Aldosterone escape occurred in 38 of 75 hypertensive patients on ACE inhibitors for 40 weeks, preventing the significant decrease in left ventricular mass index seen in patients without escape.
Observational (n=75)
Does aldosterone escape prevent the regression of left ventricular hypertrophy in essential hypertensive patients treated with ACE inhibitors?
Aldosterone escape is common during ACE inhibitor therapy for essential hypertension and may prevent the beneficial regression of left ventricular hypertrophy.
Continuous angiotensin-converting enzyme (ACE) inhibitor therapy does not necessarily produce significant decreases in plasma aldosterone levels (aldosterone escape). We examined the role of aldosterone escape in 75 essential hypertensive patients treated with an ACE inhibitor (enalapril maleate 34 patients, imidapril hydrochloride 24 patients or trandolapril 17 patients) for 40 weeks. With treatment, blood pressure decreased and plasma renin activity increased, while plasma aldosterone concentrations did not change. Aldosterone escape was observed in 38 of the 75 patients and in 17 of 37 patients with left ventricular hypertrophy before treatment. Left ventricular mass index did not change in patients with aldosterone escape but decreased significantly in patients without aldosterone escape. The present study demonstrated a high incidence of aldosterone escape in patients with essential hypertension despite the use of ACE inhibitors. The results also suggest that aldosterone escape may reverse the beneficial effects of an ACE inhibitor on left ventricular hypertrophy.
Sato et al. (Thu,) conducted a observational in Essential hypertension (n=75). Aldosterone escape vs. No aldosterone escape was evaluated on Change in left ventricular mass index. Aldosterone escape occurred in 38 of 75 hypertensive patients on ACE inhibitors for 40 weeks, preventing the significant decrease in left ventricular mass index seen in patients without escape.