[Prinzmetal's angor. Apropos of 4 cases. Review of the literature].

In the light of 4 personal observations of PPPRINZMETAL's angina, a review has been conducted of the literature in the 15 years since the condition was first described. Although the formal diagnostic criteria for this form of angina simultaneously clinical, biological and electrical - anginal attacks occurring at rest, often at night, during which elevation of the ST segment is recorded which disappears at the end of the attack without any significant rise in enzyme levels (SGOT and CPK) - the frontiers of the syndrome appear to have widened since PRINZMETAL's description: - Severe proximal stenosis of the coronary arteries is not obligatory; they may be only slightly damaged or even healthy. - Prinzmetal's angina is by no means always "spontaneous" but is often induced, either by psychic factors, which explain the fixed time of the attacks, or by organic factors, e.g. cold drinks (Observation No.2). In this event it would appear safer to speak of angina or rest as opposed to angina of effort. - In contrast to what PRINZMETAL thought, effort tests may sometimes induce angina-type pain with elevation of the ST segment, and here the borderline between this syndrome and conventional angina with ST segment elevation after effort test (5% of cases) is less clear-cut. The two nosologic entities probably reflect the same physiopathological situation, i.e. acute myocardial ischemia, and may represent the same affection in different phases of development. The prognosis is equally bad. - Attacks of rinzmetal's angina are often accompanied by severe and sometimes fatal disorders of rhythm, and this influences the therapeutic approach. - The coronary spasm posited by PRINZMETAL and others before the advent of coronarography is indeed, in the majority of cases, the immediate cause of myocardial ischemia and anginal pain, without any preliminary increase in the energy requirements of the heart as in the conventional anginal attack. - A vasoactive substance present in the circulating blood at the beginning of the affection, which may be degraded and subsequently disappear and may be secreted by the pathologic coronary artery, was demonstrated in observation No. 4: this may, in conjunction with vagal hypertonia, be the causative factor in coronary spasm. Study of its pharmacodynamic properties is now in progress.