Relation of aldosterone "escape" despite angiotensin-converting enzyme inhibitor administration to impaired exercise capacity in chronic congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

In patients with chronic congestive heart failure (CHF), aldosterone production may occur despite the administration of angiotensin-converting enzyme (ACE) inhibitors. This phenomenon has been termed aldosterone "escape"; its relation to the severity of the disease is unknown. We sought to assess whether aldosterone escape might be related to disease severity or functional impairment in patients with CHF. One hundred forty-one consecutive patients with CHF who received ACE inhibitors (> 6 months) underwent an evaluation of neurohormonal activation and body composition, an echo-Doppler examination, and a cardiopulmonary exercise test. Aldosterone escape was defined as plasma levels of aldosterone above the normal range in our laboratory (> 0.42 nmol/L). Fourteen patients (10%) had aldosterone escape. There were no differences between patients with and without aldosterone escape with regard to age, New York Heart Association class, neurohormonal activation, ACE inhibitor dose, hemodynamics, or skeletal muscle bulk. In contrast, mean peak oxygen consumption (14.2 +/- 3.5 vs 17.3 +/- 4.9 ml/min/kg, p < 0.05) and the slope of the relation between ventilation and carbon dioxide production (41 +/- 7 vs 36 +/- 6, p <0.05) were significantly worse in patients with aldosterone escape compared with those without it. Thus, aldosterone escape is associated with reduced exercise capacity in patients with CHF. This factor does not seem to be linked with hemodynamic mechanisms or with a reduced skeletal muscle bulk.