The Effect of Amlodipine and Sildenafil on the NT-ProBNP Level of Patients with COPD-Induced Pulmonary Hypertension

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 leftventricular 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. mean nt-probnp level in the first group was 1297 ± 912 pg/ml before therapy and554 ± 5 pg/ml after two weeks drug therapy, respectively. similarly, in second group nt-probnp level was 1657 ± 989 pg/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.