Beta blockers and infarct size

Abstract

Reduction of myocardial oxygen demand by beta blockers should be beneficial for treatment of the supply-demand imbalance of severe myocardial ischaemia leading to infarction. There is evidence that rate-pressure product, an index of myocardial oxygen demand, is an independent variable for determination of infarct size, and that reduction of rate-pressure product by beta blockers or by other means is beneficial. Although experimental evidence is conflicting, some animal studies have shown protection from beta blockers when a coronary artery is permanently occluded, while a majority of studies show protection when a temporary coronary artery occlusion is followed by reperfusion. Prevention of ventricular fibrillation due to coronary artery occlusion has been shown in animal studies. In patients with developing infarction, rate-pressure product is reduced by approximately 20% when a beta blocker is given intravenously, and cardiac metabolism, assessed by coronary sinus sampling, returns to a more normal "oxidative" pattern. Indirect indices of infarct size, namely serum enzyme release and precordial R wave loss are reduced in patients treated early with intravenous beta blockers compared with control patients. However there is no evidence that left ventricular function is preserved by beta blockers. Very large multicentre trials have shown reduction in mortality among treated patients by about 15% when an intravenous beta blocker is given, suggesting that routine use would save 1 life for every 100-200 patients treated.