Abstract
OBJECTIVES:
The prevalence of electrocardiographic and echocardiographic abnormalities in chronic obstructive pulmonary disease according to disease severity has not yet been established. The aim of this study was to assess the prevalence of electrocardiographic and echocardiographic abnormalities in chronic obstructive pulmonary disease patients according to disease severity.
METHODS:
The study included 25 mild/moderate chronic obstructive pulmonary disease patients and 25 severe/very severe chronic obstructive pulmonary disease patients. All participants underwent clinical evaluation, spirometry and electrocardiography/echocardiography.
RESULTS:
Electrocardiography and echocardiography showed Q-wave alterations and segmental contractility in five (10%) patients. The most frequent echocardiographic finding was mild left diastolic dysfunction (88%), independent of chronic obstructive pulmonary disease stage. The proportion of right ventricular overload (p<0.05) and blockage of the anterosuperior division of the left bundle branch were higher in patients with greater obstruction. In an echocardiographic analysis, mild/moderate chronic obstructive pulmonary disease patients showed more abnormalities in segmental contractility (p<0.05), whereas severe/very severe chronic obstructive pulmonary disease patients showed a higher prevalence of right ventricular overload (p<0.05), increased right cardiac chamber (p<0.05) and higher values of E-wave deceleration time (p<0.05). Age, sex, systemic arterial hypertension, C-reactive protein and disease were included as independent variables in a multiple linear regression; only disease severity was predictive of the E-wave deceleration time [r2 = 0.26, p = 0.01].
CONCLUSION:
Chronic obstructive pulmonary disease patients have a high prevalence of left ventricular diastolic dysfunction, which is associated with disease severity. Because of this association, it is important to exclude decompensated heart failure during chronic obstructive pulmonary disease exacerbation.
Chronic Obstructive Pulmonary Disease; Electrocardiography; Echocardiography; GOLD; Spirometry
INTRODUCTION
Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation and a
range of pathological changes in the lungs. In addition, COPD presents significant extra-pulmonary
effects and is associated with important comorbidities that may contribute to the disease severity.
Chronic airflow limitation is associated with an abnormal inflammatory response of the lungs to
noxious particles or gases, particularly cigarette smoke (11. GOLD. Global Strategy for the diagnosis, management, and prevention of chronic
obstructive pulmonary disease: GOLD Executive Summary update 2011. wwwgoldcopdorg.).
The main causes of morbidity and mortality among COPD patients are cardiovascular disease (CVD) and
lung cancer (22. Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connet JE. The effects
of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern
Med. 2005;142(4):233-9.
3. Sin DD, Wu LL, Man SF. The relationship between reduced lung function and
cardiovascular mortality: a population-based study and a systematic review of the literature. Chest.
2005;127(6):1952-9.-44. Maclay JD, McAllister DA, Macnee W. Cardiovascular risk in chronic obstructive
pulmonary disease. Respirology. 2007;12(5):634-41,
http://dx.doi.org/10.1111/j.1440-1843.2007.01136.x.
http://dx.doi.org/10.1111/j.1440-1843.20...
).
CVD is the leading cause of death worldwide (55. WHO. World Health Organization in www.who.int/cardiovascular_disease/en/acessado em julho de 2012.
www.who.int/cardiovascular_disease/en/ac...
), and
smoking is the main modifiable risk factor related to CVD (66. Howard G, Wagenknecht LE, Burke GL, Diez-Roux A, Evans GW, McGovern P, et al.
Cigarette smoking and progression of atherosclerosis: The atherosclerosis risk in communities (ARIC)
study. JAMA. 1998;279(2):119-24, http://dx.doi.org/10.1001/jama.279.2.119.
http://dx.doi.org/10.1001/jama.279.2.119...
,77. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of
potencially modifiable risk factors associated with myocardial infarction in 52 countries (the
INTERHEART study): case-control study. Lancet. 2004;364(9438):937-52,
http://dx.doi.org/10.1016/S0140-6736(04)17018-9.
http://dx.doi.org/10.1016/S0140-6736(04)...
). Among COPD patients, CVD is responsible for
approximately 50% of all hospitalizations and 20% of all deaths (88. Sin DD, Man SF. Impact of cancers and cardiovascular disease in chronic
obstructive pulmonary disease.Obstructive, occupational and environmental diseases. Curr Opin Pulm
Med. 2008;14(2):115-21, http://dx.doi.org/10.1097/MCP.0b013e3282f45ffb.
http://dx.doi.org/10.1097/MCP.0b013e3282...
). However, population-based studies have suggested that regardless of smoking status, age
or sex, a COPD diagnosis increases the risk of cardiovascular morbidity and mortality by
approximately two fold (99. Sin DD, Man SF. Why are patients with chronic obstructive pulmonary disease at
increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic
obstructive pulmonary disease. Circulation. 2003;107(11):1514-9.). In summary, COPD patients appear
to face a greater risk of dying from or being diagnosed with CVD.
Anthonisen et al. and Sin et al. have already assessed the association among COPD, CVD and
increased serum concentrations of inflammatory markers (22. Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connet JE. The effects
of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern
Med. 2005;142(4):233-9.,99. Sin DD, Man SF. Why are patients with chronic obstructive pulmonary disease at
increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic
obstructive pulmonary disease. Circulation. 2003;107(11):1514-9.). Inflammation is considered to be one of the
systemic manifestations of COPD and provides an alternative hypothesis to explain the relationship
between airflow limitation and cardiovascular risk (44. Maclay JD, McAllister DA, Macnee W. Cardiovascular risk in chronic obstructive
pulmonary disease. Respirology. 2007;12(5):634-41,
http://dx.doi.org/10.1111/j.1440-1843.2007.01136.x.
http://dx.doi.org/10.1111/j.1440-1843.20...
,99. Sin DD, Man SF. Why are patients with chronic obstructive pulmonary disease at
increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic
obstructive pulmonary disease. Circulation. 2003;107(11):1514-9.). However, the prevalence of electrocardiographic and
echocardiographic abnormalities in COPD according to disease severity has not yet been established.
Therefore, the present study aimed to assess the prevalence of electrocardiographic and
echocardiographic abnormalities in mild/moderate and severe/very severe COPD patients.
METHODS
The participants were informed of the proposed study procedures and provided written informed consent. All procedures were approved by the Committee for Research Ethics of the University Hospital at Botucatu Medical School.
We used the Fisher and Belle formula (1010. Fisher LD, Belle GV. Biostatistics: a methodology for health science. New York:
John Wiley; 1993.) to estimate the
sample size. The prevalence of cardiovascular hospitalization or mortality in COPD patients is
approximately 15% (1111. Mannino DM, Thorn D, Swensen A, Holguin F. Prevalence and outcomes of diabetes,
hypertension and cardiovascular disease in COPD. Eur Respir J. 2008;32(4):962-9,
http://dx.doi.org/10.1183/09031936.00012408.
http://dx.doi.org/10.1183/09031936.00012...
), with a 95% confidence interval (CI)
and a 10% sample error. The result was a sample size of 49 patients.
Sixty-two consecutive COPD patients recruited from the Pulmonary Outpatient Clinic of the
university hospital were evaluated. Patients aged ≥ 40 years with ≥10 pack-year
smoking histories were included. The exclusion criteria included a primary diagnosis of other
respiratory diseases [e.g., asthma, restrictive disorders (tuberculosis sequelae or
interstitial fibrosis], sleep apnea/hypopnea syndrome or lung cancer. In addition, a primary
diagnosis of unstable angina, congestive heart failure (New York Heart Association class III or IV)
or other chronic diseases, such as uncontrolled diabetes mellitus, kidney or liver failure and
cancer, also constituted grounds for exclusion. The patients were assessed on three different days
of the same week by clinical evaluations, spirometry and electrocardiogram/echocardiogram tests. The
COPD diagnosis was confirmed according to the guidelines established in the Global Initiative for
Chronic Obstructive Lung Disease (GOLD) (11. GOLD. Global Strategy for the diagnosis, management, and prevention of chronic
obstructive pulmonary disease: GOLD Executive Summary update 2011. wwwgoldcopdorg.,1212. Fabbri LM, Luppi F, Beghe B, Rabe KF. Update in chronic obstructive pulmonary
disease 2005. Am J Respir Crit Care Med. 2006;173(10):1056-65,
http://dx.doi.org/10.1164/rccm.2603005.
http://dx.doi.org/10.1164/rccm.2603005...
): a post-bronchodilator FEV1/forced vital capacity
(FVC) ratio <0.70 and an increase <15% or 200 mL in FEV1 after inhalation of a
ß2 agonist. COPD severity was categorized according to the GOLD stages, considering the
FEV1 (% predicted) and arterial blood gas values (11. GOLD. Global Strategy for the diagnosis, management, and prevention of chronic
obstructive pulmonary disease: GOLD Executive Summary update 2011. wwwgoldcopdorg.).
Measurements
Spirometry was performed using the KOKO spirometer (Ferrari KOKO, Louisville, CO 80027, USA)
before and 15 minutes after the inhalation of 400 mcg of salbutamol according to the criteria set by
the American Thoracic Society (1313. American Thoracic Society Statement. Standardization of spirometry-1987 update.
Statement of the American Thoracic Society. Am Rev Respir Dis. 1987;136(5):1285-98.). FEV1 values
are expressed in liters and as percentages of FVC or percentages of reference values (1414. Pereira CAC, Barreto SP, Simões JG, Pereira FWL, Gerstler JG, Nakatani J.
Valores de referência para a espirometria em uma amostra da população brasileira
adulta. J Bras Pneumol. 1992;18(1):10-22.). Pulse oximetry (SpO2) was assessed using an Onyx
oximeter (Model 9500 Oximeter, Nonin Medical Inc., Minneapolis, MN, USA) while the patients were
breathing room air. Body weight and height were measured by anthropometric mechanical scale
(Filizola, mod-MIC2/B-A, São Paulo, SP, Brazil). Body mass index [BMI] was calculated
using the following formula: BMI = weight [kg]/height
[m2]]. The BMI/airflow obstruction/dyspnea/exercise capacity (BODE) index
was calculated using the model described by Celli et al. (1515. Celli BR, Cote CG, Marin JM, Casanova C. The body-mass index, airflow
obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease.
N Engl J Med. 2004;350(10):1005-12.)
The BODE scores were categorized as class 1 (score 0 to 2), class 2 (score 3 to 4), class 3 (score 5
to 6) and class 4 (score 7 to 10) (1515. Celli BR, Cote CG, Marin JM, Casanova C. The body-mass index, airflow
obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease.
N Engl J Med. 2004;350(10):1005-12.). According to the
Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure, systemic hypertension was defined as a systolic blood pressure
> 140 mmHg and/or a diastolic blood pressure >90 mmHg (1616. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al.
Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure. Hypertension. 2003;42(6):1206-52,
http://dx.doi.org/10.1161/01.HYP.0000107251.49515.c2.
http://dx.doi.org/10.1161/01.HYP.0000107...
). Fasting peripheral blood was collected, and the plasma was stored at −80°C
until analysis. CRP was assessed in duplicate by high-sensitivity particle-enhanced
immunonephelometry (CardioPhase, Dade Behring Marburg GmbH, Deerfield, Illinois, USA) with a lower
detection limit of 0.007 mg/L.
Electrocardiogram (EKG)
EKGs were performed on all of the patients. A Micromed® device (Micromed Biotechnology LTDA, Wincardio, Brasília, DF, Brazil) was used with 12 simultaneous leads (DI, DII, DIII, V1, V2, V3, V4, V5, V6, aVR, aVL and aVF) and digital filters to eliminate the baseline fluctuation and interference (Wincardio 5.0.4.12, Firebird editing software). The diagnosis of EKG alteration was based on the criteria used in the literature (1717. Mivris DM, Goldberger AL. Electrocardiography. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald's Heart Disease. A test book of cardiovascular medicine. Philadelphia, PAUSA: Saunders Elsevier. 2008;149-93.). The same examiner performed all tests.
Echocardiographic analysis
The echocardiograph device was an Envisor C model (Philips Medical Systems, Andover, Massachusetts, USA) equipped with a 2.0-4.0 MHz probe capable of capturing second harmonic, tissue, pulsed, continuous and color Doppler traces, as well as one- and two-dimensional mode images. With participants positioned in left lateral decubitus and monitored using an electrocardiographic lead, the following echocardiographic cuts were performed: short parasternal axis to measure ventricles, aorta and left atrium and apical two, four and five chambers to evaluate cavities and systolic and diastolic functions of ventricles. All of the measurements were performed in accordance with the American Society of Echocardiography/European Association of Echocardiography (1818. Lang RM Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification. Eur J Ecocardiogr. 2006;7(2):79-108.) recommendations. An average of three measurements was calculated for each variable. Two operators assessed all echocardiograms; however, an individual patient's echocardiograms were assessed by the same operator. The intra-observer and inter-observer variabilities were < 3% and 5%, respectively.
The left ventricular (LV) mass (LVM) was calculated according to the following formula: LVM = 0.8×{1.04×[(LVDD+IVSDT+PWDT)3-LVDD3]}+0.6, where LVDD, IVS and PWDT represent the LV diastolic diameter, interventricular septum and posterior wall thickness, respectively. The left ventricular systolic function was evaluated by measuring the ejection fraction (EF) according to the Teichholz method. The LV diastolic function was evaluated by measuring the early (E wave) and late (A wave) diastolic mitral inflow velocities, their ratio, the E wave deceleration time (EDT) and the isovolumic relaxation time (IVRT).
Statistical analyses
The mean ± SD or the median interquartile range (25-75%) was used to present the results according to the data distribution. The patients were divided into two groups based on disease severity (COPD I/II and COPD III/IV) (11. GOLD. Global Strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD Executive Summary update 2011. wwwgoldcopdorg.). When comparing the two study groups, an unpaired t-test was used for continuous variables, and the Mann-Whitney U-test was used for ordinal variables. The Chi-squared test or Fisher's exact test was used to evaluate the qualitative variables. For multiple linear regressions, non-collinear clinically relevant variables were selected. The included categorical variables were sex (female = 0, male = 1), systemic arterial hypertension (absence = 0, presence = 1) and disease severity (COPD I/II = 0 and COPD III/IV = 1). The continuous variables were age and CRP. Mild left ventricular diastolic dysfunction was considered when the E/A ratio was <1, according to the literature.
All of the data were analyzed using the software SigmaStat 3.2 (SPSS Inc., Chicago, Illinois, USA). Statistical significance was defined as p<0.05.
RESULTS
Of the 62 patients initially evaluated, 12 were excluded from the final analyses, including 6 because of a primary diagnosis of another respiratory disease, 1 because of prostate cancer and 5 who did not complete the study protocol. Thus, 50 patients were included in the final analysis of the results. Table 1 shows the characteristics of all 50 COPD patients and also of the two groups according to the COPD severity. Age and sex did not differ statistically between the groups. As expected, the patients with severe/very severe obstruction showed lower values of spirometric variables and pulse oximetry and higher values of the BODE index Table 1.
In five (10%) patients, the electrocardiographic and echocardiographs presented alterations of the Q wave and segmental contractility, respectively. Two patients (8%) had mild/moderate disease, and three (12%) had severe/very severe disease. All of these patients had received a previous diagnosis of coronary artery disease, as documented in their medical records. The most frequent echocardiographic finding was mild left diastolic dysfunction, which was observed in 44 patients independently of their COPD stages. In addition, left atrium enlargement was diagnosed in 46% of the patients in our sample.
In the current study, differences between the electrocardiographic and echocardiographic findings were verified. Fifty-two percent of patients showed normal or near-normal EKGs, whereas only 2% had normal echocardiograms. The most common electrocardiographic findings are shown in Table 2. The proportions of right ventricular overload (p<0.05) and anterosuperior division block of the left bundle branch were higher in patients with severe/very severe COPD relative to mild/moderate COPD patients. The proportions of the other electrocardiographic findings were similar between the groups (Table 2).
In the echocardiographic analyses, the mild/moderate COPD patients presented with more abnormalities in segmental contractility (p<0.05), whereas the severe/very severe COPD patients displayed a higher prevalence of right ventricular overload (p<0.05) and increased right cardiac chamber (p<0.05). The other morphological variables did not show any statistically significant differences between the groups (Table 3).
Table 4 shows the systolic and diastolic function of the studied patients, as evaluated by Doppler echocardiography. Patients with severe/very severe obstruction presented higher values of E-wave deceleration time (EDT) (p<0.05) than mild/moderate COPD patients. The other variables did not differ statistically.
Age, sex, systemic arterial hypertension, C-reactive protein and disease severity (COPD I/II and COPD III/IV) were included as independent variables in the multiple linear regression to identify the factors associated with EDT. Only disease severity showed an association with EDT [r2 = 0.26, p = 0.01] (Table 5).
DISCUSSION
The main finding of this study was the high prevalence of mild left diastolic dysfunction in COPD patients, which was associated with increased disease severity. Only 10% of our patients displayed segmental left ventricular wall motion abnormalities, whereas, as expected, electro- and echocardiographic signs of enlargement of the right chambers were more pronounced in severe/very severe COPD patients.
Ventilation/perfusion mismatch resulting from progressive airflow limitation and emphysema is the
key driver of hypoxia in COPD patients. Hypoxia is associated with COPD severity and leads to
pulmonary vasoconstriction and right cardiac chamber enlargement, also known as cor pulmonale. Thus,
cor pulmonale is associated with COPD severity. Schena et al. evaluated patients with cor pulmonale
and pulmonary arterial hypertension secondary to COPD and found increases in the right ventricular
systolic and diastolic diameters, without left ventricular alteration (1919. Schena M, Clini E, Errera D, Quadri A. Echo-Doppler evaluation of left
ventricular impairment in chronic corpulmonale. Chest. 1996;109(6):1446-51,
http://dx.doi.org/10.1378/chest.109.6.1446.
http://dx.doi.org/10.1378/chest.109.6.14...
). However, associations were not observed between echocardiographic variables
and functional respiratory parameters (1919. Schena M, Clini E, Errera D, Quadri A. Echo-Doppler evaluation of left
ventricular impairment in chronic corpulmonale. Chest. 1996;109(6):1446-51,
http://dx.doi.org/10.1378/chest.109.6.1446.
http://dx.doi.org/10.1378/chest.109.6.14...
). In the present
study, as expected, the prevalence of right ventricular hypertrophy and right cardiac chamber
enlargement was higher in patients with severe/very severe COPD than in those with mild/moderate
obstructions.
Although cor pulmonale is a well-known echocardiographic alteration in COPD patients, few studies
have evaluated left ventricular diastolic function in the context of this disease (2020. Boussuges A, Pinet C, Molenat F, Burnet H, Ambrosi P, Badier M, et al. Left
atrial and ventricular filling in chronic obstructive pulmonary disease. An echocardiographic and
Doppler study. Am J Respir Crit Care Med. 2000;162(2 Pt1):670-5.
21. Rutten FH, Cramer MJ, Grobbee DE, Sachs AP, Kirkels JH, Lammers JW, et al.
Unrecognized heart failure in elderly patients with stable chronic obstructive pulmonary disease.
Eur Heart J. 2005;26(18):1887-94, http://dx.doi.org/10.1093/eurheartj/ehi291.
http://dx.doi.org/10.1093/eurheartj/ehi2...
22. Funk CG, Lang I, Schenk P, Valipour A, Hartl S, Burghuber OC. Left ventricular
diastolic dysfunction in patients with COPD in the presence and absence of elevated pulmonary
arterial pressure. Chest. 2008;133(6):1354-9,
http://dx.doi.org/10.1378/chest.07-2685.
http://dx.doi.org/10.1378/chest.07-2685...
-2323. Sabit R, Bolton CE, Fraser AG, Edwards JM, Edwards PH, Ionescu AA, et al.
Sub-clinical left and right ventricular dysfunction in patients with COPD. Respir Med.
2010;104(8):1171-8, http://dx.doi.org/10.1016/j.rmed.2010.01.020.
http://dx.doi.org/10.1016/j.rmed.2010.01...
). In agreement with
our results, Boussuges et al. found a high prevalence of left ventricular diastolic dysfunction in
COPD patients relative to control subjects (76% vs. 35%) (2020. Boussuges A, Pinet C, Molenat F, Burnet H, Ambrosi P, Badier M, et al. Left
atrial and ventricular filling in chronic obstructive pulmonary disease. An echocardiographic and
Doppler study. Am J Respir Crit Care Med. 2000;162(2 Pt1):670-5.). Although the frequency of diastolic dysfunction was not as high as in our
study (88%), Rutten et al. and Funk et al. also reported a prevalence >50%. (2121. Rutten FH, Cramer MJ, Grobbee DE, Sachs AP, Kirkels JH, Lammers JW, et al.
Unrecognized heart failure in elderly patients with stable chronic obstructive pulmonary disease.
Eur Heart J. 2005;26(18):1887-94, http://dx.doi.org/10.1093/eurheartj/ehi291.
http://dx.doi.org/10.1093/eurheartj/ehi2...
,2222. Funk CG, Lang I, Schenk P, Valipour A, Hartl S, Burghuber OC. Left ventricular
diastolic dysfunction in patients with COPD in the presence and absence of elevated pulmonary
arterial pressure. Chest. 2008;133(6):1354-9,
http://dx.doi.org/10.1378/chest.07-2685.
http://dx.doi.org/10.1378/chest.07-2685...
). In addition, a
recent study showed evidence of diastolic dysfunction in 47.5% (2424. Gupta NK, Agrawal RK, Srivastav AB, Ved ML, Echocardiographic evaluation of
heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of
disease. Lung India. 2011;28(2):105-9.) of COPD patients. However, Freixa et al. found a lower frequency of this
echocardiographic alteration (12%) in COPD patients in their first hospital admission (2525. Freixa X, Portillo K, Paré C, Garcia-Aymerich J, Gomez FP, Benet M, et al.
Echocardiographic abnormalities in patients with COPD at their first hospital admission. Eur Respir
J. 2012; Sep 27 [Epub ahead of print].).
Left diastolic dysfunction can be asymptomatic or associated with classical heart failure
symptoms (diastolic heart failure). The incidence of diastolic heart failure increases with age and
is more common in older women. Hypertension and cardiac ischemia are the most common causes of
diastolic heart failure. Other risk factors are obesity and diabetes mellitus (2525. Freixa X, Portillo K, Paré C, Garcia-Aymerich J, Gomez FP, Benet M, et al.
Echocardiographic abnormalities in patients with COPD at their first hospital admission. Eur Respir
J. 2012; Sep 27 [Epub ahead of print].). Note that 40% of our patients had systemic arterial hypertension, whereas 10%
had received a previous diagnosis of ischemic heart disease. In the current study, the prevalence of
ischemic heart disease was lower than that in previous studies (2626. Kazik A, Wilczek K, Polonski L. Management of diastolic heart failure.
Cardiol J. 2010;17(7):558-65.,2727. Thurnheer R, Muntwyler J, Stammberger U, Bloch KE, Zollinger A, Weder W, et al.
Coronary artery disease in patients undergoing lung volume reduction surgery for emphysema. Chest.
1997;112(1):122-8, http://dx.doi.org/10.1378/chest.112.1.122.
http://dx.doi.org/10.1378/chest.112.1.12...
). Brekke et al. observed that 27.7% of patients
who were hospitalized because of COPD exacerbation showed electrocardiographic signs of myocardial
infarction; 30% of these patients had no previous diagnosis (2727. Thurnheer R, Muntwyler J, Stammberger U, Bloch KE, Zollinger A, Weder W, et al.
Coronary artery disease in patients undergoing lung volume reduction surgery for emphysema. Chest.
1997;112(1):122-8, http://dx.doi.org/10.1378/chest.112.1.122.
http://dx.doi.org/10.1378/chest.112.1.12...
). The higher prevalence of ischemia in these studies may be have resulted from
differences in study design, sample characteristics and methods used for CVD diagnosis. For example,
in a study by Brekke et al., an electrocardiographic score was used, which was contrary to Thurnheer
et al., who employed coronarography (2727. Thurnheer R, Muntwyler J, Stammberger U, Bloch KE, Zollinger A, Weder W, et al.
Coronary artery disease in patients undergoing lung volume reduction surgery for emphysema. Chest.
1997;112(1):122-8, http://dx.doi.org/10.1378/chest.112.1.122.
http://dx.doi.org/10.1378/chest.112.1.12...
,2626. Kazik A, Wilczek K, Polonski L. Management of diastolic heart failure.
Cardiol J. 2010;17(7):558-65.). In the present study, the prevalence of ischemic changes may have been
underestimated because no additional specific investigation, beyond electrocardiography and
echocardiography, was performed on patients with no previous diagnoses of ischemic heart
disease.
Recent studies have revealed that diastolic heart failure is associated with high morbidity and
mortality. Patients with diastolic heart failure have mortality rates of 29% one year after the
diagnosis and 65% after five years (2828. Brekke PH, Omland T, Smith P, Soyseth V. Underdiagnosis of myocardial infarction
in COPD - Cardiac infarction injury score (CIIS) in patients hospitalised for COPD exacerbation.
Respir Med. 2008;102(9):1243-7, http://dx.doi.org/10.1016/j.rmed.2008.04.010.
http://dx.doi.org/10.1016/j.rmed.2008.04...
). Abusaid et al.
evaluated patients who were hospitalized for exacerbation of COPD associated with diastolic
dysfunction, and showed that left diastolic dysfunction increased the risk of hospitalization for
exacerbation (2929. Fontes-Carvalho R, Leite Moreira A. Heart failure with preserved ejection
fraction: fighting misconceptions for a new approach. Arq Bras Cardiol. 2011;96(6):504-14,
http://dx.doi.org/10.1590/S0066-782X2011000600012.
http://dx.doi.org/10.1590/S0066-782X2011...
). These data reinforce the importance of
left ventricular diastolic evaluation in COPD patients.
Note that EDT was increased in patients with severe/very severe obstruction relative to those
with mild or moderate obstruction. Although nearly all of the patients presented with mild diastolic
dysfunction, the higher EDT values in severe/very severe COPD suggest that disease severity was
associated with decreased diastolic function. Disease severity predicts EDT even after adjusting for
age, sex, systemic arterial hypertension and CRP. One explanation for this association between
disease severity and diastolic function could be systemic inflammation. Inflammation is considered
to be one of the systemic manifestations of COPD and provides an alternative hypothesis for
explaining the relationship between airflow limitation and atherosclerotic plaque formation, which
are two factors that are also associated with myocardial ischemia and left ventricular diastolic
dysfunction. Furthermore, the presence of cor pulmonale secondary to pulmonary hypertension can lead
to interventricular septum deviation toward the left ventricle, which alters left ventricular
geometry and delays filling (3131. Minai AO, Chaouat A, Adnot S. Pulmonary Hypertension in COPD: Epidemiology,
Significance, and Management: Pulmonary Vascular Disease: The Global Perspective. Chest. 2010;137(6
Suppl):39S-51S, http://dx.doi.org/10.1378/chest.10-0087.
http://dx.doi.org/10.1378/chest.10-0087...
). This mechanism could also
explain why disease severity was associated with worse diastolic function. In addition, because of
the association between left ventricular diastolic dysfunction and COPD severity, it is also
important to exclude decompensated heart failure during COPD exacerbation.
We should consider the major limitations of the present work, e.g., its small sample size and the recruitment of all patients from a single medical center. In addition, tissue Doppler imaging was not performed for evaluation of diastolic function. Further studies are needed to elucidate the specific mechanisms associated with COPD severity and left ventricular diastolic dysfunction.
In conclusion, the electro- and echocardiographic signs of right chamber enlargement are more pronounced in severe/very severe COPD patients. In addition, COPD patients have a high prevalence of left ventricular diastolic dysfunction, which is associated with disease severity. Thus, because of this association, it is important to exclude decompensated heart failure during COPD exacerbation.
Scientific knowledge of the subject
Chronic obstructive pulmonary disease (COPD) patients have a high prevalence of left ventricular diastolic dysfunction according to disease severity.
What this study adds to the field
COPD patients have a high prevalence of electrocardiographic and echocardiographic abnormalities regardless of disease severity.
COPD patients have a high prevalence of left ventricular diastolic dysfunction, which is associated with disease severity. Because of this association, it is important to exclude decompensated heart failure during COPD exacerbation.
This study received financial support from the Foundation for the Support of Research in the State of São Paulo (FAPESP), grant no. 2010/10312-1. Laura Miranda de Oliveira Caram was the recipient of a scholarship grant from CAPES.
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Publication Dates
-
Publication in this collection
June 2013
History
-
Received
20 Dec 2012 -
Reviewed
26 Jan 2013 -
Accepted
8 Feb 2013