Unstable angina: the breakthrough

It is widely perceived that unstable angina is a critical phase of coronary heart disease. The risk of acute myocardial infarction or death in these patients is high: up to 5% during hospitalization, 20% within 30 days, and 25% in 6 months. Medical and invasive treatment options for these patients have been rather discouraging, with two reasons responsible for this unsatisfactory state: first, there has been no objective marker to identify the patient at risk in the large group of patients with chest pain. Second, effective pharmacological concepts have been lacking and the results of invasive approaches controversial. However, diagnostic and therapeutic achievements in recent years may finally provide a breakthrough to improve the outcome of this high risk group of patients. Risk assessment in patients with acute chest pain is frequently a difficult and time-consuming process. The traditional approach is based on clinical symptoms, electrocardiographic findings, and measurements of creatine kinase. The limitations of this are well known: too many patients are unnecessarily hospitalized and up to 5% of patients are falsely discharged with infarction. Over the past 7 years several studies have documented that troponin T and troponin I are independent markers which best predict the acute outcome of patients with unstable angina. Approximately one third of patients presenting clinically with unstable angina have elevated troponins in the presence of no or only a minor rise in creatine kinase or creatine kinase-MB. However, an effective therapeutic concept for this high risk group of patients has been lacking. The key role of plaque rupture or erosion followed by local thrombus activation and aggregation has been recognised as the underlying pathophysiological mechanism in acute myocardial infarction as well as in unstable angina. In unstable angina, this is typically a white, platelet-rich thrombus as opposed to a red thrombus, as in myocardial infarction. Accordingly, it is reasonable that the new group of glycoprotein IIb/IIIa antagonists, the most potent anti-platelet compounds, have been found to be effective in this scenario. However, in large trials with the antibody abciximab or synthetic compounds such as tirofiban or eptifibatide the effect had a low statistical