Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction
M. Guazzi et al., Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction, CLIN PHARM, 65(3), 1999, pp. 319-327
Objective: The backward effects of left ventricular dysfunction include alt
erations in alveolar-capillary gas transfer and ventilation-perfusion coupl
ing. Because the angiotensin-converting enzyme (ACE) is highly concentrated
in the vascular endothelium of the lungs, we examined whether ACE inhibito
rs may influence the pulmonary function in patients with congestive heart f
ailure,
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 in
cluded 19 age- and sex-matched control subjects with mild primary hypertens
ion and normal left ventricular function who were given enalapril as a stan
dard 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 en
alapril; alveolar-capillary diffusion of carbon monoxide (DLCO) increased t
oward normal; exercise tolerance time, peak exercise oxygen uptake (peak V-
O2), 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 redu
ced. Changes in peak V-O2 showed a direct correlation with those in DLCO an
d an inverse correlation with those in peak VD/VT. Results at 6 and 12 mont
hs 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 wi
th ACE inhibition. These pulmonary changes may contribute to the associated
increase in exercise tolerance.