Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction.

OBJECTIVE

The backward effects of left ventricular dysfunction include alterations in alveolar-capillary gas transfer and ventilation-perfusion coupling. Because the angiotensin-converting enzyme (ACE) is highly concentrated in the vascular endothelium of the lungs, we examined whether ACE inhibitors may influence the pulmonary function in patients with congestive heart failure.

METHODS

In 20 patients with idiopathic cardiomyopathy, pulmonary function and exercise capacity were evaluated at baseline and 6 and 12 months after treatment with enalapril (10 mg twice a day) was started. The study also included 19 age- and sex-matched control subjects with mild primary hypertension and normal left ventricular function who were given enalapril as a standard treatment of high blood pressure.

RESULTS

In congestive heart failure, forced expiratory volume in 1 second, vital capacity, and total lung capacity did not vary significantly with enalapril; alveolar-capillary diffusion of carbon monoxide (DL(CO)) increased toward normal; exercise tolerance time, peak exercise oxygen uptake (peak VO2), minute ventilation and tidal volume (peak VT) also increased; and the ratio of volume of dead space (VD) to VT (peak VD/VT) at peak exercise reduced. Changes in peak VO2 showed a direct correlation with those in DL(CO) and an inverse correlation with those in peak VD/VT. Results at 6 and 12 months were comparable. Enalapril did not affect these variables in the control population.

CONCLUSIONS

In patients with idiopathic cardiomyopathy heart failure, but not in control subjects, gas transfer and ventilation-perfusion improved with ACE inhibition. These pulmonary changes may contribute to the associated increase in exercise tolerance.