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Rev. bras. fisioter. vol.16 no.5 São Carlos Sept./Oct. 2012 Epub Oct 02, 2012
Teste de exercício cardiopulmonar na fase precoce do infarto do miocárdio
Vandeni C. KunzI; Karina B. S. SerraII; Érica N. BorgesII; Paulo E. S. SerraIII; Ester SilvaI,II
ILaboratory of Cardiovascular Physical Therapy, Nucleus of Research in Physical Exercise (NUPEF), Department of Physical Therapy, Universidade Federal de São Carlos (UFSCar), São Carlos, SP, Brazil
IILaboratory of Research in Cardiovascular Physical Therapy and Functional Tests, Faculty of Health Sciences (FACIS), Universidade Metodista de Piracicaba (UNIMEP), Piracicaba, SP, Brazil
IIICardiology Clinic Tricórdis, Piracicaba, SP, Brazil
OBJECTIVE: To evaluate and to compare the cardiorespiratory and metabolic variables at the ventilatory anaerobic threshold level (AT) and at submaximal cardiopulmonary exercise testing (CPET) in both, healthy volunteers and in patients in the early phase after acute myocardial infarction (AMI).
METHOD: Twenty-six volunteers underwent a submaximal or symptom-limited cardiopulmonary exercise testing (CPET) on a cycle ergometer and were divided into AMI group (AMIG=12, 56.33±8.65 years) and healthy group (CG=14, 53.33±3.28 years). The primary outcome measures were the cardiorespiratory and metabolic variables obtained at the peak workload and at the AT of the CPET. Statistical test: independent Student's t-test, α=5%.
RESULTS: The AMIG presented lower values at the AT and the peak workload of the CPET compered to the CG: power in watts (91.06±30.10 and 64.88±19.92; 154.93±34.65 and 120.40±29.60); VO2 mL.kg-1.min-1 (17.26±2.71 and 12.19±2.51; 25.39±5.73 and 19.41±5.63); VCO2 L/min-1 (1.43±0.31 and 0.93±0.23; 2.07±0.43 and 1.42±0.36), VO2 L/min-1 (1.33±0.32 and 1.00±0.23; 1.97±0.39 and 1.49±0.36); VE L/min-1 (42.13±8.32 and 27.51±5.86; 63.07±20.83 and 40.82±11.96); HR (bpm) (122.96±14.02 and 103.46±13.38; 149.67±13.77 and 127.60±10.04), double product (DP) (bpm.mmHg.min-1) (21835.86±3245.93 and 17333.25±2716.51; 27302.33±3053.08 and 21864.00±2051.48), respectively. The variable oxygen uptake efficiency slope (OUES L/min) was lower in the AMIG (1.79±0.51) than the CG (2.26±0.37). The AMIG presented neither ECG alterations nor symptoms that limited the CPET.
CONCLUSION: The results suggest that patients with AMI Killip class I presented lower functional capacity and DP compared to the CG without presenting ischemic alterations. Thus, the study suggests that submaximal CPET can be applied at an early stage to evaluate cardiorespiratory status since it is both safe and highly sensitive to detect changes.
Keywords: oxygen consumption; myocardial infarction; physical exercise; physical therapy.
OBJETIVO: Avaliar e comparar as variáveis cardiorrespiratórias e metabólicas no nível do limiar de anaerobiose ventilatório (LAV) e no pico do teste de exercício cardiopulmonar (TECP) submáximo em voluntários saudáveis e em pacientes na fase precoce após o infarto agudo do miocárdio (IAM).
MÉTODO: Vinte e seis voluntários realizaram TECP submáximo ou sintoma limitante em cicloergômetro e foram divididos em grupo IAM (G-IAM=12, 56,33±8,65 anos) e grupo saudável (GC=14, 53,33±3,28 anos). As medidas dos desfechos principais foram as variáveis cardiorrespiratórias e metabólicas obtidas no pico e no LAV do TECP. Teste estatístico: t-Student não pareado, α=5%.
RESULTADOS: O G-IAM apresentou menores valores no LAV e no pico do TECP que o GC (p<0,05): potência em Watts (91,06±30,10 e 64,88±19,92; 154,93±34,65 e 120,40±29,60); VO2mL.kg-1.min-1 (17,26±2,71 e 12,19±2,51; 25,39±5,73 e 19,41±5,63); VCO2L/min-1 (1,43±0,31 e 0,93±0,23; 2,07±0,43 e 1,42±0,36), VO2L/min-1 (1,33±0,32 e 1,00±0,23; 1,97±0,39 e 1,49±0,36); VEL/min-1 (42,13±8,32 e 27,51±5,86; 63,07±20,83 e 40,82±11,96); FC (bpm) (122,96±14,02 e 103,46±13,38; 149,67±13,77 e 127,60±10,04); duplo produto (DP) (bpm.mmHg.min-1) (21835,86±3245,93 e 17333,25±2716,51; 27302,33±3053,08 e 21864,00±2051,48), respectivamente. A variável Oxygen Uptake Efficiency Slope (OUES L/min) do G-IAM foi 1,79±0,51 e do GC 2,26±0,37, p<0.05. O G-IAM não apresentou alterações eletrocardiográficas ou sintomas que limitassem o TECP.
CONCLUSÃO: Os resultados mostram que os pacientes com IAM Killip I apresentaram menor capacidade funcional e DP em relação ao GC, sem apresentar alterações isquêmicas. Assim, o estudo sugere que o TECP submáximo pode ser aplicado precocemente para a avaliação cardiorrespiratória por apresentar alta sensibilidade para detectar alterações de forma segura.
Palavras-chave: consumo de oxigênio; infarto do miocárdio; exercício físico; fisioterapia.
The recommendation for physical therapy treatment based on physical training within a cardiac rehabilitation program for patients after acute myocardial infarction (AMI) depends on its evolution based on clinical criteria and results of invasive and non-invasive exams1-3. Among the non-invasive examinations, the cardiopulmonary exercise testing (CPET) performed in an early-phase after the coronary event has become routine in several medical centers3-5. From this exam, it is possible to obtain more precise information regarding the integration among the pulmonary, cardiovascular and musculoskeletal systems and the changes of the functional aerobic capacity due to pathological conditions, such as in the AMI5-7. In addition, it is possible to evaluate the prognosis of the patient in relation to risk stratification for new cardiac events2,3.
The literature reports that the maximal oxygen consumption (VO2max) is one of the most investigated variables8,9. However, the VO2max is hardly achieved by cardiac patients, whose the exercise performance is limited by peripheral muscle fatigue, dyspnea, and the presence of significant cardiac alterations10. Moreover, the exercise performance depends on the motivation and perception of the subjects. In this case, the determination of the ventilatory anaerobic threshold (AT), which is an important physiologic parameter, has been recommended since it provides information regarding the physiological changes from the aerobic to the anaerobic metabolism11. Therefore, it has been considered more objective for the prescription of aerobic physical training, demonstrating good reproducibility9,12,13.
Furthermore, in the AT level there is a balance between the supply and consumption of O2 in the working muscles, preventing acidosis; the sympathetic nervous system is not over stimulated, and thus minor changes occur in the release of the epinephrine and norepinephrine hormones, which allows that, in this exercise level, these patients become able to maintain a working frequency for a prolonged period of time14.
Additionally, from the CPET it is possible to evaluate the variables VE/VCO2 slope and the Oxygen Uptake Efficiency Slope (OUES), which indicate the ventilatory efficiency for the production of carbon dioxide and oxygen consumption, respectively. Thus, from these variables it is possible to obtain clinical information about the functional status, disease severity15-17, and also information about the prognosis of coronary diseases, without exposing the patient to maximal CPET9,18,19. Moreover, it can be used to evaluate and prescribe the intensity of physical exercise in a cardiac rehabilitation program19,20.
The submaximal CPET has been used to evaluate the variables of cardiac patients, since during this test the oxygen supply to tissues while performing the exercise is not limited. Submaximal tests are more appropriate for patients with cardiovascular disorders because they provide greater efficacy and safety for the prescription of physical training in physical therapy treatment programs14,21,22.
The hypothesis of the present study was that patients may be submitted to submaximal CPET, after hospital discharge due to AMI, to evaluate clinical, hemodynamic, metabolic and electrocardiographic responses to submaximal CPET. Therefore, the aim of this study was to evaluate and to compare the cardiorespiratory and metabolic variables at the AT level and at the peak of the submaximal CPET in healthy subjects and in patients in the early phase after the AMI.
Study design and ethic approval
This was a cross-sectional study, with the approval of the Ethics Committee of Research of the Universidade Metodista de Piracicaba (UNIMEP), Piracicaba, SP, Brazil, nº 63/06. The participants agreed and signed an informed consent form according to the Resolution nº 196/96 of the Brazilian Health National Council.
Sample size calculation
The sample size was calculated for the variable VO2 in mL.kg-1.min-1, with a 95% confidence level and statistical power of 80%, capable to detect a difference between-groups (two-tailed test) suggested a number of 12 subjects for each group, (Graph Pad Stat Mate, version 1.01i, 1998).
One hundred and six subjects (72 with AMI and 34 healthy) with ages ranging between 50 and 65 years were screened for study participation. Of these, 12 patients with the diagnosis of AMI (56.33±8.65 years-old) and 14 healthy subjects (53.33±3.28 years-old) completed the study. The flow of the participants through the study can be observed in Figure 1.
The participants of the AMI group (AMIG) were selected in the Coronary Units of the Hospital dos Fornecedores de Cana de Piracicaba, SP and Santa Casa de Misericórdia de Limeira, SP, Brazil. The patients from the AMIG underwent to the doppler echocardiogram and cardiac catheterization with chemical or mechanical reperfusion in the first hours after the AMI; were taking beta-blockers (atenolol, 46±9.4mg/day); with left ventricular ejection fraction (LVEF) within the limits of normality (0.61±0.06); and with clinical classification of Killip I. To compose the healthy group (CG), 34 subjects were evaluated (CG), being included 14 subjects whom had not participated in physical training programs; presented an aerobic classification as weak23, did not have any indication of cardiovascular, respiratory, musculoskeletal and/or metabolic abnormalities, were not taken medications and were not smokers or alcohol drinkers.
Subjects from both groups underwent clinical and cardiovascular evaluation and also performed blood biochemical tests (total and fraction cholesterol (HLD, LDL) blood glucose, triglycerides, creatinine and uric acid).
The diagnosis of AMI had been confirmed by the presence of two or more criteria: 1) chest or retrosternal pain (constricting or burning pain), with or without radiation for the upper limbs, neck and upper back, lasting >30 minutes with no relief of symptoms to the vasodilator; 2) ST-segment elevation >1 mV in at least two or more contiguous electrocardiogram (ECG), 3) elevation of myocardial necrosis markers CK-MB and CPK, twice the normal values24.
All the participants underwent clinical evaluation performed by a cardiologist before the performance of the CPET.
The experimental procedures were held in acclimatized laboratory, with temperature and relative humidity around 23ºC and 60% respectively. The tests were performed in the afternoon to minimize the interferences of the circadian cycle on the cardiovascular responses. The participants were previously familiarized with the laboratory environment, with the experimental procedures and with the equipments that were used in the experiment. All subjects were instructed not to ingest caffeine, alcoholic beverages and do not perform physical exercise on the day before and in the day of the experiments. During the experiments, the AMIG should maintain the medication in use. Before beginning the tests, the volunteers were asked about the occurrence of a normal night's sleep and, in addition, examined in order to guarantee that they were with their basal conditions within the normality limits25.
The experiment consisted of a CPET, ramp-type continuous physical exercise, performed in a cycle ergometer with electromagnetic breaking (QuintonCorival 400, Seattle, WA, USA), with seat height adjusted to allow knee flexion of 5-10 degrees. The participants were instructed not to perform an isometric contraction of the upper limbs, while holding the handlebars of the bicycle, and to maintain pedaling cadence at 60 rpm.
The protocol consisted of a pre-test rest sitting on a cycle ergometer for a period of 60 seconds; starting the exercise with free load during a period of 240 seconds, followed by an increase of power on every 60 seconds, individually calculated according to the formula described by Wasserman et al.14, being of 10 watts (W) for the patients of the AMIG and 15W for the volunteers of the CG. For both groups, the CPET was submaximal, being interrupted when the submaximal heart rate (HR) was reach or in the presence of signs and/or symptom-limiting26.
The HR was captured through a heart rate monitor of one channel (MINISCOPE II Instramed-Porto Alegre, RS, Brazil) and processed through an analog to digital converter Lab. PC+ (National Instruments Co. Austin, TX, USA), which represents an interface between the heart rate monitor and a microcomputer. The signal was recorded in real time, after A/D conversion, in a sampling rate of 500 Hz27; and the blood pressure (BP) was measured using the auscultatory method based on Korotkoff sound on every 2 minutes, using a mercury sphygmomanometer (WanMed, São Paulo, SP, Brasil) and a stethoscope (Littman, St. Paul, MN, USA).
Ventilatory and metabolic variables, such as pulmonary ventilation (VE) in BTPS L/min-1, VO2mL.kg-1.min-1, and VCO2 in L/min-1, respiratory exchange ratio (R) and HR were recorded simultaneously during the entire CPET, breath by breath, through a measurement system of the expired gases (CPX/D Med Graphics Breeze, St. Paul, Minesota, USA), which was calibrated before each test. These variables were subsequently processed and calculated as moving means every eight respiratory cycles for better kinetic observation of responses during physical exercise.
Analysis of ventilatory and metabolic variables
The determination of AT was performed through the graphic visual analysis method of the responses of the metabolic and ventilatory variables, performed by three observers with previous experience in the administration of the procedures used for such purpose. The criterion for the quantification of the AT was the moment that a disproportional increase of VCO2 in relation to a linear increase of VO2 was observed by analyzing the graphic in the ergospirometer monitor11,27. For this analysis, it was selected the slope interval between the early response of the ventilatory and metabolic variables at increasing power until the respiratory compensation point (RCP) or until the end of the exercise, if the participant did not present the RCP. This analysis was based in the method V-slope described by Wasserman and McIlroy28, which is considered a gold-standard. From this, there were verified the power values in watts, HR in bpm, VO2 in ml.kg-1.min-1 and L/min, VCO2 and L/min R, VE in L/min, respiratory exchange rate (R) and correspondening to the AT and the peak of exercise. The AT value was considered as the mean of the data obtained from the analysis of the three observers. The inter-rater reliability measured by the intraclass correlation coefficient (ICC) was of 0.9629.
The slope VE/VCO2 was calculated by linear regression models, from the beginning of increase of power during the test until the peak of exercise, using the values of the increased minute ventilation in relation to the carbon dioxide production, obtained during the CPET30.
The OUES, which represents the relation between VO2 and VE during the incremental exercise test, was calculated by logarithm expression of ventilation, in which OUES is defined as the regression slope "a" in VO2=a.logVE+b. A high or sharpened OUES represents greater efficiency of VO2, whereas a low OUES represents a greater VE in relation to VO220. For the calculation of the predicted values of OUES, we used the equation published by Hollenberg and Tanger31, in which men is represented by OUES (L/min)=[1320-(26.7 x age)+(1394 x body surface area)]/1000.
Data analysis was performed using the softwarw SPSS, version 16. The normal distribution of all variables was verified using the Shapiro-Wilk test. Independent Student's t-test, with significance level of α=5%, was used for the between-group comparison. The results for age, anthropometric characteristics and cardiovascular variables during rest were expressed as means and standard-deviation. The results of the clinical characteristics were expressed in number of volunteers and percentage. The values of cardiorespiratory variables obtained in the CPET were expressed as mean and standard deviation, mean difference and its 95% confidence intervals (CI).
Anthropometric characteristics, age and cardiovascular variables during rest did not differ between the groups studied (Table 1). The risk factors present at AMIG were tabagism, hyperglycemia, hypercholesterolemia, hypertriglyceridemia, systemic arterial hypertension. On the other hand, the CG did not present any of the risk factors mentioned above. The clinical characteristics related to the AMIG data concerning the localization and clinical classification of the AMI, left ventricle ejection fraction (LVFE), type of myocardial reperfusion and the use of medications are presented in Table 1.
Analysis of the ventilatory and metabolic variables
The ventilatory and metabolic variables obtained during peak exercise and the AT, concerning to power, VO2, VCO2, VE, HR e DP of the AMIG were significantly lower compared to CG (p<0.05). The values of the variables slope VE/VCO2 and OUES predicted did not present significant between-group difference. The OUES obtained in the AMIG was lower than the CG (p<0.05). However, the variables R, SBP and DBP at peak exercise and at AT did not present between-group difference (p>0.05) (Table 2).
Signs and symptoms during the cardiopulmonary exercise testing
The electrocardiographic data during rest and during CPET are described in Table 3. Patients presented an abnormal resting ECG related to AMI, and in the effort ECG any patient presented alterations in the ST-segment and the changes observed during resting was maintained. The data related to the symptoms of AMIG present at the peak of exercise and at the AT during the CPET is described in Table 3. In the AT, all patients reported absence of symptoms during effort and at peak of exercise, two patients had dyspnea associated to hypertension reactive to the effort, one patient and presented dyspnea and nine patients had fatigue of the lower limbs, evaluated based on the non-maintenance of the rpm.
The early evaluation of the aerobic functional capacity in patients suffering from AMI using beta blockers is of fundamental importance for the risk stratification, recommendation about the limitations to perform physical activity, as well as to prescribe the appropriate physical training intensity14,32. In this sense, the AMIG underwent to sub-maximal CPET 22±4 days (on average) after the AMI, as well as in the studies of Tabet et al.33 and Duru et al.34, which evaluated the patients at 18 and 36 days (on average) after the AMI, respectively. During the CPET, the AMIG have not presented any signs or symptoms that limited its performance.
In our study, we observed that the AMIG showed lower aerobic functional capacity both in the AT and at peak exercise compared to the CG, demonstrated by the power, HR, VO2, VCO2 and VE, obtained during the CPET. The AMIG presented VO2 values in the AT of 12.19±2.51 mL.kg-1.min-1, being this result lower that the findings by Tabet et al.33 (15.9±5.1 mL.kg-1.min-1) which have evaluated sedentary infarction patients using atenolol (69±4 mg). At peak exercise, the values obtained from VO2 were 17.27±2.71 and 25.39±5.73 mL.kg-1.min-1 for the AMIG and CG, respectively, being these values similar to those found in studies of Giallauria et al.30 and Tabet et al.33.
The lowest functional capacity values presented by AMIG, in both at the AT and at peak exercise, can be attributed to two distinct mechanisms: 1) the presence of pathology and 2) to the use of betablocker therapy.
Intolerance to exercise in patients with AMI is a common problem. These patients usually present a reduction in the central and peripheral blood flow during exercise, since the increased peripheral vascular conduction is strongly associated to cardiac output response. Thus, after the AMI, the changes in ventricular function that compromise cardiac output may be responsible for the decline in aerobic functional capacity of these patients35-37. Therefore, the lowest values of VO2 found in the AMIG, both in the AT and in the peak of the sub-maximal CPET, may be attributed to reduced cardiac output and increased peripheral vascular conductance. This condition may lead the patient, during exercise, to a situation of lactate accumulation and lower limb fatigue38-40, which contributes for lower exercise tolerance and possibly justify the findings of this study.
Another important aspect in this study is related to beta-blocker therapy used by AMIG, being these medications are routine and first choice for treatment of this pathology41. These drugs improve survival and reduce hospitalization in this group of patients, and its action on exercise tolerance is still contradictory30,33,43,42.
The beta-blockers are able to partially antagonize the sympathetic activity, which reduces HR, the myocardial oxygen consumption and increases the time of left ventricular filling, with improve myocardial perfusion44. The beta-blocker may also partially inhibit inflammatory activity, with effects on apoptosis and hypertrophy of cardiomyocytes, leading to increase left ventricular ejection fraction and, consequently, increase cardiac output. Therefore, the beta-blocker therapy may influence the hemodynamic adjustment needed to maintain the increasing needs of muscle metabolic demand44,45, although some studies suggest that these drugs improve exercise tolerance, but do not improve the performance of the exercise and the consumption of oxygen9,45. It is likely that, in our study, patients after AMI have been benefited by the use of beta-blocker therapy, however presenting lower values of oxygen consumption in relation to the CG.
Although the SBP and the DBP at the peak and at AT has not differ during the CPET, the DP, which is estimated by multiplying the HR by SBP, was significantly higher for the CG. This indicates an increased myocardial oxygen consumption, which may be explained by the fact that the CG have reached higher power (watts), indicating greater functional aerobic capacity. In addition, the AMIG was in beta-blocker therapy and showed lower HR values at peak exercise and at AT. Accordingly, it is important to concurrently measure the HR and BP to safely assess the cardiovascular stress during exercise, since high values of DP at the peak of the exercise test must be related to preserved ventricular function and absence of ischemia46.
In addition to the variables already discussed, we emphasize that the assessment of the slope VE/VCO2 and OUES is of fundamental importance, since we can obtain information from pulmonary perfusion capability and cardiac output in an indirect way. Our results show median values of VE/VCO2 of 26.89±3.54 for AMIG and 28.21±4.79 for CG, which are considered within the normal range. Previous studies have determined values of normality for VE/VCO2 slope lower than 30 and changed values between 30 and 70, which are usually found in patients with cardiac alterations9,42. In this way, the results suggest that both groups evaluated did not present reduced pulmonary perfusion capability and cardiac output, since this variable present a significant correlation with preserved function of mecanorreceptores and ergorreceptores, thereby contributing to the normal respiratory test response to exercise. However, in the study of Giallauria et al.30 in patients after 36 days of AMI, the relationship of VE/VCO2 was 33.80±4.00. These results differ from those observed in our study. On the other hand, for healthy individuals aged 50-60 years-old, Sun et al.47 found VE/VCO2 values of 27.20±3.00, which is similar to our findings.
Addition to the evaluated parameters described above, it is also possible to estimate the cardiopulmonary functional reserve of patients with AMI through the OUES variable20 without therefore submitting them to maximal exercise testing, The OUES is physiologically based on the development of metabolic acidosis, which is controlled by the redistribution of blood flow to the activate muscles. The OUES is also based on physiologic dead space, which is affected by pulmonary perfusion9. In this study, we found OUES values for AMIG below the predicted, being the obtained value of 1.79±0.51 L/min and the predicted values of 2.38±0.35 L/min. However, the results of the AMIG are similar to the findings of the studies from Van Laethem et al.9, Davies et al.20 (1.60±0.70 L/min) and Van de Veire et al.48 (1.30±0.43 L/min).
Therefore, the AMIG presents a reduction of cardiopulmonary functional reserve index in addition to the reduction of functional capacity, which perhaps may be justify by the fact that the presence of pathologies and in elderly people occur changes in the ventilatory responses to exercise due to abnormalities in the musculoskeletal system (increased ergorreflex activity, reduced efficiency of muscle fibers of type 1) and decreased lung capacity and volumes, resulting in lower OUES values.
The results of the present study reinforce the importance of determining the functional capacity and the aerobic cardiopulmonary reserve of coronary patients, as these variables will contribute to guide the physical activity prescription for this population37.
Moreover, during the CPET, is also possible to determine clinical changes that usually include the presence of chest pain and dyspnea due to physical effort, and also muscle fatigue. During the performance of the CPET the patients from AMIG were asymptomatic at AT reporting only dyspnea and fatigue of the lower limbs at peak exercise (Table 3). With regards to the electrocardiographic data during the CPET, no patient presented changes in the ST-segment, indicating the absence of ischemic event during the effort. There was also no changes were observed for the electrocardiogram alteration that already existent during rest. These findings demonstrate that even those patients that have presented reduced functional aerobic capacity, they have not presented clinical changes regarding the symptomatology that could limited the CPET. Therefore, these patients can be safely included in physical training programs to improve functional capacity and exercise tolerance, aiming to reduce modifiable risk factors for cardiovascular disease, to stabilize and slow down or even reverse the progression of atherosclerotic processes, reducing morbidity and mortality.
The impossibility to generalize our results can be considered a limitation of the present study, since only AMI Killip class I patients, asymptomatic, clinically stable and using beta-blockers were evaluated. More detailed studies with samples that involve patients with Killip II clinical classification, as well as patients with AMI not receiving beta-blocker therapy, would be relevant to assess whether they can perform physical activity safely without the supervision of a specialist in the area of cardiac rehabilitation.
The results show that patients with AMI Killip I had lower functional capacity in relation to CG, without presenting ischemic changes. The results of the VE/VCO2 slope and OUES indicate that the AMIG has normal ventilatory response to exercise, however with reduced cardiorespiratory functional response. Thus, the study suggests that the sub-maximal CPET can be early administered to cardio-respiratory assessment since it offers high sensitivity to detect changes in a safely manner.
Implications for physical therapy
For some time, the physical therapy area has sought scientific basis to guide clinical practice and subsidize the choice of interventions. Detailed analyses of the CPET may be used as a diagnostic tool for assessing the cardiopulmonary responses to physical exercise.
In addition, the relationship of the AT with heart alterations refers to the importance of the physiotherapeutic treatment be directed to minimize the overload to the cardiovascular system, providing better exercise tolerance and reduced symptoms such as dyspnea and fatigue of the lower limbs.
Therefore, the introduction of the CPET executed by health professionals aim to encourage the use of this non-invasive technique in the cardiac rehabilitation filed and, therefore to evaluate and re-evaluate the functional capacity of the AT level before and after physiotherapy interventions.
To the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPQ), Brasília DF, Brazil (579408/2008-6, 478601/2010-7 e 308348/2009-5) for the financial support and to the doctors responsible for the Coronary Units of the Hospital dos Fornecedores de Cana de Piracicaba, SP (Luiz Antônio Gubolino) and of the Santa Casa de Misericórdia de Limeira, SP (Luciano D. Dantas).
1. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined A consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol. 2000;36(3):959-69. [ Links ]
2. Goto Y, Sumida H, Ueshima K, Adachi H, Nohara R, Itoh H. Safety and implementation of exercise testing and training after coronary stenting in patients with acute myocardial infarction. Circ J. 2002;66(10):930-6. [ Links ]
3. Thompson PD. Exercise prescription and proscription for patients with coronary artery disease. Circulation. 2005;112(15):2354-63. [ Links ]
4. Fuchs ARCN, Meneghelo RS, Stefanini E, De Paola AV, Smanio PEP, Mastrocolla LE, et al. Exercise may cause myocardial ischemia at the anaerobic threshold in cardiac rehabilitation programs. Braz J Med Biol Res. 2009;42(3):272-8. [ Links ]
5. Fletcher GF, Balady GJ, Amsterdam EA, Chaitman B, Eckel R, Fleg J, et al. Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association. Circulation. 2001;104(14):1694-740. [ Links ]
6. Wasserman K, Hansen JE, Sue DY, Stringer WW, Whipp BJ. Principles of exercise testing and interpretation. 3ª ed. Philadelphia: Wiliams & Wilins; 1999. [ Links ]
7. Regenga MM, Peondini GB, Mafra JMS. Reabilitação precoce do paciente infartado. In: Regenga MM. Fisioterapia em cardiologia: da UTI a Reabilitação. São Paulo: Rocca; 2000. [ Links ]
8. Lavie CJ, Milani RV, Mehra MR. Peak exercise oxygen pulse and prognosis in chronic heart failure. Am J Cardiol. 2004;93(5):588-93. [ Links ]
9. Van Laethem C, Bartunek J, Goethals M, Nellens P, Andries E, Vanderheyden M. Oxygen uptake efficiency slope, a new submaximal parameter in evaluating exercise capacity in chronic heart failure patients. Am Heart J. 2005;149(1):175-80. [ Links ]
10. Braga AMFW, Rondon MUPB, Negrão CE, Wajngarten M. Predictive value of ventilatory and metabolic variables for risk of death in patients with cardiac failure. Arq Bras Cardiol. 2006;86(6):451-8. [ Links ]
11. Higa MN, Silva E, Neves VF, Catai AM, Gallo Júnior L, Silva de Sá MF. Comparison of anaerobic threshold determined by visual and mathematical methods in healthy women. Braz J Med Biol Res. 2007;40(4):501-8. [ Links ]
12. Myers J, Gullestad L. The role of exercise testing and gas-exchange measurement in the prognostic assessment of patients with heart failure. Curr Opin Cardiol. 1998;13(3):145-55. [ Links ]
13. Barmeyer A, Meinertz T. Anaerobic threshold and maximal oxygen uptake in patients with coronary artery disease and stable angina before and after percutaneous transluminal coronary angioplasty. Cardiology. 2002;98(3):127-31. [ Links ]
14. Wasserman K, Hansen JE, Sue D, Whipp BJ, Casaburi R. Principles of exercise testing and interpretation. 4ª ed. Philadelphia: Williams & Wilkins; 1999. [ Links ]
15. Arena R, Humphrey R, Peberdy MA. Prognostic ability of VE/VCO2 slope calculations using different exercise test time intervals in subjects with heart failure. Eur J Cardiovasc Prev Rehabil. 2003;10(6):463-8. [ Links ]
16. Defoor J, Schepers D, Reybrouck T, Fagard R, Vanhees L. Oxygen uptake efficiency slope in coronary artery disease: clinical use and response to training. Int J Sports Med. 2006;27(9):730-7. [ Links ]
17. Pinkstaff S, Peberdy MA, Kontos MC, Fabiato A, Finucane S, Arena R. Usefulness of decrease in oxygen uptake efficiency slope to identify myocardial perfusion defects in men undergoing myocardial ischemic evaluation. Am J Cardiol. 2010;106(11):1534-9. [ Links ]
18. Arena R, Brubaker P, Moore B, Kitzman D. The oxygen uptake efficiency slope is reduced in older patients with heart failure and a normal ejection fraction. Int J Cardiol. 2010;144(1):101-2. [ Links ]
19. Arena R, Myers J, Guazzi M. The clinical importance of cardiopulmonary exercise testing and aerobic training in patients with heart failure. Rev Bras Fisioter. 2008;12(2):75-87. [ Links ]
20. Davies LC, Wensel R, Georgiadou P, Cicoira M, Coats AJS, Piepoli M, et al. Enhanced prognostic value from cardiopulmonary exercise testing in chronic heart failure by non-linear analysis: oxygen uptake efficiency slope. Eur Heart J. 2006;27(6):684-90. [ Links ]
21. Paschoal MA. Avaliação fisioterapêutica cardiovascular realizada durante o esforço físico. In: Paschoal MA. Fisioterapia cardiovascular: avaliação e conduta na reabilitação cardíaca. 1ª ed. Barueri: Manole; 2010. P. 122-44. [ Links ]
22. Sacilotto MC, Del Grossi RT, Sirol FN, Pessotti ER, Catai AM, Sakabe DI, et al. Relação da freqüência cardíaca e da potência pico do teste ergométrico e no nível do limiar de anaerobiose de homens de meia-idade saudáveis e de hipertensos. Fisioter Mov. 2007;20(4):43-53. [ Links ]
23. American Heart Association. Committee on exercise. Exercise testing and training of apparently health individuals. A handbook for physicians. Dallas: American Heart Association; 1972. [ Links ]
24. Piegas LS, Feitosa G, Mattos LA, Nicolau JC, Rossi Neto JM, Timerman A, et al. Sociedade Brasileira de Cardiologia. Diretriz da Sociedade Brasileira de Cardiologia sobre tratamento do infarto agudo do miocárdio com supradesnível do segmento ST. Arq Bras Cardiol. 2009; 93(6 Supl 2):e179-264. [ Links ]
25. Mion Jr D, Kohlmann Jr O, Machado CA, Amodeo C, Gomes MAM, Praxedes JN, et al. V Diretrizes brasileiras de hipertensão arterial. Arq Bras Cardiol. 2007;89(3):e24-79. [ Links ]
26. Andrade J, Brito FS, Vilas Boas F, Castro I, Oliveira JA, Guimarrães JI, et al. II Diretrizes da Sociedade Brasileira de Cardiologia sobre teste ergométrico. Arq Bras Cardiol. 2002;78(Supl 2):1-17. [ Links ]
27. Silva E, Catai AM, Trevelin LC, Guimarães JO, Silva Jr LP, Silva LMP, et al. Design of a computerized system to evaluate the cardiac function during dynamic exercise [abstract]. Phys Med Biol. 1994;33:409. [ Links ]
28. Wasserman K, McIlroy MB. Detecting the threshold of anaerobic metabolism in cardiac patients during exercise. Am J Cardiol. 1964;14:844-52. [ Links ]
29. Weir JP. Quantifying test-retest reliability using the intraclass correlation coefficient and the SEM. J Strength Cond Res. 2005;19(1):231-40. [ Links ]
30. Giallauria F, Galizia G, Lucci R, D'Agostino M, Vitelli A, Maresca L, et al. Favourable effects of exercise-based Cardiac Rehabilitation after acute myocardial infarction on left atrial remodeling. Int J Cardiol. 2010;136(3):300-6. [ Links ]
31. Hollenberg M, Tanger IB. Oxygen uptake efficiency slope: an index of exercise performance and cardiopulmonary reserve requiring only submaximal exercise. J Am Coll Cardiol. 2000;36(1):194-201. [ Links ]
32. Pithon KR, Martins LEB, Gallo Jr L, Catai AM, Silva E. Comparação das respostas cardiorrespiratórias entre exercício de carga constante e incremental abaixo, acima e no limiar de anaerobiose ventilatório. Rev Bras Fisioter. 2006;10(2):163-9. [ Links ]
33. Tabet JY, Meurin P, Ben Driss AB, Thabut G, Weber H, Renaud N, et al. Determination of exercise training heart rate in patients on B-blockers after myocardial infarction. Eur J Cardiovasc Prev Rehabil. 2006;13(4):538-43. [ Links ]
34. Duru F, Candinas R, Dziekan G, Goebbels U, Myers J, Dubach P. Effect of exercise training on heart rate variability in patients with new-onset left ventricular dysfunction after myocardial infarction. Am Heart J. 2000;140(1):157-61. [ Links ]
35. Koike A, Shimizu N, Tajima A. Relation between oscillatory ventilation at rest before cardiopulmonary exercise testing and prognosis in patients with left ventricular dysfunction. Chest. 2003;123(2):372-9. [ Links ]
36. Ogawa T, Spina RJ, Martin WH 3rd, Schechtman KB, Holloszy JO, Ehsani AA. Effects of aging, sex, and physical training on cardiovascular responses to exercise. Circulation. 1992;86(2):494-503. [ Links ]
37. Motohiro M, Yuasa F, Hattori T, Sumimoto T, Takeuchi M, Kaida M, et al. Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction. Am J Phys Med Rahabil. 2005;84(9):684-91. [ Links ]
38. Sakate Y, Yoshiyama M, Hirata K, Fujita H, Takeuchi K, Tachibana K, et al. Relationship between doppler-derived left ventricular diastolic function and exercise capacity in patients with myocardial infarction. Jpn Circ J. 2001;65(7):627-31. [ Links ]
39. Wilson JR, Martin JL, Schwartz D, Ferraro N. Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle. Circulation. 1984;69(6):1079-87. [ Links ]
40. Tajima A, Itoh H, Osada N, Omiya K, Maeda T, Ohkoshi N, et al. Oxygen uptake kinetics during and after exercise are useful markers of coronary artery disease in patients with exercise electrocardiography suggesting myocardial ischemia. Circ J. 2009;73(10):1864-70. [ Links ]
41. Shakar SF, Lowes BD, Lindenfeld J, Zolty R, Simon M, Robertson AD, et al. Peak oxigen consumption and outcome in heart failure patients chronically treated with beta-blockers. J Card Fail. 2004;10(1):15-20. [ Links ]
42. Guimarães GV, Silva MSV, D'Ávila VM, Ferreira SMA, Silva CP, Bocchi EA. Peak VO2 and VE/VCO2 slope in betablockers era in pathients with heart failure: a Brazilian experience. Arq Bras Cardiol. 2008;91(1):39-48. [ Links ]
43. Zugck C, Haunstetter A, Krüger C, Kell R, Schellberg D, Kübler W, et al. Impact of beta-blocker treatment on the prognostic value of currently used risk predictors in congestive heart failure. J Am Coll Cardiol. 2002;39(10):1615-22. [ Links ]
44. Wolk R, Johnson BD, Somers VK, Allison TG, Squires RW, Gau GT, et al. Effects of beta-blocker therapy on ventilatory responses to exercise in patients with heart failure. J Card Fail. 2005;11(5):333-9. [ Links ]
45. Corrà U, Mezzani A, Bosimini E, Scapellato F, Temporelli PL, Eleuteri E, et al. Limited predictive value of cardiopulmonary exercise indices in patients with moderate chronic heart failure treated with carvedilol. Am Heart J. 2004;147(3):553-60. [ Links ]
46. Fornitano LD, Godoy MF. Duplo produto elevado como preditor de ausência de coronariopatia obstrutiva de grau importante em pacientes com teste ergométrico positivo. Arq Bras Cardiol. 2006;86(2):139-44. [ Links ]
47. Sun XG, Hansen JE, Garatachea N, Storer TW, Wasserman K. Ventilatory efficiency during exercise in healthy subjects. Am J Respir Crit Care Med. 2002;166(11):1443-8. [ Links ]
48. Van de Veire NR, Van Laethem C, Philippé J, De Winter O, De Backer G, Vanderheyden M, et al. VE/VCO2 slope and oxygen uptake efficiency slope in patients with coronary artery disease and intermediate peak VO2. Eur J Cardiovasc Prev Rehabil. 2006;13(6):916-23. [ Links ]
Ester da Silva
Universidade Federal de São Carlos
Rodovia Washington Luís, km 235
CEP 13565-905, São Carlos, SP, Brasil
Received: 12/16/2011 Revised: 03/13/2012 Accepted: 04/23/2012