b-Adrenergic antagonists have antiarrhythmic, anti-ischemic, and antihypertensive properties. During AMI, they diminish myocardial oxygen demand by decreasing heart rate, systemic arterial pressure, and myocardial contractility. Prolongation of diastole may augment perfusion to ischemic myocardium. 32
Immediate b-antagonist administration in AMI reduces chest pain, wall stress, infarct size, incidence of cardiovascular complications, and mortality rate for patients not treated with fibrinolytics. The International Collaborative Study Group randomized 144 patients with AMI to treatment with timolol or placebo. 36 The timolol group had a reduction in pain, analgesic use, and infarct size. The Metoprolol in Acute Myocardial Infarction (MIAMI) trial randomized 5ZZ8 patients to metoprolol or placebo. Metoprolol reduced mortality rate in high-risk patients, and infarct size was reduced in patients treated within Z h of symptom onset. 37 ISIS-1 randomized 16,027 patients to atenolol or placebo and found a 14 percent sustained reduction in mortality rate equating to 6 lives saved per 1000 patients. 38
For patients treated with fibrinolytics, the TIMI-II trial showed that b antagonists decrease the risk of nonfatal reinfarction and recurrent ischemia if given within 2 h after symptom onset. Mortality rate and ventricular function were not affected.39
The ACC/AHA guidelines recommend that all patients with Q-wave AMI who do not have a contraindication to b antagonists be treated with these agents within 12 h of onset of infarction, regardless of whether they have received fibrinolytic therapy. 4 Patients with recurrent ischemia and tachyarrhythmias should receive b-antagonist therapy. The role of b antagonists in non-Q-wave infarctions is less clear. The AHCPR guidelines do recommend that patients with unstable angina receive treatment with b antagonists, when possible.24
Relative contraindications to b-adrenergic antagonists are heart rate less than 60 beats per minute, systolic blood pressure less than 100 mmHg, moderate to severe left ventricular failure, signs of peripheral hypoperfusion, PR interval more than 0.24 s, second-degree or third-degree atrioventricular block, severe chronic obstructive pulmonary disease, history of asthma, severe peripheral vascular disease, and insulin-dependent diabetes mellitus. 4 Use of b antagonists should be individualized for patients with these conditions. Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE) inhibitors reduce left ventricular dysfunction and left ventricular dilatation and slow the development of congestive heart failure during AMI. Studies have consistently shown a reduction in mortality rate for patients treated with oral ACE inhibitors during and soon after AMI. 32 A meta-analysis of 15 trials including over 100,000 patients supports a 6.5 percent reduction in short-term mortality rate, with an absolute benefit of 4.6 fewer deaths per 1000 patients treated with early ACE inhibitor therapy.40 Intravenous enalaprilat was associated with increased hypotension and is not recommended for use during AMI.
The ACC/AHA guidelines recommend that patients with AMI and ST-segment elevation in two or more anterior precordial leads or with clinical heart failure in the absence of contraindications receive treatment with ACE inhibitors.4 Contraindications to ACE inhibitors include hypotension, bilateral renal artery stenosis, renal failure, or history of cough or angioedema due to prior ACE inhibitor use. The efficacy of ACE inhibitors in unstable angina has not been well evaluated.
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