Practical algorithms for pharmacologic management of the post myocardial infarction patient.
The pharmacologic management of the patient post myocardial infarction (MI) aims to achieve several goals. Chief among these is to prevent subsequent events, which include death, reinfarction, and rehospitalization. Secondary goals include preventing arrhythmias, minimizing left ventricular (LV) remodeling, and preventing progression to heart failure. This review describes practical algorithms for use in the pharmacologic management of the patient post MI based on American Heart Association/American College of Cardiology guidelines. The intensity of drug treatment is determined guided by the degree of LV dysfunction and the presence or absence of ischemia and arrhythmic risk markers. All patients post MI require an angiotensin-converting enzyme (ACE) inhibitor and antiplatelet therapy, usually with aspirin. In individuals who cannot tolerate an ACE inhibitor, an angiotensin receptor blocker (ARB) is an adequate substitute. Numerous studies document the efficacy of ACE inhibitors, which decrease mortality and the risk of heart failure and stroke. Aldosterone blockade is recommended long-term for patients post MI with an LV ejection fraction < or = 40% and either symptomatic heart failure or diabetes. Use of a beta blocker is an important addition to most post-MI drug regimens. Beta blockers decrease mortality and are especially effective in patients with impaired LV function. Among the beta blockers, carvedilol, which also has alpha-adrenergic receptor blocking activity, was found to decrease mortality significantly in patients with low ejection fractions and heart failure. Another drug therapy of value in post-MI treatment is use of calcium-channel blockers. These are restricted to patients with conserved LV function in whom congestion is absent and in whom beta blockers are contraindicated. Current guidelines also recommend that patients post MI with elevated cholesterol levels should be prescribed lipid therapy with a statin at hospital discharge.
Reiffel
James A
JA
Cardiology Division, Department of Medicine, Columbia University, New York, New York, USA. jar2@columbia.edu
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000465:Algorithms; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D005395:Fish Oils / Q000627:therapeutic use; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012720:Severity of Illness Index; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000209:etiology; D020257:Ventricular Remodeling / Q000187:drug effects*
D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D002317:Cardiovascular Agents; D005395:Fish Oils; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D010975:Platelet Aggregation Inhibitors