Research Article

Presence of Left Ventricular Diastolic Dysfunction in Patients of Chronic Obstructive Pulmonary Disease

Kaleem Ullah1, Zafar Niaz2, Sami Ullah Mumtaz3, Sajid Abaidullah4*

1Senior Registrar Medicine Unit-III, Nishtar Medical University / Nishtar Hospital Multan; 2Assistant Professor, North Medical Ward, King Edward Medical University / Mayo Hospital Lahore; 3Senior Registrar, North Medical Ward, King Edward Medical University / Mayo Hospital Lahore; 4Professor of Medicine, North Medical Ward, King Edward Medical University / Mayo Hospital Lahore.

Received | May 12, 2017; Accepted | January 18, 2018; Published | April 28, 2018

*Correspondence | Dr. Sami Ullah Mumtaz,King Edward Medical University, Mayo Hospital Lahore; Email: drsumumtaz@gmail.com

Citation | Ullah, K., Z. Niaz, S.U. Mumtaz and S. Abaidullah. 2018. Presence of left ventricular diastolic dysfunction in patients of chronic obstructive pulmonary disease. Annals of King Edward Medical University, 24(1): 19-23.

DOI | https://doi.org/10.21649/akemu.v24i1.2306

Keywords | Chronic Obstructive Pulmonary Disease, Left ventricular diastolic dysfunction, Echocardiography

Introduction

Chronic obstructive pulmonary disease (COPD) is characterized by fibrosis and lung tissue destruction resulting in decreased elasticity.(1) Many times it describes chronic or persistent cough, breathlessness on exertion or even vague chest pains or non-specific radiological findings on chest x-ray described as bronchitic, fibronodular or reticulonodular changes.(2) Worldwide, it is the fifth leading cause of death.(3) In UK, some 7% of all days of sickness absence from work results from this ailment.(4,5) It is caused by tobacco smoke, alpha1-antitrypsin deficiency, or caused by occupational and environmental factors.(6)

It is asymptomatic in early stages, however, after teenage, there is yearly 25 to 30 mL decrease in FEV1 in non-smokers, compared with an average decline of 45 to 60 mL in smokers. About 20% smokers had an accelerated decline in FEV1 annually up to 150 to 200 mL. The tobacco smoke is directly proportional to decline in forced expiratory volume in one second (FEV1). Among the effected 50% smokers, 15%–20% develop significant disease.(7) Majority of patients lose 50% of their lung capacity at the time of diagnosis.(8)The relationship between COPD and cardiovascular diseases strongly exists.(9) The rate of FEV1 decline is directly related to cardiovascular mortality.(10) Diastolic dysfunction is commonly reported in COPD patients.(11) In a recent study, 54 of 109 patients affected by HF with preserved systolic function had an FEV1 <70%.(12) Presence of heart failure with no left ventricular systolic dysfunction results in diastolic dysfunction.(13) The rate of ventricular filling (diastolic dysfunction) is decreased as the ventricular walls thickened, and tachycardia shortens the duration of ventricular filling.(14)

Both COPD and heart failure had common symptoms and signs such as dyspnea, rales, tachycardia and oedema(15). The chest X rays and ECG increases diagnostic accuracy(16). The LV dysfunction is high in COPD because of common risk factors with coronary disease like age, male gender and cigarettes smoking.(17) As the disease progresses, it involves both left ventricle (LV) and right ventricle (RV), and their systolic and diastolic functions. Routine echocardiography is required for assessment of LV dysfunction.(18)Currently, data on association between left ventricular diastolic dysfunction and chronic obstructive pulmonary disease is lacking in Pakistan. Results presented in this study would establish bases in early diagnosis and management and would improve the quality of life, and functional status of these patients.

Material and Methods

This cross sectional study was carried out in Mayo Hospital Lahore during a period of one year. After ethical approval of the study, 50 patients were included from indoor department through non-probability purposive sampling technique. Informed written consent was obtained from all patients before inclusion in study. The age range was 40-80 years, with either gender, history of smoking with >10 years, persistent symptoms of dyspnea, wheezing, productive cough and chest tightness lasting for >3 months along with clinical signs of nicotine staining, barrel shaped chest, vesicular breathing with prolonged expiration, bronchi and coarse crepitation, positive chest radiography findings and FEV1 <60% and FEV1/FVC <70% of predicted were included. Only the patients with already confirmed diagnosis of heart failure on the basis of clinical signs of orthopnea, paroxysmal nocturnal dyspnea rales, ECG and Chest X-Ray findings were excluded. They were examined for positive clinical signs and were sent for ECG, x-ray chest PA view (cardiothoracic ratio) and pulmonary function tests. They were then subjected to echocardiography and the left ventricular diastolic dysfunctions were noted. Confounders were controlled by stratification.

The statistical analysis was performed using SPSS version 16. Parameters such as age, years of smoking, FEV1, FVC, FEV1/FVC ratio, left ventricular internal diameter in systole and diastole, ejection fraction, peak mitral filling velocity (E), peak mitral filling rate (A), E/A ratio, isovolumetric relaxation time (IVRT), mitral deceleration time, and atrial flow reversal were quantitative variables and were presented as mean and standard deviation. Gender and left ventricular dysfunction was qualitative variables and were presented as frequency and percentages.

Results

The mean age of all subjects was 60.7±6.2 years. There were 45 (90%) male and 5 (10%) female patients in this study. There were 43 (86%) patients with a history of smoking and 13 (26%) patients with occupational history of smoking. The mean FEV1 of the patients was 45.7±13.1% with a range of 20 - 60. The mean FVC of the patients was 78.6±7.8% with a range of 60 to 90.The mean FEV1/FVC ratio was 56.9±14.3 with a range of 30 to 70 (Table 1).

Table 1: Characteristics of patients studied in this cohort

The mean left ventricular internal diameter in systole was 29.2±2.1 & in diastole was 46.5±3.4. The mean ejection fraction was 60.6±4.6 with a range of 50 to 70. The mean peak mitral filling velocity (E) of the patients was 69.8±15.9 with a range of 50 to 100.The mean peak mitral filling rate (A) was 57.2±30.9 with the range of 40 to 90 while mean E/A ratio was 1.3±0.3. The mean IVRT was 84.2±14.7 minutes. The mean mitral deceleration time was 187.4±25.1 msec. The mean atrial flow reversal was 0.28±0.04 (Table 2). There were 14 (28%) patients of LVDD and 36 (72%) patients had normal ventricular function (Figure 1).

Table 2: Echocardiographic findings

Discussion

The mean age of the patients in our study was 60.7±6.2 years which is comparable with the study of Dzudie et al(19) in which mean age of the patients was 55 years with age range of 26 to 82 years. Similarly in Suchoe et al(20) study, the mean age was 62.1±7.7 years, which is almost same and comparable with our study. In our study 86% patients had history of smoking which is comparable with the study of Abroug et al(21) where they seen 83% history of smoking, which is same and comparable with our study.

In our study the mean FEV1 was 45.7±13.1 which is comparable with the study of Suchoe et al(20) where it was 40±8.9. In our study the mean left ventricular systolic internal diameter was 29.2±2.21. It is comparable with the study of Suchoe et al(20) where mean was 33.2±4.2.In our study the mean left ventricular diastolic internal diameter was 46.5±3.4. In the study of Suchoe et al.,(20) it was 38.0±11.2. In another study conducted by Boussouges et al.,(11) it was 48±4.5, which is same and comparable with our study.

In our study the mean EF of the patients was 60.6±4.6% which is comparable with the study of Rocha et al.,(22) where it was 69±9%.The mean E/A ratio of the patients was 1.3±0.3 comparable with the study of Alchanatis et al.,(23) where it was 1.07± 0.3. The mean isovolumetric relaxation time of the patients was 84.2±14.7 msec that was comparable with the study of Alchanatis et al.,(23) where it was 85.6±8.8msec. 28% patients had left ventricular diastolic dysfunction which is comparable with the study of Abroug et al.,(21) where it was 31.1%. In Paudel et al24study, it was 26.7%, and was directly proportional to the severity of the disease.(24)

Conclusion

COPD patients had left ventricular diastolic dysfunction and it was related to increase in pulmonary artery pressure, while no left ventricular systolic dysfunction was noted. Therefore, every COPD patient must have a routine echocardiography for early detection of cardiac involvement.

References

1. Casaburi R, Kukafka D, Cooper CB, Witek TJ Jr, Kesten S. Improvement in exercise tolerance with the combination of tiotropium and pulmonary rehabilitation in patients with COPD. Chest 2005; 127: 809-17. https://doi.org/10.1378/chest.127.3.809
2. Khan MS. Chronic obstructive pulmonary disease-an update in management. Rawal Med J 2000; 27: 29-44.
3. Pauwels RA, Rabe KF. Burden and clinical features of chronic obstructive pulmonary disease (COPD). Lancet 2004; 364: 613-20. https://doi.org/10.1016/S0140-6736(04)16855-4
4. Frew A, Holgate ST. Respiratory diseases. In: Kumar & Clark Clinical Medicine. 5th ed. London: WB Saunders; 2002: 863.
5. Ahmad N, Aamir AH, Hussain I, Ghulam S. Annual Prevalence of various diseases in Hospitalized patients in a tertiary level teaching hospital at Peshawar. Pakistan J Med Res 2004; 43:166-71.
6. Hnizdo E, Glindmeyer HW, Petsonk EL, Enright P, Buist AS. Case definition of chronic obstructive pulmonary disease. J COPD 2006; 3: 1-6. https://doi.org/10.1080/15412550600651552
7. Willemse BWM, Postma DS, Timens W. The impact of smoking cessation on respiratory symptoms, lungs function, airway hyper responsiveness and inflammation. Eur Respir J 2004; 23:464-76 https://doi.org/10.1183/09031936.04.00012704
8. Khan MA, Qureshi FA, Alam J. Management of dyspnoea due to chronic obstructive pulmonary disease. Pak J Med Sci 2002; 18: 83-5.
9. Sin D, Hand SFP. Chronic obstructive pulmonary disease as to risk factor for cardiovascular morbidity and mortality. Proc Am Thorac Soc 2005; (2): 8-11. https://doi.org/10.1513/pats.200404-032MS
10. Sunyer J, Ulrink CS. Level of FEV1 as a predictor of all cause and cardiovascular mortality: an effect beyond smoking and physical fitness? Eur Respir J 2005; 25: 587-8. https://doi.org/10.1183/09031936.05.00011105
11. Boussouges A, Pinet C, Molenat F, Burnet H, Ambrosi P, Badier M, et al. Left atrial and ventricular filling in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 162: 670-75. https://doi.org/10.1164/ajrccm.162.2.9908056
12. Caruana L, Petrie MC, Davie AP et al. Do patients with suspected heart failure and preserved left ventricular systolic function suffer from “diastolic heart failure” or from misdiagnosis? A prospective descriptive study. Br Med J 2000; 321: 215-8. https://doi.org/10.1136/bmj.321.7255.215
13. Ali L, Abid AR, Mohyuddin MT, Azhar M. Echocardiographic evaluation of patients with diastolic dysfunction. Pakistan J Cardiol 2005; 16:143-8.
14. Carbajal EV, Deedwania PC. Cogestive Heart Failure. In: Current diagnosis and tre15. Wang CS, FitzGerald JM, Schulzer M, et al. This dyspneic patient inthe emergency department have congestive heart failure? JAMA 2005; 294: 1944-56.
15. Wang CS, FitzGerald JM, Schulzer M, et al. This dyspneic patient inthe emergency department have congestive heart failure? JAMA 2005; 294: 1944-56. https://doi.org/10.1001/jama.294.15.1944
16. Rutten FH, Cramer MJM, Grobbee DE, Sachs APE, Kirkels JH Lamers JWJ et al. Unrecognized heart failure in elderly patients with stable chronic obstructive pulmonary disease. Eur Heart J 2006; 27:372 https://doi.org/10.1093/eurheartj/ehi677
    https://doi.org/10.1093/eurheartj/ehi676
17. Sin DD, McAlister FA, Man SFP, Anthonisen NR. Contemporary Management of Chronic Obstructive Pulmonary Disease: Scientific Review. JAMA 2003; 290: 2301-12. https://doi.org/10.1001/jama.290.17.2301
18. Paudel B, Dhungel S, Paudel K, Pandru K, Paudel R. When left ventricular failure complicates chronic obstructive pulmonary disease: hypoxia plays the major role. Kathmandu Univ Med J 2008; 6: 37-40.
19. Dzudie A, Kengne AP, Mbahe S, Menanga A, Kenfack M, Kingue S. Chronic heart failure, selected risk factors and co-morbidities among adults treated for hypertension in a cardiac referral hospital in Cameroon. Eur J Heart Fail 2008; 10: 367-72. https://doi.org/10.1016/j.ejheart.2008.02.009
20. Suchoe E, Tracz W, Podolec P, Pieculewicz M, Peazak W, Prokop A, et al. Evaluation of left ventricular function in patients with chronic obstructive pulmonary disease. Pol Arch Med Wewn 2007; 117: 26-30.
21. Abroug F, Ouanes-Besbes L, Nciri N, Sellami N, Addad F, Hamda KB et al. Left heart dysfunction and severe exacerbation of COPD: diagnostic performance of cardiac biomarkers. AJRCCM 2006; 10: 201-26.
22. Rocha N, Stelmach R, Cukier A, Parga JR, Avila LF, Caldas M, et al. Assessment of the ventricular function of patients with advanced chronic obstructive pulmonary disease by using magnetic resonance imaging. Arq Bras Cardiol 2004; 83: 326-31.
23. Alchanatis M, Paradellis G, Pini H, Tourkohoriti G, Jordanoglou J. Left ventricular function in patients with obstructive sleep apnoea syndrome before and after treatment with nasal continuous positive airway pressure. Respiration 2000; 67: 367-71. https://doi.org/10.1159/000029532
24. Paudel B, Dhungel S, Paudel K, Pandru K, Paudel R. When left ventricular failure complicates chrnic obstructive pulmonary disease: hypoxia plays the major role. Kathmandu Univ Med J (KUMJ) 2008; 6: 37-40.