Effects of Captopril Combined with Oxygen Therapy at Rest and on Exercise in Patients with Chronic Bronchitis and Pulmonary Hypertension

Abstract

The aim of this study was to determine the effects of captopril combined with oxygen therapy on pulmonary hemodynamics and gas exchange in chronic obstructive pulmonary disease (COPD) patients with pulmonary hypertension. Eleven subjects, with severe airflow obstruction (FEV₁/FVC: 42 ± 11%) and chronic respiratory failure (PaO₂: 54 ± 6 mm Hg, PaCO₂:46 ± 8 mm Hg) treated with long-term oxygen, underwent two successive hemodynamic and arterial gas studies, at rest and during exercise. All the studies were performed whilst the patients were breathing oxygen, at rest and during exercise and 1 h after intake of 12.5 mg of captopril. The second study was performed in 9 out of the 11 patients after 8 weeks of treatment with 12.5 mg captopril 3 times daily. At rest, there was no significant effect of captopril. Mean pulmonary arterial pressure (PAP) showed a trend towards decrease after 8 weeks treatment. During exercise, there was a statistically significant decrease of mean PAP, pulmonary capillary wedge pressure and total pulmonary vascular resistance, without any deleterious effect on blood gases. However, the clinical significance of these variations during exercise is poor. We conclude that a low dose of captopril associated with oxygen therapy has no significant clinical effect on pulmonary hemodynamics at rest and during exercise in COPD

Angiotensin-converting enzyme 2 in lung diseases

“…By contrast, tissue ACE-deficient mice, which exhibit undetectable lung ACE activity but retain 34% of the ACE activity in plasma, show the same remodeling of pulmonary arterioles as do wild-type mice [41]. In addition, despite earlier studies of acute ACE inhibition [42][43][44], a recent pilot study on patients with pulmonary hypertension secondary to COPD showed that treatment with the AT 1 receptor blocker losartan (50 mg) showed no statistically significant beneficial effect in terms of pulmonary artery pressure, exercise capacity or breathlessness score [45]. The discrepancy between hypoxic rat studies and this human trial might be caused by differences in the pathogenesis of hypoxic rats versus patients with COPD-related pulmonary hypertension.…”

The role of the renin‐angiotensin and natriuretic peptide systems in the pulmonary vasculature.

“…Studies with ACE inhibitors in PPH have produced conflicting results in terms of pulmonary haemodynamic benefit [9,[25][26][27] and consequently these agents have not found a place in the treatment of these patients. In cor pulmonale, acute dosing studies have demonstrated variable effects on pulmonary haemodynamics [28][29][30][31][32][33] whereas chronic dosing studies have been short-term and have included only small numbers of patients [34,35] ( Table 1). The inclusion criteria for many of these studies (see Table 1) have been extremely variable with the inclusion of a heterogeneous group of subjects some of whom did not have pulmonary hypertension and were not hypoxaemic/hypercapnic.…”

Right Heart Catheterization During Exercise in Patients with COPD—An Overview of Clinical Results and Methodological Aspects

“…The acute (after 60 min) and chronic (after 8 weeks) hemodynamic effects of angiotensin-converting enzyme (ACE) inhibition in combination with oxygen were examined in patients with COPD at rest and during exercise (91). Only the exercise data improved, and this effect was judged to be clinically irrelevant by the authors.…”