Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor ramipril

Background-Electrocardiographic markers of left ventricular hypertrophy (LV H) predict poor prognosis. We determined whether the ACE inhibitor ramipril prevents the development and causes regression of ECG-LVH and whether thes e changes are associated with improved prognosis independent of blood press ure reduction. Methods and Results-In the Heart Outcomes Prevention Evaluation (HOPE) stud y, patients at high risk were randomly assigned to ramipril or placebo and followed for 4.5years. ECGs were recorded at baseline and at study end. We compared prevention/regression and development/persistence of ECG-LVH in th e two groups and related these changes to outcomes. At baseline, 676 patien ts had LVH (321 in the ramipril group and 355 in the placebo group) and 760 5 patients did not have LVH (3814 in the ramipril group and 3791 in the pla cebo group). By study end, 336 patients in the ramipril group (8.1%) compar ed with 406 in the placebo group (9.8%) had development/persistence of LVH; in contrast, 3799 patients in the ramipril group (91.9%) compared with 374 0 in the placebo group (90.2%) had regression/prevention of LVH (P=0.007). The effect of ramipril on LVH was independent of blood pressure changes. Pa tients who had regression/prevention of LVH had a lower risk of the predefi ned primary outcome (cardiovascular death, myocardial infarction, or stroke ) compared with those who had development/persistence of LVH (12.3% versus 15.8%, P=0.006) and of congestive heart failure (9.3% versus 15.4%, P <0.00 01). Conclusions-The ACE inhibitor ramipril decreases the development and causes regression of ECG-LVH independent of blood pressure reduction, and these c hanges are associated with reduced risk of death, myocardial infarction, st roke, and congestive heart failure.