The Journal of Medical Sciences
Volume 7 | Issue 2 | Year 2021

Two-dimensional Echocardiographic Study of Left Ventricular Volume and Function in COPD Patients Admitted in Tertiary Care Hospital in Kolkata

Lalawmpuia PC1, Satyabrata Ganguly2, Venu Gopala Reddy P3

1Department of Medicine, Civil Hospital, Aizawl, Kolkata, West Bengal, India

2Department of Internal Medicine, AMRI Hospitals, Kolkata, West Bengal, India

3Department of General Surgery, Zoram Medical College, Falkawn, Mizoram, India

Corresponding Author: Lalawmpuia PC, Department of Medicine, Civil Hospital, Aizawl, Kolkata, West Bengal, India, Phone: +91 8974739488, e-mail:


Aim and objective: To estimate the two-dimensional echocardiographic study of left ventricular volume and function in chronic obstructive pulmonary disease (COPD) patients admitted in tertiary care hospital.

Introduction: COPD affects pulmonary blood vessels, right ventricle, as well as left ventricle leading to the development of pulmonary hypertension (PH), cor pulmonale (COR-P), right and left ventricular dysfunction. The present study was conducted to determine the relation between severity of airway obstruction (stages) of COPD and left ventricular dysfunction. Secondary objective was to assess the correlation between smoking and left ventricular (LV) dysfunction.

Materials and methods: A cross-sectional descriptive study was conducted in the tertiary Medical College and Hospital. A total of 52 COPD patients were included by convenience sampling into the study. The echo study addressed pericardial condition, cardiac dimensions, LV systolic and diastolic function, and hemodynamic of pulmonary circulation. LV dysfunction was outcome variable and IBM SPSS version 22 were used for statistical analysis.

Results: Majority of the participants were aged between 61 and 70 years. LV diastolic dysfunction was observed in eight (15%) participants and LV systolic dysfunction was observed in five (10%) participants. The mean E/A ratio significantly decreased as the severity of COPD increased (p = 0.024). A weak negative correlation was observed between duration of smoking and E/A ratio and left ventricular end diastolic diameter.

Conclusion: LV defects, specifically E/A ratio was inversely proportional to the severity of the COPD.

How to cite this article: Lalawmpuia PC, Ganguly S, Reddy PVG. Two-dimensional Echocardiographic Study of Left Ventricular Volume and Function in COPD Patients Admitted in Tertiary Care Hospital in Kolkata. J Med Sci 2021;7(2):17-20.

Source of support: Nil

Conflict of interest: None

Keywords: Airway obstruction, COPD, Pulmonary hypertension, Ventricular dysfunction, 2D echocardiography


Chronic obstructive pulmonary disease (COPD) or chronic obstructive lung disease (COLD) is a pulmonary condition which is characterized by airflow obstruction due to chronic bronchitis or emphysema which is not fully reversible and is usually progressive in nature.1 According to the Global Burden of Disease (GBD), COPD is the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030.2 An estimated 328 million people have COPD worldwide. In 15 years, COPD is expected to become the leading cause of death worldwide.3

Chronic obstructive pulmonary disease leads to secondary pulmonary arterial hypertension (PAH) and right ventricular hypertrophy or “cor pulmonale” and ultimately right heart failure.4 An increase in right ventricular (RV) afterload induces a left ventricular (LV) diastolic dysfunction because of biventricular interdependence as RV and LV are enclosed in a relatively nondistensible pericardium. Hence, changes in right ventricular volume will affect left ventricular volume.5 An increase in RV afterload is common in COPD patients. Secondly, forward failure of the RV, as indicated by a reduced RV ejection fraction will hamper an adequate filling of the LV. Increase in pulmonary arterial pressure results in impairment of RV function and underfilling of the LV, leading to a failing stroke volume response.5

Existent but undocumented LV dysfunction secondary to ischemic heart disease (IHD), is high in COPD patients because they share many risk factors in common such as age, male predominance, cigarette smoking.6 Other factors such as hypoxia, and hyperviscosity of blood secondary to polycythaemia and shifting of interventricular septum toward left side may also contribute to the LV dysfunction.7

Echocardiography provides a rapid, noninvasive portable, and accurate method to evaluate the right ventricle function, right ventricular filling pressure, tricuspid regurgitation, left ventricular function, and valvular function. It is worth noting that an echocardiographic-detected left ventricular hypertrophy is a strong predictor of cardiovascular events, especially in COPD patients.8

Both syndromes have been studied extensively, but separately, with COPD in the domain of the pulmonologist and heart failure in the domain of the cardiologist. Studies on the prevalence of left ventricular dysfunction (failure) in COPD patients or vice versa are scarce. The present study was conducted to determine the relation between severity of airway obstruction (stages) of COPD and left ventricular dysfunction. Secondary objective was to assess the correlation between smoking and left ventricular dysfunction.


A cross-sectional descriptive study was conducted in the department of general medicine and intensive care unit (ICU) at a tertiary medical college and hospital, from June 2011 to May 2012. A total of 52 COPD patients were included by convenience sampling into the study. Both male and female COPD patients diagnosed by physical examination, chest X-ray, pulmonary function tests were included in the study. Ethical committee approval was obtained from the institutional review board and informed consent was taken from all the participants.

Cases diagnosed with bronchial asthma, lung cancer, poorly controlled hypertension (BP >140/90 with antihypertensives), significant valvular disease and known coronary artery diseases (angina, ischemic changes in resting ECG, or documented history of myocardial infarction), bronchiectasis were excluded from the study. Very poor echogenic subjects in whom meaningful echocardiographic examination could not be performed were also excluded from the study.

A thorough clinical examination including general survey and detailed systemic examination as per proforma were done. Routine measurement of blood pressure (BP), pulse, and respiratory rate were done. Echocardiography, chest X-ray and spirometry are the main of the study.

2D-echocardiography was done by a VIVID 7 model of GE healthcare system with a multifrequency probe with a range of 2-4.3 MHz both 2D and M-mode studies were done. All echo-doppler studies were carried out by the same cardiologist. The echo study addressed pericardial condition, cardiac dimensions, LV systolic and diastolic function, and hemodynamic of pulmonary circulation.

Measures of Left Ventricular Functions

Left ventricular function was also assessed by using the following parameters: EF (ejection fraction) = measure of how much end-diastolic value is ejected from LV with each contraction (56-78%).

FS (fractional shortening) = it is a percentage change in LV dimension with each LV contraction (28-44%).

LV mass = left ventricular mass (88-224 g).

E/A = diastolic filling of left ventricles usually classified initially on the basis of the peak mitral flow velocity of the early rapid filling wave (E), peak velocity of the late filling wave caused by atrial contraction (A). In normal subjects LV elastic recoil is vigorous because of normal myocardial relaxation, therefore more filling is completed during early diastolic, so left ventricular diastolic dysfunction (LVDD) is said to be present when E/A is < 1.3 (age group 45-49 years), <1.2 (age group 50-59 years), <1.0 (age group 60-69 years), and <0.8 (age group ≥70 years).9

All the patients investigated by spirometry were classified according to GOLD guidelines (postbronchodilator FEV1/forced vital capacity (FVC) ratio <7 0% predicted). The best of at least three technically acceptable values for forced expiratory volume in one second (FEV1) forced vital capacity (FVC), Forced expiratory flow 25-75 (FEF25-75) and peak expiratory flow rate and flow-volume curves were selected.

Left ventricular dysfunction was considered as outcome variables. Stages of COPD, duration of smoking, demographic variables were considered as explanatory variables. Descriptive analysis was carried out by mean and standard deviation for quantitative variables, frequency and proportion for categorical variables. The association between categorical explanatory variables and quantitative outcome was assessed by comparing the mean values. ANOVA was used to assess statistical significance. p- value < 0.05 was considered statistically significant. IBM SPSS version 22 was used for statistical analysis.


A total of 52 subjects were considered into final study. Among the study population, three (5.7%) participants were aged between 30 and 40 years, seven (13.46%) were aged between 41 and 50 years, 17 (32.69%) were aged between 51 and 60 years, 21 (40.38%) were aged between 61 and 70 years, and four (7.6%) participants were aged between 71 and 80 years. Males were 46 (88.5%) and females were six (11.5%). Majority of 36.54% participants were in stage 3, followed by stage 1 (30.76%), stage 2 (25%), and stage 4 (7.69%). In the study population, eight (15%) participants had LV diastolic dysfunction and five (10%) participants had LV systolic dysfunction (Table 1).

Table 1: Summary of baseline characteristics in the study population (N = 52)
Parameter Summary N (%)
Age group
30-40 3 (5.7
41-50 7 (13.46
51-60 17 (32.69
61-70 21 (40.38)
71-80 4 (7.6)
Male 46 (88.5)
Female 6 (11.5)
Stage 1 16 (30.76)
Stage 2 13 (25)
Stage 3 19 (36.54)
Stage 4 4 (7.69)
Duration of smoking (no. of packs)
5 16 (30.76)
10 8 (15.38)
15 12 (23.07)
20 10 (19.23)
25 6 (11.54)
LV diastolic dysfunction
Yes 8 (15)
No 44 (85)
LV systolic dysfunction
Yes 5 (10)
No 47 (90)

The mean E/A ratio with in stage1 was 1.04, 0.87 in stage 2, 0.73 in stage 3, and 0.72 in stage 4. Taking stage 1 as base line, the mean difference of E/A ratio was statistically significant (p -value 0.024). The mean left ventricular ejection fraction in stage 1 was 63.62, 61.08 in stage 2, 61.21 in stage 3, and 54.4 in stage 4. The mean left ventricular end diastolic diameter in stage 1 was 42.5, 38.9 in stage 2, 47.8 in stage 3 and 47.8 in stage 4 (Table 2).

Table 2: Comparison of different parameters across stages of COPD (N = 52)
Parameter Stages of COPD p-value
Stage 1 Stage 2 Stage 3 Stage 4
E/A ratio 1.04 ± 0.7 0.87 ± 0.4 0.73 ± 0.32 0.72 ± 0.25 0.024
Left ventricular ejection fraction 63.62 ± 15.6 61.08 ± 14.9 61.21 ± 15.01 54.4 ± 14.2 0.863
Left ventricular end diastolic diameter 42.5 ± 8.6 38.9 ± 7.2 43.16 ± 8.2 47.8 ± 9.1 0.072

*p-value < 0.05 (statistically significant)

A week negative correlation (r = 0.0207) between duration of smoking and E/A ratio was observed as per the scatter plot (Fig. 1).

Figure 1: Relationship between diastolic function (E wave/A wave) with years of smoking

A week negative correlation (r = 0.0458) was observed between duration of smoking and Left ventricular end-diastolic diameter (LVEDD) as per the scatter plot (Fig. 2).

Figure 2: Relationship between LVEDD with years of smoking


In the present study, we assessed the left ventricular function in COPD patients and have found that majority of them had statistically significant decreased E/A ratio in stage 4 COPD (p < 0.05). The interaction between COPD and cardiovascular comorbidity is complex and bidirectional. Several studies have reported cardiac abnormalities in COPD with the right ventricle.

In the current study, eight (15%) participants had LV diastolic dysfunction and five (10%) participants had LV systolic dysfunction. In a study by Funk et al. reported that 7.50% COPD patients had LV systolic dysfunction and 47.5% patients had evidence of LV diastolic dysfunction.10 Other studies have reported LV systolic dysfunction in the range of 4-32% among COPD patients.11,12 Sorel M et al. highlighted that in COPD patients, LV diastolic function was significantly impaired and its magnitude was related to increase in pulmonary artery pressure. The cause of left ventricular diastolic dysfunction in COPD patients could be due to chronic hypoxemia leading to the changes in myocardial relaxation, distension, and lung hyperinflation making the parietal pleura stiff.7

The present study demonstrated a week negative correlation between duration of smoking and E/A ratio. It is supported by the fact that cigarette smoking and other exposure factors lead to inflammatory changes which disrupt the vascular pulmonary endothelium.

There was week negative correlation between duration of smoking and LVEDD. This can be explained as there is a lower preload in left cardiac chambers mediated by an intrathoracic hypovolemia and a decrease of the pulmonary vascular bed caused by dynamic hyperinflation.13 This mechanism may explain not only the reductions in LV diameters and volumes but also the lower stroke volumes and the supposed LV diastolic dysfunction found at the transmitral doppler analysis. Indeed, the inflow pattern is not only an index of ventricular relaxation and compliance, but it is also influenced by others variables such as the preload and the HR.14,15 A lower preload can mimic an impaired LV relaxation in normal functioning heart.16

One of the limitations of our study was a smaller sample size, and the method used to assess the lung function was spirometry, whereas lung volume measurements would have been more accurate. Further well-designed cohort studies and use of future three-dimensional echocardiography with optimal sample size will be helpful in defining the left ventricular dysfunction in COPD patients.


Left ventricular defects specifically differences in E/A ratio were present in patients with all stages of COPD severity. The pathophysiological mechanisms involved can act independently or synergically, given the complex heart-lung interaction. These findings pave the way for future research, and to new diagnostic and therapeutic strategies. Treatment and prevention of smoking can have a great impact on the natural history of coexisting COPD and CVD.


We acknowledge the technical support in data entry, analysis, and manuscript editing by “Evidencian Research Associates.”


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