There is now evidence that infarct size in man can be reduced by early treatment and that some cases of threatened infarction can be aborted. Beta blockade, given intravenously within about 6-8 hours after the onset of pain can reduce infarct size and abort some infarctions. So far we have no conclusive data on mortality. Beta blockers may act by a number of mechanisms, namely reduction of cardiac contractility, heart rate and blood pressure thus reducing cardiac work and oxygen requirement, prevention of cardiac rupture by the same mechanism, and by an early effect on R on T ectopic beats and hence serious ventricular arrhythmia. Early myocardial revascularization either by coronary graft, percutaneous angioplasty or intracoronary streptokinase are all promising but so far unproven by adequate clinical trial. Randomized trials suggest that intravenous streptokinase may be effective and hyaluronidase appears promising, possibly by promotion of collateral vessel flow. Calcium channel blockade may also be helpful and there are some early studies which support this. Lowering work by sodium nitroprusside also reduces infarct size. Heparin may have a place in the treatment of threatened infarction. After recovery it now appears established that beta 1-blockade will lower mortality. We do not know how long this effect persists. Other agents are less well established perhaps because the trials have been too small. Anticoagulants may have a place but their use is not widespread. Anti-platelet agents are also controversial. Studies of dipyridamole and sulphinpyrazone have been suggestive but not conclusive; the studies of aspirin are moderately encouraging, when all trials are pooled. Anti-arrhythmic therapy after infarction has been disappointing, with the exception of beta blockade. Perhaps more emphasis should also be put upon changes in lifestyle, notably stopping smoking, reduction of fat intake and encouraging regular exercise.