<qa>  What is the name of the ACE inhibitor therapy that causes aldosterone secretiThe persistent elevation of ANG II and aldosterone concentrations during ACE inhibitor therapy is often termed escape. Aldosterone secretion from the adrenal cortex persists in response to ANG II produced by the non ACE enzymatic conversions of ANG I and a rise in plasma potassium. Comparison of the effects of adding ANG II receptor blockers ARB and aldosterone receptor antagonists to ACE inhibitors in heart failure trials suggests that it is aldosterone escape that exerts the greater pathophysiological effects. In ValHeFT the addition of valsartan to ACE inhibitor therapy had no detectable effect on mortality. In both the RALES and EPHESUS trials however, mortality was significantly reduced by the addition of spironolactone RALES or eplerenone EPHESUS to standard therapy including ACE inhibitors. 