Current therapeutic strategies in unstable angina

Unstable angina is a heterogeneous condition which marks the transition from stable coronary heart disease to a state in which the patient is at high risk of progressing to myocardial infarction (MI) or death. The number of hospital admissions for this condition is increasing, although it is not certain whether this reflects a genuine increase in prevalence; unstable angina is certainly a significant clinical burden. The risk of MI or death is highest in the first few weeks after the onset of symptoms. Unstable angina and MI share a common underlying pathogenesis: disruption of an atherosclerotic plaque followed by platelet aggregation and thrombus formation. Initial medical management is directed at relieving the symptoms of ischaemia and inhibiting thrombus formation. There is considerable controversy over the most appropriate choice of strategy, an early invasive approach or a more conservative one, and little data from controlled trials to guide the decision. The key role of platelets in unstable angina has led to the development of new antiplatelet agents such as the glycoprotein (GP) IIb/IIIa receptor blockers. A large number of these have been developed and several have been extensively evaluated in clinical trials in patients undergoing percutaneous coronary intervention and in acute coronary syndromes without persistent ST-segment elevation. Eptifibatide is a small-molecule (heptapeptide) GP IIb/IIIa receptor blocker that was shown in the PURSUIT trial to reduce significantly the combined end-point of death or MI in patients presenting with unstable angina/non-Q wave MI.