Comparison of the Factors Influencing Pulmonary Arterial Pressure in Smoker and Non-smoker COPD Patients with Pulmonary Hypertension

BACKGROUND: There are several prognostic factors in patients with Chronic Obstructive Pulmonary Disease (COPD) that include Forced expiratory volume in one second (FEV1), Body Mass Index (BMI), dyspnea severity, exercise capacity and Pulmonary Hypertension (PH). PH is one of the most important factors. PH pathogenesis in patients with COPD has not been clarified thoroughly and factors such as alveolar hypoxemia, polycythemia, acidosis and pulmonary vessels obstruction have been suggested. The authors assessed some of these contributing factors in smoker and non-smoker patients with COPD. MATERIALS AND METHODS: This comparative-descriptive study included COPD patients suspected to have cor pulmonale without exacerbation in the last four weeks. Echocardiographic evaluation of Pulmonary Arterial Pressure (PAP) was done and Pulmonary Hypertension (PH) was defined as systolic Pulmonary Arterial Pressure (PAP) greater than 40 mmHg. Complete Blood Count (CBC) and Arterial Blood Gas (ABG) were also studied in all patients. RESULTS: Echocardiography was done for 142 patients who were suspected to have PH and 110 patients had measurable PAP. All of the patients were in stage II – IV of COPD according to GOLD criteria. 90 patients had PH of which 47 were smokers and 43 were non-smokers. In smoker patients, significant correlation between PAP and PaO(2) was seen (r=−0.291, p-value=0.047). But in non-smoker patients, this correlation was absent. A significant correlation between PAP and FEV1 (r=−0.341, P value=0.025) was seen in non-smoker patients. This correlation was absent in smoker patients. There was no correlation between PAP and hemoglobin, hemoglobin and FEV, and also PaO(2) and FEV1 in smoker and non-smoker COPD patients. CONCLUSION: In non-smoker patients with COPD, degree of pulmonary parenchymal lesions and bronchial obliteration plays a more important role than hypoxia in the pathogenesis of pulmonary hypertension.