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Unstable angina pectoris is a clinical syndrome with multiple underlying pathophysiologic mechanisms. This presentation is concerned with primary angina pectoris exclusively. In the majority of cases a rupture of an atherosclerotic plaque and an intracoronary thrombus are responsible for instable angina. The practitioner's role is to identify those patients who will develop complications with the aid of clinical parameters. Prinzmetal's angina is also instable, occurs at rest and leads to ST-segment elevation. It is most likely due to coronary spasm, developing in disease-free and atherosclerotic coronary segments alike. This variant of unstable angina is treated most successfully with calcium antagonists. The recognition of the responsible pathophysiologic mechanism permits adjustment of treatment of every patient taking into consideration the seriousness of his prognosis.

The authors report original appearances (sinusoid or "saw tooth" aspect) of computerised analysis of the ST segment in 3 cases, corresponding to ST changes during exercise stress testing. This is due to alternating ST elevation and depression probably related to abnormal vasomotor tone given the fact that the recording was normalised by coronary vasodilator therapy.

Spontaneous spasm and methylergometrine maleate-provoked spasm are defined, the latter being observed in nearly all cases of so-called Prinzmetal angina, in approximately one out of three cases of angina at rest, and a certain number of cases of unstable angina: it has even been demonstrated during effort tests with coronarography. Several studies have demonstrated its possible implication in myocardial infarction. Continuous electrocardiogram recordings and isotopic studies have also shown the frequency of silent spasms, or those associated with other ECG modifications than an increased STT latency period. It is now well-established that this type of angina is provoked by reduction in myocardial oxygen supply. To explain the triggering mechanism of the spasm, various factors have been successively evoked: alpha- and beta-receptor disequilibrium, a vagal effect, the very important role played by thromboxane A2 of platelet origin. Emphasis is also placed on circadian variations observed during the spasm, but the course of spastic angina is often unpredictable, leading to necrosis or sudden death in a fairly large number of cases. Medical treatment is essentially by long-acting nitrate derivatives and calcium inhibitors (beta-blockers are considered, according to different teams, as being useless or even dangerous). Surgical treatment may be by aortocoronary shunt or transluminal angioplasty in cases that are stable with trinitrate compounds; associated plexectomy has given good results according to teams in Lille; while heart transplantation has been performed in rare cases. Choice of therapy is difficult in cases with apparently non-surgical moderate stenosis and recurrent spastic angina.

Aorto-coronary by pass, widely accepted in the treatment of patients with coronary artery disease is still controversial in the treatment of Prinzmetal variant angina. Recurrence of attacks, occlusion of grafts and post-operative infarction were frequent by described and seem to be related with the persistence of coronary spasm. Authors propose the association of myocardial revascularization and coronary denervation by resection of periaortic plexi. Results of 50 surgical plexectomies associated with coronary by pass appear far better than by pass alone (mortality 4%, myocardial necrosis 4%, persistence of attacks 4%).

The authors report the case of a 38 year old man who experienced at two month' interval, hypersensitivity reactions to the ingestion of 200 mg tablets of glafenine, complicated on the first occasion by a transmural anterior wall myocardial infarction as the first manifestation of coronary artery disease and on the second occasion by Prinzmetal angina due to posterior wall ischaemia. Coronary angiography was more or less normal. The timing of the symptoms in the context of an anaphylactic reaction and their repetition when the same molecule was reintroduced are strong arguments in favour of the pathogenic role of glafenine, even in the absence of biological criteria which are always variable. The mechanism of the coronary problems is discussed with reference to mediators released during the anaphylactic reaction: coronary vasoconstriction due to histamine and leukotriene release; inhibition of prostaglandin synthesis causing potentiation of the effects of histamine; lowering of the vasodilatory and antiaggregant prostacyclin enhancing the vasoconstrictor and platelet aggregant action of thromboxane A2. All the conditions favouring the initiation of coronary spasm with eventual coronary thrombosis, the one aggravating the other, are therefore present.

The authors review the literature on arrhythmias and ST changes, the principal causes of sudden death in the mid systolic click-late systolic murmur (SC-SM) syndrome, having recorded the ECG during sudden death of a patient with this syndrome by Holter monitoring. This would also appear to be the first reported case of sudden death recorded by this technique. It showed that death was caused by ventricular fibrillation which was preceded by a clinical and electrical episode of Prinzmetal angina. Hypotheses explaining the abnormalities of ventricular repolarisation and rhythm in so-called "idiopathic" SC-SM syndrome are reviewed. Special attention is paid to studies suggesting the participation of coronary spasm and autonomic nervous system disturbances. In conclusion, the authors underline: - the value of ambulatory electrocardiography in patients with the SC-SM syndrome and especially in a defined high risk group; - the value of testing for coronary spasm when coronary angiography is envisaged; - the need for better management with antiarrhythmic therapy. The indications of betablockade are discussed as these drugs are thought to favourise coronary spasm.

In a series of 2000 coronary arteriographies, spasm of the coronary artery was found in 52 cases, which were divided into three groups: 41 cases of "iatrogenic" spasm caused by stimulating the ostium of the coronary artery (usually the right) with the tip of the catheter; 8 cases of spasm on top of an organic fixed lesion; 4 cases of coronary spasm on a coronary artery which was reported as "radiologically normal". The study includes a review of the circumstances which favour or impede discovery of coronary spasm, as well as a provocation test using methyl ergometrine. This test seems to be specific in that it only produced coronary spasm in patients with Prinzmetal's syndrome, and excluded the cases of angina with normal coronary arteriography. The patients with spasm on top of a fixed organic lesion underwent a successful aorto-coronary bypass graft together with resection of the pre- and sub-aortic nerve plexus. Patients with a spasm in an artery which was "arteriographically normal" were treated medically by nitrate compounds and vaso-dilators. Three of these patients had an excellent result with medical treatment. Treatment failed in the fourth patient, who then obtained benefit from straight-forward resection of the pre- and sub-aortic nerve plexus with an excellent result which has been maintained for over six months.