|Year : 2011 | Volume
| Issue : 2 | Page : 105-109
Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease
NK Gupta, Ritesh Kumar Agrawal, AB Srivastav, ML Ved
Department of Tuberculosis and Chest Diseases, R N T Medical College, Udaipur, Rajasthan, India
|Date of Web Publication||30-Apr-2011|
Ritesh Kumar Agrawal
Rajkumar Cloth Store, Rauja Bazar Mau, Mau Nath Bhanjan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Chronic obstructive pulmonary disease (COPD) has considerable effects on cardiac functions, including those of the right ventricle, left ventricle, and pulmonary blood vessels. Most of the increased mortality associated with COPD is due to cardiac involvement. Echocardiography provides a rapid, noninvasive, portable, and accurate method to evaluate the cardiac changes. Aims: To assess the cardiac changes secondary to COPD by echocardiography and to find out the correlation between echocardiographic findings and severity of COPD, if there is any. Materials and Methods: A total 40 of patients of COPD were selected and staged by pulmonary function test (PFT) and evaluated by echocardiography. Results: On echocardiographic evaluation of COPD, 50% cases had normal echocardiographic parameters. Measurable tricuspid regurgitation (TR) was observed in 27/40 cases (67.5%). Pulmonary hypertension (PH), which is defined as systolic pulmonary arterial pressure (sPAP) > 30 mmHg was observed in 17/27 (63%) cases in which prevalence of mild, moderate, and severe PH were 10/17 (58.82%), 4/17 (23.53%), and 3/17 (17.65%), respectively. The frequencies of PH in mild, moderate, severe, and very severe COPD were 16.67%, 54.55%, 60.00%, and 83.33%, respectively. Right atrial pressure was 10 mmHg in 82.5% cases and 15 mmHg in 17.5% cases. Cor pulmonale was observed in 7/17 (41.17%) cases; 7.50% cases had left ventricle (LV) systolic dysfunction and 47.5% cases had evidence of LV diastolic dysfunction defined as A ≥ E (peak mitral flow velocity of the early rapid filling wave (E), peak velocity of the late filling wave caused by atrial contraction (A) on mitral valve tracing). Left ventricle hypertrophy was found in 22.5% cases. Conclusion : Prevalence of PH has a linear relationship with severity of COPD and severe PH is almost associated with cor pulmonale. Echocardiography helps in early detection of cardiac complications in COPD cases giving time for early interventions.
Keywords: Chronic obstructive pulmonary disease, cor pulmonale, echocardiography, pulmonary hypertension
|How to cite this article:|
Gupta N K, Agrawal RK, Srivastav A B, Ved M L. Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease. Lung India 2011;28:105-9
|How to cite this URL:|
Gupta N K, Agrawal RK, Srivastav A B, Ved M L. Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease. Lung India [serial online] 2011 [cited 2021 Jan 21];28:105-9. Available from: https://www.lungindia.com/text.asp?2011/28/2/105/80321
| Introduction|| |
Chronic obstructive pulmonary disease (COPD), defined by GOLD as a preventable and treatable disease with some significant extrapulmonary effects, is a very common clinical entity in clinical practice. COPD is a leading cause of death and disability worldwide. According to World Bank data it is expected to move from its status in 2000 as the 4 th and 12 th most frequent cause of mortality and morbidity, respectively, to the 3 rd and 5 th leading cause of mortality and morbidity, respectively, in 2020. , COPD is associated with significant extrapulmonary (systemic) effects among which cardiac manifestations are most common. Cardiovascular disease accounts for approximately 50% of all hospitalization and nearly one third of all deaths, if forced expiratory volume in one second (FEV 1 ) > 50% of predicted.  In more advanced disease cardiovascular disease account for 20%-25% of all deaths in COPD.  COPD affects pulmonary blood vessels, right ventricle, as well as left ventricle leading to development of pulmonary hypertension, cor pulmonale, right ventricular dysfunction, and left ventricular dysfunction too. 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.  Many studies have confirmed that echocardiographically derived estimates of pulmonary arterial pressure co-relate closely with pressures measured by right heart catheter (r > 0.7). ,
Hence the present study was undertaken with the following aims and objectives:
- To assess the cardiac changes secondary to COPD by echocardiography, and
- To find out the correlation between echocardiographic findings and the severity of COPD using GOLD guidelines.
| Materials and Methods|| |
Forty patients of COPD confirmed by clinical history, radiology of chest, and pulmonary function test were selected from Chest and T.B. Hospital of R.N.T. Medical College, Udaipur, Rajasthan. During selection, patients with H/O of chronic lung disease other than COPD, hypertension, any primary cardiac disease, any systemic disease that can cause pulmonary hypertension, patients with poor echo window, and patients who were unable to perform spirometry were excluded from the study.
All selected patients were subjected to routine investigations, including complete blood count, lipid profile, blood sugar, blood urea, serum creatinine, electrocardiography, and so on, as needed.
All the patients were investigated by spirometry and diagnosed and classified according to GOLD guidelines (postbronchodilator FEV 1 /forced vital capacity (FVC) ratio < 70% predicted), mild (FEV 1 ≥ 80% of predicted), moderate (50% ≤ FEV 1 < 80% predicted), severe (30% ≤ FEV 1 < 50% predicted), and very severe (FEV 1 < 30% predicted), respectively.
All patients were subjected to resting two-dimension transthoracic Doppler echocardiography in the cardiology department of R.N.T. Medical College and associated hospitals by expert cardiologists. The machine used was VIVID 7 model of GE health care system with a multifrequency probe with a range of 2-4.3 MHz. Both 2D and M-Mode studies were done.
Echocardiography was reviewed to assess the pericardium, valvular anatomy and function, left and right side chamber size and cardiac function. Tricuspid regurgitant flow was identified by color flow Doppler technique and the maximum jet velocity was measured by continuous wave Doppler without the use of intravenous contrast. Right ventricular systolic pressure was estimated based on the modified Bernoulli equation and was considered to be equal to the sPAP in the absence of right ventricular outflow obstruction: sPAP (mmHg) = right ventricular systolic pressure = trans-tricuspid pressure gradient (TTPG) + right atrial pressure (RAP), where trans-tricuspid gradient is 4v2 (v = peak velocity of tricuspid regurgitation, m/s). ,, RAP was empirically estimated as 15 mmHg before 1997. Since 1997, RAP was estimated to be 5, 10, or 15 mmHg based on the variation in the size of inferior vena cava with inspiration as follows: complete collapse, RAP = 5 mmHg; partial collapse, RAP = 10 mmHg; and no collapse, RAP = 15 mmHg. 
Pulmonary hypertension (PH) was defined in this study as sPAP ≥ 30 mmHg.  This value was chosen according to the definition of pulmonary hypertension. PH was classified into mild, moderate, and severe category as sPAP 30-50, 50-70, >70 mmHg, respectively (using Chemla formula, mean pulmonary arterial pressure (MPAP) =0.61 PASP + 2 mmHg and putting value of 25-35, 35-45, and >45 mmHg of MPAP for mild, moderate, and severe pulmonary hypertension, respectively). 
Right ventricle dimension was measured by M-Mode echo and right ventricular dilation or cor pulmonale was said to be present when it exceeded the normal range of 0.9-2.6 cm. Right ventricle contractility was also noted and right ventricular systolic dysfunction was said to be present when it was hypokinetic.
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). 
| Results|| |
A total of 40 patients were recruited in our study and out of them, the number of patients with mild, moderate, severe, and very severe COPD were 18/40 = 45%, 11/40 = 27.5%, 5/40 = 12.5%, and 6/40 = 15%, respectively [Table 1].
On echocardiography 20 patients (20/40 = 50%) had normal study.
Measurable tricuspid regurgitation (TR) was observed in 27 patients (27/40 = 67.5%). Mean TTPG for the entire group in which TR could be measured was 37.04 mmHg.
PH defined as sPAP > 30 mmHg was observed in 17 patients (17/40 = 42.5% of the total study population) (17/27 = 63% of measurable TR). Out of those 17 patients with pulmonary hypertension, 10 patients were in mild PH (sPAP 30-50 mmHg) (10/40 = 25%) (10/17 = 58.82%), 4 were in moderate PH (sPAP 50-70 mmHg) (4/40 = 10%) (4/17 = 23.53%), and 3 were in severe PH (sPAP > 70 mmHg) (3/40 = 7.5%) (3/17 = 17.65%) [Table 2]. The frequencies of PH in mild, moderate, severe, and very severe COPD were 3/18 = 16.67%, 6/11 = 54.55%, 3/5 = 60%, 5/6 = 83.33%, respectively; thus we can see that there is a good co-relation between the frequency of PH and severity of COPD [Table 3].
The frequencies of cor pulmonale in patients with mild, moderate, and severe PH were 10%, 75%, and 100%, respectively; so we can see a good co-relation between severity of PH and the development of cor pulmonale [Table 4] and [Table 5].
Comparative study of various stages of severity of COPD reveals that as severity of COPD increases the prevalence of cardiac dysfunction increases, so more severe COPD is associated with more prevalent and more severe cardiac manifestations [Table 6].
| Discussion|| |
The cardiac manifestations of COPD are numerous. Impairment of right ventricular dysfunction and pulmonary blood vessels are well known to complicate the clinical course of COPD and co-relate inversely with survival. Significant structural changes occur in the pulmonary circulation in patients with COPD. The presence of hypoxemia and chronic ventilator insufficiency is associated with early evidence of intimal thickening and medial hypertrophy in the smaller branches of the pulmonary arteries. Coupled with these pathological changes are pulmonary vasoconstriction arising from the presence of alveolar hypoxemia, destruction of pulmonary vascular bed, changes in intrinsic pulmonary vasodilator substances (such as decrease in PGI 2 s (prostacyclin synthase), decrease in eNOS (endothelial nitric oxide synthase), and increase in ET1 (endothelin1) leads to remodeling, increase in blood viscosity, and alteration in respiratory mechanics. All these lead to a significant increase in pulmonary vascular resistance, the consequence of which is pulmonary hypertension. Severe PH increases right ventricular after load with a corresponding increase in right ventricular work, which results in uniform hypertrophy of the right ventricle. In patients with COPD, hypoxic vasoconstriction is associated with not only right ventricular hypertrophy but also right ventricular dilation which eventually leads to clinical syndrome of right heart failure with systemic congestion and inability to adapt right ventricular output to the peripheral demand on exercise.
Although the true prevalence of PH in COPD is unknown, an elevation of pulmonary arterial pressure is reported to occur in 20%-90% of patients when measured by right heart catheterization with some evidence that pulmonary hemodynamic worsens with worsening airflow obstruction. ,,,,, Two studies have shown an abnormal increase in mean pulmonary arterial pressure (Ppa) in COPD of 0.4-0.6 mmHg per year. These studies illustrate that PH in COPD progresses slowly and occurs in mild as well as severe forms of disease. ,
The level of PH has a prognostic value in COPD patients that has been demonstrated by several studies. In one of these studies, the 5-year survival rates were 50% in patients with mild PH (20-30 mmHg), 30% in those with moderate-to-severe PH (30-50 mmHg), and 0% in the small group of patients with very severe PH (>50 mmHg). Thus a high degree of PH bears a poor prognosis, and this also has been observed in COPD patients receiving long-term oxygen therapy.  The present study finding reveals 42.5% patients of various severity of COPD have findings of pulmonary hypertension, that is similar in prevalence of previous studies. The frequencies of PH in mild, moderate, severe, and very severe COPD were 16.67%, 54.55%, 60.00%, and 83.33%, respectively. In one study it was found to be 25%, 43%, and 68% in mild, moderate, and severe COPD, respectively.  In our study it is also observed that severe PH is present only in severe or very severe COPD. In conclusion, the incidence of PH is directly proportional to severity of disease. Previous studies showed the frequencies of severe PH in COPD from about 1%-3%, , but in our study it is 4.7%; this may be due to small study population comprising more percentage of severe and very severe COPD patients.
Cor pulmonale is present in 17.5% of patients in our study. Approximately 25% patients with COPD eventually develop cor pulmonale.  Cor pulmonale was found in 40% patients with COPD in one autopsy study. , It is estimated that every year between 10% and 30% of all hospital admissions for heart failure in the United States are due to cor pulmonale  and approximately 85% patients with cor pulmonale have COPD. 
Some studies indicate that LV function remains normal in persons with COPD, whereas others suggest that LV dysfunction may be present. , Abnormal LV performance in persons with COPD may be due to a number of factors, such as hypoxemia and acidosis; concurrent coronary artery disease; ventricular interdependence (because the right ventricle (RV) and LV share a common septum, RV dilatation may lead to bulging of the septum into the LV, which would in turn increase LV end-diastolic pressure, decrease venous return, and diminish LV stroke volume and cardiac output (CO) and large swings in intrathoracic pressure (pronounced negative pleural pressure would increase Ppa and diminish LV stroke volume due to ventricular interdependence, negative pleural pressures may also increase LV after load). 
In our study, left ventricular systolic dysfunction (LVSD) is present in 7.5% patients, in previous studies it was present in 4%-32% patients of COPD. ,,, LVDD was seen in COPD patients with normal pulmonary arterial pressure and it increased with right ventricular after load.  In our study LVDD is present in 47.5% of patients, out of which 16 patients had PH and 3 did not have PH, various mechanisms might explain the presence of left diastolic dysfunction in COPD patients. This may be due to chronic hypoxemia leading to abnormalities of myocardial relaxation, lung hyperinflation, and distension leading to increased stiffness of the parietal pleura and thus of the wall of cardiac fossa leading to added load on ventricle, and also due to ventricular interdependence.
Left ventricular hypertrophy (LVH) was present in 22.5% patients in our study, in one previous study LVH was found in 25%-60% patients dying of COPD mainly in patient who also had right ventricular hypertrophy. 
| Conclusion|| |
To conclude, the present study shows high prevalence of pulmonary hypertension, cor pulmonale, left ventricular dysfunction complicating COPD, more so with more severe COPD. We suggest screening of all COPD patients for cardiac complications. This would contribute to the assessment of prognosis in these patients and assist in identifying individuals likely to suffer increased mortality and morbidity warranting close monitoring and intense treatment.
| References|| |
|1.||Murray CJ, Lopez AD. Evidence based health policy-lessons from the Global Burden of disease Study. Science 1996;274:740-3. |
|2.||World Health Report. Geneva: World Health Organisation; 2000. Available from: http://www.who.int/whr/2000/en/statistics.htm. [Last accessed on 2004 Jan]. |
|3.||Anthonisen N, Connett JE, Kiley JP, Altose MD, Bailey WC, et al. Effects of Smoking Intervention and the Use of an Inhaled Anticholinergic Bronchodilator on the Rate of Decline of FEV1. JAMA 1994;272:1497-1505. |
|4.||Sin DD, Anthonisen NR, Soriano JB, Agusti AG. Mortality in COPD: Role of comorbidities. Eur Respir J 2006;28:1245-57. |
|5.||Daniels LB, Krummen DE, Blanchard DG. Echocardiography in pulmonary vascular disease. Cardiol Clin 2004;22:383-99. |
|6.||Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70:657-62. |
|7.||Tramarin R, Torbicki A, Marchandise B, Laaban JP, Morpurgo M. Doppler echocardiographic evaluation of pulmonary artery pressure in chronic obstructive pulmonary disease. A European multicentre study. Eur Heart J 1991;12:103-11. |
|8.||Currie PJ, Seward JB, Chan KL, Fyfe DA, Hagler DJ, Mair DD, et al. Continuous wave Doppler estimation of right ventricular pressure: A simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750-6. |
|9.||Chan KL, Currie PJ, Seward JB, Hagler DJ, Mair DD, Tajik AJ. Comparison of three Doppler ultrasound methods in the prediction of pulmonary artery pressure. J Am Coll Cardiol 1987;9:549-54. |
|10.||Bredikis AJ, Liebson PR. The echocardiogram in COPD: Estimating right heart pressures. J Respir Dis 1998;19:191-8. |
|11.||Rappaport E. Cor pulmonale. In, Murray JJ, Nadel JA, Mason RM, Boushey H (eds). Textbook of respiratory medicine, 4 th Edition. Philadelphia, W.B. Saunders 2000;1631-48. |
|12.||Chemla D, Castelain V, Humbert M, Simonneau JLHG, Lecarpentier Y, Hervé P. New Formula for Predicting Mean Pulmonary Artery Pressure Using Systolic Pulmonary Artery Pressure: Chest 2004;126;1313-17. |
|13.||Braunwald′s Heart Disease. 8 th Edition. By Libby P, Bonow RO, Zipes DP, Mann DL. Philadelphia: Saunders 2008. p. 251. |
|14.||Weitzenblum E, Hirth C, Ducolone A, Mirhom R, Rasaholinjanahary J, Ehrhart M. Prognostic value of pulmonary artery pressure In chronic COPD: Thorax 1981;36:752-8. |
|15.||Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Hirth C, Roegel E. long term course of pulmonary artery pressure In chronic COPD. Am Rev Respir Dis 1984;130:993-8. |
|16.||Burrows B, Kettel LJ, Niden AH, Rabinowitz M, Diener CF. Patterns of cardiovascular dysfunction in COPD. N Engl J Med 1972;286:912-8. |
|17.||Fishman AP. State of the art: Chronic cor pulmonale. Am Rev Respir Dis 1976;114:775-94. |
|18.||Pietra G. Pathology of the pulmonary vasculature and heart. In; Cherniack N, editor. COPD. Philadelphia: WB Saunders; 1996. p. 21-6. |
|19.||Thabut G, Dauriat G, Stern JB, Logeart D, Lévy A, Marrash-Chahla R, et al: Pulmonary haemodynamics in advanced COPD candidates for lung volume reduction surgery or lung transplantation. Chest 2005;127:1531-6. |
|20.||Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Pelletier A. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985;131:493-8. |
|21.||Kessler R, Faller M, Weitzenblum E, Chaouat A, Aykut A, Ducolone´A, et al. "Natural history" of pulmonary hypertension in a series of 131 patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001;164:219-24. |
|22.||Oswald-Mammosser M, Weitzenblum E, Quoix E, Moser G, Chaouat A, Charpentier C, et al. Prognostic factors in COPD patients receiving long-term oxygen therapy. Chest 1995;107:1193-8. |
|23.||Higham MA, Dawson D, Joshi J, Nihoyannopoulos P, Morrell NW. Utility of echocardiography in assessment of pulmonary hypertension secondary to COPD. Eur Respir J 2001;17:350-5. |
|24.||Chaouat A, Bugnet AS, Kadaoui N, Schott R, Enache I, Ducoloné A, et al. Severe pulmonary hypertension and chronic obstructive pulmonary disease. Am J Respire Care Med 2005;172:189-94. |
|25.||Thabut G, Dauriat G, Stern JB, Logeart D, Lévy A, Marrash-Chahla R, et al. Pulmonary Haemodynamics in advanced COPD candidate for lung volume reduction surgery or lung transplantation. Chest 2005;127:1531-6. |
|26.||Springhouse. Respiratory disorders. In, Springhouse (ed). Professional Guide to Diseases.9 th Edition.Philadelphia, Lippincott William and Wilkins 2008;120. |
|27.||Rigolin VH, Robiolio PA, Wilson JS, Harrison JK, Bashore TM. The forgotten chamber: The importance of the right ventricle. Cathet Cardiovasc Diagn 1995;35:18-28. |
|28.||Fishman AP. State of the art: Chronic Cor Pulmonale. Am Rev Respire Dis 1976;114:775-94. |
|29.||Macnee W. Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease. Part One. Am J Respire Crit Care Med 1994;150:833-52. |
|30.||Murphy ML, Adamson J, Hutcheson F. Left ventricular hypertrophy in patients with chronic bronchitis and emphysema. Ann Intern Med 1974;81:307-13. |
|31.||Fluck DC, Chandrasekar RG, Gardner FV. Left ventricular hypertrophy in chronic bronchitis. Br Heart J 1966;28:92-7. |
|32.||Robotham JL, Lixfeld W, Holland L, MacGregor D, Bryan AC, Rabson J. Effects of respiration on cardiac performance. J Appl Physiol 1978;44:703-9. |
|33.||Render, ML, Weinstein, AS, Blaustein, AS Left ventricular dysfunction in deteriorating patients with chronic obstructive pulmonary disease. Chest 1995;107:162-8. |
|34.||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. |
|35.||Jardin F, Gueret P, Prost JF, Farcot JC, Ozier Y, Bourdarias JP. Two-dimensional echocardiographic assessment of left ventricular function in chronic obstructive pulmonary disease. Am Rev Respir Dis 1984;129:135-42. |
|36.||Louridas G, Patakas D, Stavropoulos C. Left ventricular function in patients with chronic obstructive pulmonary disease. Cardiology 1981;67:73-80. |
|37.||Funk GC, 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;133:1354-9. |
|38.||Poddar AK, Chakraborti BN, Ghosh JL, Nandy S, Hazra S. Assessment of left ventricular function in patients of COPD :Ind J Tub. 1997; 44-181 |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
|This article has been cited by|
||78-Year-Old-Woman With Dyspnea on Exertion
| ||Chad W. McRee,Jordan C. Ray,Brian P. Shapiro |
| ||Mayo Clinic Proceedings. 2014; 89(11): e109 |
|[Pubmed] | [DOI]|
||Enfermedad pulmonar obstructiva crónica y ventrículo izquierdo
| ||Karina Portillo,Jorge Abad-Capa,Juan Ruiz-Manzano |
| ||Archivos de Bronconeumología. 2014; |
|[Pubmed] | [DOI]|
||Oxidative status and chymotrypsin-like activity in right and left ventricle hypertrophy in an experimental model of emphysema
| ||Jair Tonon,Flávia Alessandra Guarnier,Cláudia Roberta Brunnquell,Sara Santos Bernardes,Alessandra Lourenço Cecchini,Rubens Cecchini |
| ||Pathophysiology. 2013; |
|[Pubmed] | [DOI]|
||Evaluation of left ventricular function in patients with chronic obstructive pulmonary disease with or without pulmonary hypertension
| ||Rabab A. El Wahsh,Mahmoud K. Ahmed,Rehab I. Yaseen |
| ||Egyptian Journal of Chest Diseases and Tuberculosis. 2013; |
|[Pubmed] | [DOI]|
||Right Ventricular Morphology and Function in Chronic Obstructive Pulmonary Disease Patients Living at High Altitude
| ||Tolga Sinan Güvenç,Hatice Betül Erer,Seref Kul,Gökhan Perinçek,Sami Ilhan,Nurten Sayar,Binnaz Zeynep Yildirim,Coskun Dogan,Yavuz Karabag,Bahattin Balci,Mehmet Eren |
| ||Heart, Lung and Circulation. 2013; 22(1): 31 |
|[Pubmed] | [DOI]|
||Association between left ventricular diastolic dysfunction and severity of chronic obstructive pulmonary disease
| ||Caram, L.M.O. and Ferrari, R. and Naves, C.R. and Tanni, S.E. and Coelho, L.S. and Zanati, S.G. and Minicucci, M.F. and Godoy, I. |
| ||Clinics. 2013; 68(6): 772-776 |
||Right Ventricular Morphology and Function in Chronic Obstructive Pulmonary Disease Patients Living at High Altitude
| ||GÃ¼venÃ§, T.S. and Erer, H.B. and Kul, T. and PerinÃ§ek, G. and Ilhan, S. and Sayar, N. and Yildirim, B.Z. and DoÄan, C. and KarabaÄ, Y. and Balci, B. and Eren, M. |
| ||Heart Lung and Circulation. 2013; 22(1): 31-37 |
||Les pÃ©ricardites tuberculeuses au centre hospitalier universitaire de bobo-dioulasso, burkina faso
| ||YamÃ©ogo, A.A. and Kyelem, C.G. and NikiÃ©ma, Z. and Birba, E. and YamÃ©ogo, T.M. and ZabsonrÃ©, P. |
| ||Pan African Medical Journal. 2012; 12(1) |
||Frequency of pulmonary hypertension in patients with COPD due to biomass smoke and tobacco smoke
| ||Sertogullarindan, B. and Gumrukcuoglu, H.A. and Sezgi, C. and Akil, M.A. |
| ||International Journal of Medical Sciences. 2012; 9(6): 406-412 |