    » link
  • 190
    The World anti-doping code. The 2007 prohibited list international standard. [Acessed in 2011 Oct 13]. Available from: http://www.wada-ama.org
  • Guideline in Cardiology of Sport and Exercise of the Brazilian Society of Cardiology and the Brazilian Society of Sports Medicine

    Ghorayeb N., Costa R.V.C., Daher D.J., Oliveira Filho J.A., Oliveira M.A.B. et al.
  • Publication Dates

    • Publication in this collection
      04 Apr 2013
    • Date of issue
      Jan 2013
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