Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane

Conductance of alveolar capillary membrane (D-M) and capillary blood volume (V-C) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLco). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced D-M and subsequent impairment of DLco. Ang iotensin-converting enzyme inhibition improves DLco in patients with chroni c heart failure. This study was aimed at investigating which of the two sub components of DLco is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (gro up 1) and 13 age- and sex-matched normal subjects underwent pulmonary funct ion testing with determination of D-M and V-C, while receiving placebo and 48 h and 1 and 2 months after starting enalapril treatment (10 mg twice dai ly). Nine similar patients (group 2) received isosorbide dinitrate (40 mg t hrice daily) for a month then enalapril for another month, and underwent pu lmonary function testing at 48 h and 1 month after starting treatments. Eff ects of angiotensin-converting enzyme inhibition in normal controls were no t significant in the short- or mid-term. In group 1 patients, the only chan ge observed at 48 h was a reduction in V-C (probably due to a decrease in c apillary pulmonary pressure). There was a marked increase in D-M to a simil ar extent at 1 and 2 months, resulting in a significant improvement in DLco despite a decrease in V-C. In group 2 patients, nitrates failed to improve DLco and D-M, whereas enalapril was as effective as in group 1. These obse rvations suggest a modulatory effect of angiotensin-converting enzyme inhib ition on the membrane function which emerges gradually and persists over ti me and is probably dissociated from changes in pulmonary capillary pressure and V-C. Chronic heart failure disturbs the alveolar capillary interface a nd increases gas diffusion resistance; angiotensin-converting enzyme inhibi tion restores the diffusive properties of the membrane and gas transfer, an d protects the lung when the heart is failing.