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Results for “Angina Pectoris, Variant”

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Ergonovine test in coronary disease.

The authors present the role of the Ergonovine test in establishing the diagnosis of the angina produced by coronary spasm. ECG alterations induced by Ergonovine, like transparietal ischemia (monophasic wave) or subendocardic ischemia, not only make possible a correct diagnosis, but they also underline the mechanism of angina and the therapeutical measures. Severe arrhythmias and the danger of sudden death are the two elements illustrating the importance of this coronary spastic mechanism. Nitroglycerine, isosorbidinitrate and calcium antagonists are the drugs of election for the prevention and also for the treatment of coronary spasm.

Adult↗
PubMed1982

[Clinical experiences with intra-aortic balloon pumping].

The clinical experience with intraaortic balloon pumping (IABP) in 16 patients in a hospital without cardiac surgery is described. The indications for IABP were cardiogenic shock in 8 cases, preshock in extensive myocardial infarction in 2 cases, unstable angina in 4 cases and ventricular septal rupture after acute myocardial infarction in 2 cases. The prognosis in cardiogenic shock after extensive acute myocardial infarction (CPK average 1545 U/l) or after reinfarction was poor in spite of treatment with IABP (survival only 25%). Important insertion of balloon pumping technique are percutaneous insertion of balloon catheters and transport of patients by ambulance with functioning IABP.

Adult↗
PubMed1982

[Vasospastic angina: relation to myocardial infarct and electrocardiographic variations].

The vasospastic angina can manifest itself electrocardiographically in the classical form with morphasic deformation of the ST-T segment (type A), but also as decrease of the ST segment of subepicardial or subendocardial origin (type B). On the basis of own observations the two forms are compared, it is referred to connections with the myocardial infarction, adequate causes are discussed and attention is paid to particularly endangered patients.

Angina Pectoris, Variant↗
PubMed1982

[Complicated ventricular arrhythmias in angina at rest].

To assess the incidence of serious ventricular arrhythmias (SVA) during transient ischemic attacks (IA), 27 patients with severe angina at rest were submitted to Holter monitoring for a total period of 1344 hours. The recorded IA's were 565. To evaluate the time/relation between SVA and ST segment changes, the IA's complicated by SVA were divided in 2 parts: one for the upstroke and plateau phase of ST changes; Hse other for the period of resolution of ST changes and the first 3 minutes after ST return to baseline. SVA's were found in 12 of the 27 patients (44.4%), but only in 29 of the 565 IA's (5.1%). The recorded arrhythmias consisted of: frequent ventricular premature beats (VPB) (greater than or equal to 5/min) in 8 patients, multifocal VPB in 6, paired VPB in 10, ventricular tachycardia in 5, R on T phenomenon in 2. No correlations were found between the occurrence of SVA during IA and type of ST changes, location of ST changes, occurrence of the same arrhythmias outside the IA's. SVA's were significantly more frequent during IA associated with pain than during silent IA. When considering only IA associated with ST elevation, a relation was found between the occurrence of SVA and amplitude and duration of ST displacement. The same relation was not observed when IA's associated with ST depression were taken in consideration. Among the 29 IA's complicated by SVA, 22 showed the arrhythmias during the first phase (3.8% of all IA's) and 7 during the second phase (1.3% of all IA's); 6 of these 7 IA's were associated with ST elevation.

Adult↗
PubMed1982

[Spasm of the coronary arteries].

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.

Angina Pectoris, Variant↗