Management in unstable angina.

That unstable angina is a serious and potentially dangerous condition which requires immediate attention is a statement with which few clinicians would disagree. However, if it is examined more closely and attempts are made to establish exactly just how serious and how dangerous, an apparent confusion emerges. Furthermore, if clinicians start to discuss the details of the immediate attention, it becomes abundantly clear that there is not only a huge choice of treatment available, but also that there is considerable debate as to the circumstances in which a particular therapy might best be used. There are several reasons for this controversy and they are worth elaborating in order to determine whether there is some order within the confusion. Firstly, the term itself is applied to a clinical state which can be caused by a variety of pathophysiological abnormalities.1 The term was adopted to describe a condition which is neither stable angina pectoris nor myocardial infarction. It includes other diagnostic labels such as preinfarction angina, acute coronary insufficiency, intermediate coronary syndrome, crescendo angina and threatening infarction. Secondly, many papers about the management of patients with unstable angina are based on the experience of a secondary or tertiary referral centre. They are largely concerned with patients who have failed to respond to conventional medical treatment. Confusion has been caused by extrapolating from these reported experiences to the patients presenting to a district general hospital or to their general practitioner. Thirdly, there have been few studies that have examined the natural history of unstable angina. In those that have, it is often difficult to be certain that similar groups of patients are being described. Finally, it is important to allude to the dangers of a high technology approach. The proximity to, and availability of, investigational facilities such as coronary arteriography has a considerable influence on the likelihood of the patient being investigated. The urge to do something active and invasive can become a force that is difficult for the doctor to resist. As a result a dependence on the investigation may begin to develop. Unstable angina will inevitably have a mortality and morbidity whatever the treatment used; failure is perhaps easier to accept when everything possible has been done. If the high technology approach is of demonstrable benefit, then this is good clinical practice. But what if it is not beneficial? A better understanding of the complex pathophysiology of unstable angina may help produce some order out of the confusion.' For many years it was believed that unstable angina was due to episodic changes in myocardial oxygen demand superimposed on rapidly advancing or completed coronary thrombosis. It is now apparent that alternative or additional mechanisms need to be considered. These include episodic reductions in the myocardial oxygen supply due to coronary artery spasm, platelet activation, thrombus formation and fibrinolysis.