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ORIGINAL ARTICLE |
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Year : 2015 | Volume
: 14
| Issue : 2 | Page : 87-91 |
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Left ventricular dysfunction and its correlates in chronic obstructive pulmonary disease patients
Gajanan S Gaude, Gautam Suresh, Vinay Mahishale
Department of Pulmonary Medicine, Jawaharlal Nehru Medical College, KLE University, Belgaum, Karnataka, India
Date of Web Publication | 21-Nov-2015 |
Correspondence Address: Gajanan S Gaude Department of Pulmonary Medicine, Jawaharlal Nehru Medical College, KLE University, Belgaum - 590 010, Karnataka India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2384-5589.170165
Background: In chronic obstructive pulmonary disease (COPD) patients, left ventricular (LV) systolic dysfunction is rare. Objectives: To evaluate the prevalence of LV systolic or diastolic dysfunction in patients with COPD. Materials and Methods: A cross-sectional study was conducted in a tertiary care hospital for a period of 2 years from January 2012 to December 2013. These patients underwent physical examination and standard two-dimensional (2D) echocardiographic views, and peak flow velocity of early diastolic filling [early filling velocity (E-Max)], peak flow velocity of late atrial filling [atrial filling velocity (A-Max)], and early flow velocity peak/late flow velocity peak [early to late (E/A)] ratio were measured according to the criteria of the American Society of Echocardiography. Statistical analysis was carried out using SPSS software. Results: A total of 102 patients diagnosed with COPD as per the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines were enrolled. Of the 102 COPD patients, the maximal A-Max increased and E-Max decreased in 76 patients (74.5%) (P < 0.001). The early flow velocity peak/late flow velocity peak (E/A) ratio also markedly decreased in these 76 patients (P < 0.001) indicating LV dysfunction. The atrial contribution to total left diastolic filling increased in patients with COPD. This was also observed in COPD patients with normal pulmonary artery pressure (PAP) (P < 0.001). Grade IV COPD (P - 0.000), the duration of illness (P < 0.001), and smoking >10 packs for years (P < 0.001) were the risk factors that were associated with the development of LV diastolic dysfunction in COPD patients. Conclusion: The prevalence of LV diastolic dysfunction was 74.5%. As the severity of COPD increased, the risk of LV diastolic dysfunction increased. The screening of severe COPD patients for LV function might improve the outcome. Keywords: Chronic obstructive pulmonary disease (COPD), left ventricular (LV) dysfunction, pulmonary arterial pressure (PAP)
How to cite this article: Gaude GS, Suresh G, Mahishale V. Left ventricular dysfunction and its correlates in chronic obstructive pulmonary disease patients. Afr J Med Health Sci 2015;14:87-91 |
How to cite this URL: Gaude GS, Suresh G, Mahishale V. Left ventricular dysfunction and its correlates in chronic obstructive pulmonary disease patients. Afr J Med Health Sci [serial online] 2015 [cited 2021 Mar 8];14:87-91. Available from: http://www.ajmhs.org/text.asp?2015/14/2/87/170165 |
Introduction | |  |
Chronic obstructive pulmonary disease (COPD) is a syndrome of progressive airflow limitation caused by the abnormal inflammatory reaction of the airway and lung parenchyma. It is now considered a systemic disease with widespread extrapulmonary manifestations. [1] It remains a major public health problem and is projected to rank fifth in 2020 among disease burdens worldwide. [2] Abnormal patterns of left ventricular (LV) diastolic filling have been reported in patients with increased right ventricular (RV) pressure and/or volume load, suggesting that LV filling dynamics are influenced by RV loading conditions. [3] Several studies [4],[5] have demonstrated decreased RV volumes, reflecting RV afterload in patients with COPD and mild pulmonary artery hypertension. In a recent study, Dario-Vizza et al. assessed the frequency of systolic dysfunction to be less than 5%. [4] Derangement of the LV function in such patients, in the absence of other disorders affecting the LV function, has not been clearly established. [3] Hence, the present study was conducted to determine the prevalence of LV diastolic dysfunction in COPD patients in a tertiary care referral hospital.
Materials and Methods | |  |
This cross-sectional study was conducted in a tertiary care hospital in Belgaum, Karnataka, India from January 2012 to December 2013. Patients with a diagnosis of COPD as per the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines [2] were included in the study. Patients with valvular heart disease, angina pectoris, ischemic heart disease, cardiomyopathy, and rheumatic heart disease were excluded.
Procedure
The COPD diagnosed cases, as per GOLD guidelines, were counseled for the study, and those who gave written informed consent were included in the study. Baseline and demographic characteristics were collected for all the patients. The patients were subjected to pulmonary function tests and echocardiogram (ECHO) to stage the severity of COPD and for cardiac evaluation. Pulmonary function test was carried out using RMS Helios 702 spirometer (Recorders and Medicare Systems Pvt. Ltd. MEDSPIROR, Chandigarh, India), and forced expiratory volume in the 1 s (FEV 1 ) , forced vital capacity (FVC), and FEV 1 /FVC ratios were recorded to stage COPD. [2] Standard two-dimensional (2D) ECHO was carried out with Acuson SC2000 Cardiac Ultrasound System (Acuson, Arizona) to measure systolic and diastolic LV dimensions and for the calculation of LV fractional shortening. The measurements of interventricular septum thickness were also taken.
Diastolic dysfunction
The heart failure with preserved ejection fraction (diastolic dysfunction) was defined on the basis of clinical finding congestive heart failure with ECHO findings of preserved LV ejection fraction. Diastolic flow from the left atrium and left ventricle across the mitral valve has two components: E wave, early diastolic filling and A wave, atrial contraction. In late diastole, E wave velocity is influenced by both the rate of early diastolic relaxation and the left atrial pressure. An alteration in the pattern of E wave velocity reflects the degree of LV diastolic dysfunction and prognosis. The peak velocity of blood flow across the mitral valve during early diastolic filling corresponds to the E wave. Similarly, atrial contraction corresponds to the A wave. From these findings, the early to late (E/A) ratio was calculated. Under normal conditions, E is greater than A and the E/A ratio is approximately 1.5 m/s. In early diastolic dysfunction, relaxation is impaired and with vigorous atrial contraction, the E/A ratio decreases to less than 0.75 m/s. As the disease progresses, LV compliance is reduced, which increases left atrial pressure and in turn, increases early LV filling despite impaired relaxation. This paradoxical normalization of the E/A ratio is called pseudonormalization. In patients with severe diastolic dysfunction, LV filling occurs primarily in early diastole, creating an E/A ratio greater than 2.0 m/s.
Grading of diastolic dysfunction (or diastolic filling pattern)
Grade 1 (mild dysfunction): Mitral E velocity is decreased and A velocity is increased, producing an E/A ratio of less than 0.75 m/s. Grade 2 (moderate dysfunction): As diastolic function worsens, the mitral inflow pattern goes through a phase resembling a normal diastolic filling pattern, that is, an E/A ratio of 1-1.5 m/s and normal deceleration time (DT) (160-240 ms). Grade 3 and grade 4 (severe irreversible dysfunction): Restrictive filling with severe diastolic dysfunction is characterized by increased E velocity and decreased A velocity with an E/A ratio higher than 2 m/s.
Ethical clearance for the study was obtained from the institutional ethical review board.
Statistical analysis
All analyses within the groups were carried out using SPSS computer software (SPSS version 13.0 SPSS Inc., Chicago, IL, USA). Data were analyzed by chi-square (X 2 ) test and logistic regression analysis. LV diastolic dysfunction was correlated with risk factors of COPD by one-way analysis of variance (ANOVA) test. Descriptive statistics are reported as means and standard deviation (SD). For significant main effects, post hoc pair-wise comparisons were performed between levels using t tests with a modified Bonferroni procedure. A P value less than 0.05 was considered as statistically significant. For analysis of risk factors for LV dysfunction, univariate and multivariate logistic regression analyses were used.
Results | |  |
A total of 102 patients with COPD were included in the study [Table 1]. About 62% of the cases were males and nearly two-third patients had more than 5 years history of COPD illness. A total of 45.1% of the patients were smokers and 60.8% had normal body mass index (BMI) while nearly 10% were underweight and 21.6% were overweight.
A total of 76 patients (74.5%) had LV diastolic dysfunction while the remaining 24 patients had normal LV function. Among these 76 patients with diastolic dysfunction, 6 patients (5%) had associated systolic dysfunction and 70 patients (95%) had only diastolic dysfunction. A total of 29 (38.2%) patients in stage III COPD and 32 (42.1%) patients in stage IV COPD had diastolic dysfunction [Table 2]. Atrial filling velocity (A-Max) was increased as compared to early filling velocity (E-Max) and thus, E/A ratio decreased in patients with diastolic dysfunction compared with patients without diastolic dysfunction (P < 0.000). Stage I COPD and stage II COPD disease had less prevalence of LV dysfunction. Also, it was observed that as the severity grade of COPD increased, the risk of LV dysfunction also increased [Table 3].
Comparative evaluation was carried out among patients with COPD with the presence of pulmonary arterial hypertension (PAP) and with normal arterial pressure. It was observed that the A-Max increased and the E-Max decreased in patients with COPD with increased PAP. The atrial contribution to total left diastolic filling increased in patients with COPD with increased PAP (P < 0.000) [Table 4]. | Table 4: Diastolic dysfunction in patients with COPD patients and its relation to pulmonary arterial pressure (PAP)
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Discussion | |  |
The main finding of the present study was the presence of LV diastolic dysfunction in patients with COPD, with 76 patients (74.5%) having diastolic dysfunction and rest having normal LV function. Among these, 95% had only diastolic dysfunction. Dario-Vizza et al. [4] also observed that the frequency of systolic dysfunction to be less than 5% in COPD cases. Malerba et al. [6] has observed the incidence of left diastolic dysfunction in COPD to be 65% while in another study, Steinberg et al. [7] observed the incidence of diastolic dysfunction to be 78% in COPD patients. Kjaergaard [8] in a cross-sectional study observed that the incidence of diastolic dysfunction increased more sharply with age in women and stated that there was an increased female predominance in diastolic dysfunction.
The incidence of systolic dysfunction in COPD ranges from 8% to 46% and that of diastolic dysfunction ranges from 54% to 92%. [Table 5] summarizes the prevalence of LV dysfunction in COPD in various studies. [9],[10],[11],[12],[13] The varied difference in different study groups can be attributed to the methodological differences in the assessment of LV dysfunction. In the present study, among the COPD patients diagnosed with diastolic dysfunction, 30 (40%) had associated pulmonary arterial hypertension (PAH) and 46 (70%) had normal pulmonary arterial pressure (PAP). Funk et al. [14] has observed that the maximal atrial filling velocity increased and the early filling velocity decreased in COPD patients with pulmonary arterial hypertension as compared with the control subjects. This is in accordance with our study where diastolic dysfunction was present in 46 (70%) patients with normal PAP. We also observed that there was an increase in the A-Max and E-Max was decreased with an inverse E/A ratio.
Several factors might influence the LV diastolic dysfunction in COPD patients. COPD patients experience chronic hypoxemia, which might result in abnormalities of myocardial relaxation as a consequence of myocyte hypoxia due to intracellular calcium transport disturbances, and with advancing age the LV relaxation decreases leading to increase in the isovolumetric time causing diastolic dysfunction. [15] The cardiac fossa is a physiologic constraint at normal heart volumes. The physiologically useful interventricular interdependence is thereby promoted. The effect of lung inflation in tensing the walls of the fossa may also at times embarrass both ventricles. Together with the raised intrathoracic pressure, it is responsible for the fall in LV and RV volumes and output during positive pressure ventilation. [16]
It was also observed that an increased atrial contribution leading to total diastolic filling in patients with COPD indicates reduced E-max and a compensatory increase in late diastole at a time when septal geometry was less deranged. These concepts of left diastolic dysfunction are based on the presence of pulmonary hypertension and/or hypoxemia in COPD patients. Boussuges et al. [16] has observed similar results in moderate-to-severe COPD patients using combined analysis of pulmonary venous and mitral blood flow velocities. It was observed that there was an impaired LV filling and an increased contribution of atrial contraction to LV filling despite normal systolic LV function as compared with the control subjects. Aldrich et al. [17] has observed that positive-end expiratory pressure (auto-PEEP) is common in patients with airway obstruction due to dynamic hyperinflation and even without overt ventilatory failure, and its severity is generally in proportion to the severity of the hyperinflation and the airway obstruction, thus limiting the venous return leading to diastolic dysfunction in COPD patients. The atrial contribution to total left diastolic filling increased and this was also observed in COPD patients with normal PAP. [18]
The greater prevalence of LV diastolic dysfunction was observed in stage IV disease (31%) as compared to other stages in the present study. Systemic inflammation might provide the biological link between the two, that is, a common tumor necrosis factor-alpha (TNF-α) mediated pathogenesis underlying these diseases. Systemic inflammation is now believed to be a contributory factor in the clinical manifestations and natural history of COPD, and is an essential component of the COPD disease process and in diastolic dysfunction. [19],[20],[21]
The study has some limitations. First, the sample size was small. Second, this is a single study center, and hence, the data cannot be generalized for the general population at large. Third, there was no control group in the present study. 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 LV diastolic dysfunction.
Thus, it can be concluded that all patients with COPD should be screened for diastolic dysfunction using echocardiography, which is considered for the early diagnosis and proper therapy of this condition can be advised at the earliest. This will help in improving the quality of life in these patients and prolonging their survival.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Murray CJ, Lopez AD. Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet 1997;349: 1436-42. |
2. | Rabe KF, Hurd S, Anzueto A, Barnes PJ, Buist SA, Calverley P, et al. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. GOLD executive summary. Am J Respir Crit Care Med 2007;176:532-55. |
3. | Nootens M, Wolfkiel CJ, Chomka EV, Rich S. Understanding right and left ventricular systolic function and interactions at rest and with exercise in primary pulmonary hypertension. Am J Cardiol 1995;75:374-7. |
4. | Vizza CD, Lynch JP, Ochoa LL, Richardson G, Trulock EP. Right and left ventricular dysfunction in patients with severe pulmonary disease. Chest 1998;113:576-83. |
5. | Kerber RE, Dippel WF, Abboud FM. Abnormal motion of the interventricular septum in right ventricular volume overload: Experimental and clinical echocardiographic studies. Circulation 1973; 48:86-96.  [ PUBMED] |
6. | Malerba M, Ragnoli B, Salameh M, Sennino G, Sorlini ML, Radaeli A, et al. Sub-clinical left ventricular diastolic dysfunction in early stage of chronic obstructive pulmonary disease. J Biol Regul Homeost Agents 2011;25:443-51. |
7. | Steinberg BA, Zhao X, Heidenreich PA, Peterson ED, Bhatt DL, Cannon CP, et al.; Get With the Guidelines Scientific Advisory Committee and Investigators. Trends in patients hospitalized with heart failure and preserved left ventricular ejection fraction: Prevalence, therapies, and outcomes. Circulation 2012;26:65-75. |
8. | Kjaergaard J, Akkan D, Iversen KK, Kjoller E, Køber L, Torp-Pedersen C, et al. Prognostic importance of pulmonary hypertension in patients with heart failure. Am J Cardiol 2007;99:1146-50. |
9. | Steele P, Ellis JH, Van Dyke D, Sutton F, Creagh E, Davies H. Left ventricular ejection fraction in severe chronic obstructive airways disease. Am J Med 1975;59:21-8.  [ PUBMED] |
10. | Berger HJ, Matthay RA, Loke J, Marshall RC, Gottschalk A, Zaret BL. Assessment of cardiac performance with quantitative radionuclide angiocardiography: Right ventricular ejection fraction with reference to findings in chronic obstructive pulmonary disease. Am J Cardiol 1978;41:897-905.  [ PUBMED] |
11. | MacNee W, Xue QF, Hannan WJ, Flenley DC, Adie CJ, Muir AL. Assessment by radionuclide angiography of right and left ventricular function in chronic bronchitis and emphysema. Thorax 1983;38: 494-500.  [ PUBMED] |
12. | Zema MJ, Masters AP, Margouleff D. Dyspnea: The heart or the lungs? Differentiation at bedside by use of the simple Valsalva maneuver. Chest 1984;85:59-64.  [ PUBMED] |
13. | McCullough PA, Hollander JE, Nowak RM, Storrow AB, Duc P, Omland T, et al.; BNP Multinational Study Investigators. Uncovering heart failure in patients with a history of pulmonary disease: Rationale for the early use of B-type natriuretic peptide in the emergency department. Acad Emerg Med 2003;10:198-204. |
14. | Funk GC, Lang I, Schenk P, Valipour I, Hartl S, Burghuber OC. Left ventricular dysfunction in patients with COPD in the presence and absence of elevated pulmonary arterial pressure. Chest 2008; 133:1354-9. |
15. | Cargill RI, Kiely DG, Lipworth BJ. Adverse effects of hypoxaemia on diastolic filling in humans. Clin Sci (Lond) 1995;89:165-9. |
16. | 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;162:670-5. |
17. | Aldrich TK, Hendler JM, Vizioli LD, Park M, Multz AS, Shapiro SM. Intrinsic positive end-expiratory pressure in ambulatory patients with airways obstruction. Am Rev Respir Dis 1993;147:845-9. |
18. | Caram LM, Ferrari R, Naves CR, Tanni SE, Coelho LS, Zanati SG, et al. Association between left ventricular diastolic dysfunction and severity of chronic obstructive pulmonary disease. Clinics (Sao Paulo) 2013; 68:772-6. |
19. | 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;26:1887-94. |
20. | 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;104:1171-8. |
21. | Abusaid GH, Barbagelata A, Tuero E, Mahmood A, Sharma G. Diastolic dysfunction and COPD exacerbation. Postgrad Med 2009;121:76-81. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
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