Angiotensin Converting Enzyme inhibitors reduce mortality in heart failure. One therapeutic mechanism is believed to be the reduction of circulating angiotensin II and aldosterone. However, the Renin-Angiotensin-Aldosterone axis (RAAS) is not uniformly suppressed during therapy for heart failure. This effect has been referred to as 'angiotensin II reactivation' and 'aldosterone escape' and their reactivation may herald clinical deterioration. In the CONSENSUS I trial, correlations were seen between mortality, and angiotensin II and aldosterone. Furthermore, mortality was lower in those with good angiotensin II suppression. Therefore, neurohormonal elevation despite adequate treatment may associate with a poorer prognosis.
Lee, A. F. C., MacFadyen, R. J., & Struthers, A. D. (1999). Neurohormonal reactivation in heart failure patients on chronic ACE inhibitor therapy: a longitudinal study. European Journal of Heart Failure, 1(4), 401-406. https://doi.org/10.1016/S1388-9842(99)00046-X