Beta-blockade in acute myocardial infarction.
Coronary heart disease is the most common cause of death in many Westernized countries. Patients who experience either a threatened myocardial infarction (MI) or an acute MI within the last 12 h or so can benefit from interventions that decrease myocardial oxygen demand. Beta-Blockade fulfills such a purpose mainly through diminishing the product of heart rate x systolic blood pressure. Added benefits of beta-blockade include (a) a redistribution of myocardial blood supply in favour of ischaemic areas, (b) inhibition of catecholamine-induced myocardial necrosis, and (c) a decrease in the Q-Tc interval and an increase in the threshold to ventricular fibrillation. Beta 1-Selective blockade is the essential ingredient; the possession of intrinsic sympathomimetic activity (ISA) may diminish benefit. Intravenous, followed by oral, beta-blockade within 12 h (preferably 6 h) of the onset of chest pain results in (a) a marked reduction in chest pain, (b) a reduction in infarct size by about 30%, (c) a diminished likelihood of threatened infarction progressing to overt infarction, (d) a reduction in the number of life-threatening ventricular arrhythmias, and (e) a reduction in the incidence of cardiac arrest and reinfarction. Intravenous, followed by oral, beta 1-selective blockade (atenolol) significantly reduces vascular mortality by about 15% at 1 week post-MI, and the benefit is maintained at 1 year. Such an intervention, provided contraindications to beta-blockade are respected, is safe and well tolerated. Probably about 50% of patients are eligible for such treatment. Such an approach is highly cost effective.
Cruickshank
J M
JM
Wythenshawe Hospital, Manchester, England.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*
D000319:Adrenergic beta-Antagonists