The effect of amlodipine and sildenafil on the NT-proBNP level of patients with COPD-induced pulmonary hypertension.

Document Type: Supplement (special issue)

Authors

1 Lung Transplantation Research Center, NRITLD, Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

2 Clinical Pharmacy Department, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

3 Clinical Pharmacy Department, School of Pharmacy, Shahid Behehshti University of Medical Sciences, Tehran , Iran.

4 Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Pharmaceutical Care Department,Tehran,Iran

5 Lung Transplantation Research Center, NRITLD, Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

6 1-Clinical Pharmacy Department, School of pharmacy, Shahid Beheshti University of Medical Sciences 2-Chronic Respiratory Disease Research Center, NRILTD, Masih Daneshvari Hospital, Shahid Beheshti Universityof Medical Sciences, Tehran, Iran.

Abstract

Pulmonary hypertension (PH) is an important cause of heart failure in chronic obstructive pulmonary disease (COPD). The pro brain natriuretic peptide N-terminal (NT-proBNP) has been suggested as a noninvasive marker to evaluate ventricular function. However, there is no evidence to support the use of NT-proBNP in monitoring the benefits of vasodilators in COPD induced PH. Thus, we used NT-proBNP as a biomarker to evaluate the effect of oral vasodilators on cardiac function in COPD-induced PH.
Forty clinically-stable PH patients were enrolled with history of COPD, normal left ventricular ejection-fraction (LVEF), right ventricular systolic pressure (RVSP) > 45 mmHg and baseline blood NT-proBNP levels >100 pg/ml. Patients were randomized into two groups, one group received sildenafil and second group were given amlodipine for two weeks. NT-proBNP and systolic pulmonary arterial pressure (systolic PA-pressure) were measured at the beginning and the end of study.
NT-proBNP levels in the first group was 1297±912 pg/ml before therapy and 554±5 pg/ml after two weeks drug therapy, respectively. Similarly, in second group NT-proBNP level was 1657±989pg/ml and 646±5 pg/ml before and after treatment. Amlodipine or sildenafil significantly reduced NT-proBNP levels in COPD-induced PH patients (p<0.05).
Our study shows that amlodipine and sildenafil have a similar effect on NT-proBNP levels. In both groups NT-proBNP levels were significantly reduced after treatment. Therefore, our findings support the potential benefits of treatment with vasodilators in COPD induced PH.

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