Propranolol and practolol in the treatment of spontaneous angina pectoris.
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Biomedical subjects
Publications and source records attributed to M Guazzi.
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Attacks of Prinzmetal's variant form of angina pectoris are spontaneous, recur cyclically, and present unequivocal electrocardiographic alterations: they are ideal for a detailed haemodynamic study.Four patients with this form of angina were investigated. In each of them episodes occurred of electrocardiographic abnormalities either accompanied or unaccompanied by pain. During the same session, the cardiogram, heart rate, arterial pressure, and right atrial pressure were continuously recorded during periods ranging from 5 to 7 hours in each patient. Cardiac output was measured at selected times. Left ventricular ejection time, isovolumic contraction time, mean rate of isovolumic pressure development, and mean systolic ejection rate were also determined. In the 38 recorded anginal episodes, no circulatory change preceded the cardiographic modifications. From the onset of the electrocardiographic abnormalities to the beginning of their reversion, the following circulatory events were observed: (1) obvious reduction of cardiac output; (2) arterial hypotension; (3) lengthening of isovolumic contraction time and mean rate of isovolumic pressure development; (5) reduction of mean systolic ejection rate. It is concluded: (1) that no circulatory factor interfering with work or oxygen consumption of the heart is responsible for eliciting these anginal episodes; (2) that conspicuous left ventricular impairment occurs during the increasing and steady period of the electrocardiographic abnormalities. As the electrocardiogram started reverting to the pre-attack aspect, cardiac performance rapidly improved and, after a ;supernormal' phase, returned in about 2 minutes to basal levels. It is possible that this phase is dependent on a temporary sympathetic compensatory mechanism. No significant qualitative differences were detected between the circulatory pattern of various anginal episodes. The difference was mainly quantitative and the magnitude of the haemodynamic changes correlated well with the degree of the electrocardiographic abnormalities. Pain, when present, seemed just a concomitant symptom not significantly interfering with the circulatory changes associated with the episodes of this form of angina pectoris.
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Four patients with Prinzmetal's variant angina pectoris were subjected to continuous electrocardiographic recording. In three of them several episodes of ST segment elevation unaccompanied by pain were recorded. In one patient, identical electrocardiographic alterations were observed both in presence or in absence of pain, while in the others a good correlation was evident between pain and severity of the electrocardiographic abnormalities. In two patients transmural myocardial infarction complicated the course of the angina. In contrast to the classical findings, in these patients the attacks of chest pain did not cease after the infarction, but became more frequent and severe. The electrocardiographic alterations of the anginal episodes occurred in the same myocardial areas involved by the infarction, so that a reversible superposition of electrocardiographic signs of acute ischaemia on those of recent necrosis was observed. Continuous electrocardiographic recording provided the best means of investigation of these patients with the variant form of angina pectoris.
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