Unstable angina is not a specific disease but a clinical syndrome, more akin to hypertension than to streptococcal endocarditis. The classification of unstable angina has, until now, been based on simple clinical descriptors, such as whether the ischaemic pain is on exertion and accelerating, or whether it occurs at rest,1 and whether or not ischaemia persists despite vigorous anti-ischaemic treatment. The ECG, particularly the presence or absence of changes in the ST segment, has also been useful as a classification tool. In addition, markers of myocardial damage, such as the cardiac specific troponins T or I are being used increasingly in the classification of these patients.2

Such clinical and laboratory descriptors are valuable in predicting prognosis, but they provide little or no information about the aetiology of unstable angina. Such information is important because it allows specific rather than empiric management. To return to the analogy with hypertension, the identification of specific subtypes such as renovascular hypertension or mineralocorticoid induced hypertension has allowed specific and more effective treatment to be developed. Similar advances may be anticipated in unstable angina.

The work of Maseri has been fundamental in the development of our thinking about the cause of unstable angina.3 From an aetiological perspective, unstable angina may be classified as thrombosis, severe progressive arterial obstruction, coronary vasospasm/vasoconstriction, inflammation and increased myocardial oxygen consumption.4