Strongly Consider Starting an Angiotensin-Converting Enzyme Inhibitor or Angiotensin Receptor Blocker after Myocardial Infarction
Ying Wei Lum MD
The renin-angiotensin-aldosterone system (RAAS) regulates aldosterone release in the body via the action of angiotensin II on angiotensin I receptors. Angiotensin II by itself is also a potent vasoconstrictor (even more than norepinephrine), leading to hypertension (Fig. 30.1). Its other harmful effects include the promotion of atherosclerosis and hypertrophic changes in the blood vessels and left ventricle. Angiotensin-converting enzyme (ACE) inhibitors, by blocking the conversion of angiotensin I to angiotensin II, are believed to attenuate ventricular dilatation and remodeling. Furthermore, ACE inhibitors block the degradation of bradykinin, which is thought to have antihypertensive effects. The accumulation of bradykinin is believed to be the cause of the chronic cough associated with use of ACE inhibitors. Angiotensin II receptor blockers (ARBs), on the other hand, work further downstream in the RAAS by blocking angiotensin II at the receptor site.
In general, patients initiated on ACE inhibitors during myocardial infarction (MI) have demonstrated a reduction in overall mortality by about 20% to 30%. This benefit is most profound in patients with symptomatic congestive heart failure and their therapy should be continued indefinitely. However, therapy in patients without evidence of left ventricular dysfunction may be ceased after 4 to 6 weeks. These patients should then be re-evaluated in 4 to 6 months to reassess ventricular function. Patients who are intolerant to ACE inhibitors (because of severe cough, etc.) may take an ARB as a suitable alternative. Valsartan was recently compared with captopril and found to be as effective at reducing mortality, heart failure hospitalizations, and reinfarction.