Left ventricular (LV) dysfunction and/or heart failure (HF) are frequent complications of
hypertension and myocardial infarction (MI), placing affected patients at increased risk of
significant morbidity and premature death. Given that the renin-angiotensinaldosterone
system (RAAS) is activated and of pathophysiological importance in such patients, a strong
therapeutic rationale exists to target the main effector mechanism (that is, angiotensin II [Ang
II]) in order to lessen the associated morbidity and mortality burden. Angiotensin-converting …