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PubMed1991

Coronary artery spasm and vascular biology. Cholinergic constriction.

Coronary artery spasm is undoubtedly one of the causative factors of ischemic heart disease, particularly variant-type angina pectoris and myocardial infarction, but the disease mechanisms involved are still unclear. The present review describes the clinical background of coronary artery spasm in relation to ischemic heart disease, including a brief history of studies in this field, and also suggests future guidelines for experimental investigations based on the characteristics of coronary artery spasm, focusing particularly on data we have obtained in our laboratory from studies of cholinergic constriction. The pig may be a suitable animal in which coronary artery spasm could be provoked with cholinergic agents following endothelial denudation. The use of such large animals would allow the study of spastic arterial segments by various methods with angiographic confirmation. After endothelial denudation it is possible that phenotypic changes in cholinergic receptors might occur in smooth muscle cells, and that such changes might remain even after endothelial repair.

Acetylcholine↗
PubMed1994

Antianginal effects of FK409, a new spontaneous NO releaser.

1. The aim of this study was to compare antianginal effects of (+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamide (FK409), a new spontaneous nitric oxide releaser, with those of isosorbide dinitrate (ISDN). We used two types of rat angina model; methacholine- and arginine vasopressin (AVP)-induced coronary vasospasm models. 2. In the in vitro study, FK409 showed 80 times more potent vasorelaxant effect in dog isolated coronary artery than ISDN (EC50 = 16.7 +/- 4.8 and 1340 +/- 320 nM, respectively). 3. In the rat methacholine-induced coronary vasospasm model, FK409 suppressed the elevation of ST segment dose-dependently and significantly at 0.1 mg kg-1, i.d. On the other hand, ISDN suppressed it significantly at 3.2 mg kg-1, i.d. In addition, the efficacy of 3.2 mg kg-1 ISDN in the model was almost the same as that of 0.1 mg kg-1 FK409. 4. In the above experiments, FK409 and ISDN decreased mean blood pressure significantly at the maximum dose tested (1.0 mg kg-1, i.d. and 3.2 mg kg-1, i.d., respectively) but did not change heart rate at these doses. Therefore, the hypotensive effect of FK409 was 10 times weaker than the antianginal effect of the compound, while those of ISDN were almost the same. 5. In the rat AVP-induced coronary vasospasm model, 32 mg kg-1 FK409 significantly inhibited the depression of ST segment 60 min after oral administration. On the other hand, 32 mg kg-1 ISDN did not inhibit it at 60 and 120 min after oral administration. 6. In conclusion, FK409 inhibits coronary vasospasm more potently in two types of rat angina models than ISDN. In addition, FK409 shows an antianginal effect more selectively that a hypotensive effect,compared with ISDN.

Angina Pectoris, Variant↗
PubMed1982

Alternans of the ST segment of T wave. A sign of electrical instability in Prinzmetal's angina.

In an effort to determine the incidence of ventricular arrhythmias associated with ST segments alternans, the patterns of ST segment and T-wave electrical alternans (STEA) were analyzed in 93 patients during spontaneous Prinzmetal's angina. Twenty-eight of 93 patients, or 30% (Group I), showed STEA during episodes of ST segment elevation. SIxty-five of 93 patients, or 70% (Group II), showed no alternans during episodes of ST segment elevation. In Group I, ventricular arrhythmias, defined as all ventricular ectopic activity greater than 5 beats per minute and complex Lown grades III to V, occurred during 52 of 55 episodes, or 95%; whereas in Group II, ventricular arrhythmias occurred in only 51 of 125 episodes, or 41% (p less than 0.01). The difference in the incidence of ventricular fibrillation (VF) or ventricular tachycardia (VT) in the two groups was more striking. VT or VF occurred in 20 of 55 in Group I (36%) versus 5 of 125 in Group II (4%). Although there were no significant differences in age or sex between Group I and II patients, there was a significant difference in the magnitude of the maximum ST segment elevation (5 mm in Group I versus 3 mm in Group II, p less than 0.01). This study demonstrates that the occurrence of STEA and T wave alternans frequently heralds the onset of ventricular arrhythmias in Prinzmetal's angina. Both the arrhythmias and the alternans occur during the time of maximal ST segment elevation.

Angina Pectoris, Variant↗
PubMed1997

Repolarization alternans: techniques, mechanisms, and cardiac vulnerability.

Sudden cardiac death continues to be the leading cause of mortality in developed countries. Electrical alternans of the ST segment and the T wave on the surface ECG as a noninvasive marker of patients at risk is a phenomenon that was initially observed early in this century and was seen then to be associated with cardiac rhythm disturbances. Substantial evidence indicates that T wave alternans (TWA) is related to myocardial ischemic as a harbinger of malignant ventricular arrhythmias because it reflects dispersion and heterogeneity of repolarization. Recent data have demonstrated a significant correlation between TWA and vulnerability to ventricular arrhythmias in individuals with or without organic heart disease, it also predicts the results of electrophysiological testing and arrhythmia-free survival in patients with a variety of cardiac diseases. This article reviews the historical background of TWA and discusses the early experimental and recent clinical evidence implying an integral link between TWA and ischemia-induced cardiac vulnerability.

Angina Pectoris, Variant↗
PubMed1994

Electrophysiologic basis for T wave alternans as an index of vulnerability to ventricular fibrillation.

Substantial evidence indicates that T wave alternans is an intrinsic property of ischemic myocardium. The electrophysiologic basis appears to be spatial and temporal heterogeneity of repolarization resulting from changes in action potential morphology rather than in activation sequence. Ischemia-induced changes in postrepolarization refractoriness and depressed electrical restitution of action potential duration have also been implicated. The main underlying ionic basis for T wave alternans during coronary occlusion appears to be derangements in intracellular cycling of calcium. Accumulation of potassium in the extracellular space adjoining ischemic cells and disruption in electrogenic sodium-calcium exchange may also be involved. In humans, T wave alternans has been observed in Prinzmetal's and classical angina, angioplasty, and bypass graft occlusion. Under these conditions associated with acute myocardial ischemia, alternans is restricted to the ischemic zone, and alternation in action potential morphology is an underlying factor. Recently, repolarization alternans has been shown to be a statistically significant predictor of the results of electrophysiologic testing and arrhythmia-free survival in individuals with and without organic heart disease. Collectively, these observations provide a rationale for quantitation of T wave alternans magnitude for assessment of vulnerability to life-threatening ventricular arrhythmias both in response to and independent of the effects of myocardial ischemia.

Angina Pectoris, Variant↗
PubMed1980

Beneficial effects of intravenous glyceryl trinitrate in a case of Prinzmetal angina.

A case is described of the successful use of intravenous glyceryl trinitrate in controlling ischaemia-induced high-grade ventricular ectopic activity occurring in a patient during a Prinzmetal angina attack. The intravenous form of glyceryl trinitrate is probably more effective than the sublingual form in controlling arrhythmias arising during acute ischaemic episodes because of prompt delivery of the drug to the coronary circulation where vasodilation occurs. In addition,the ability to control the quantity and rate of drug delivery with an intravenous infusion offers distinct advantages in cases of coronary spasm occurring during situations such as coronary arteriography where it can be administered with careful electrocardiographic and haemodynamic monitoring.

Angina Pectoris↗
PubMed1981

Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm.

Vascular responses to ergometrine were compared in groups of patients subject to coronary artery spasm, or oesophageal spasm, or neither. We measured the degree of diffuse narrowing at different coronary artery sites (not in spasm), and the rise in blood pressure. The data provide no evidence for a generalised sensitivity to alpha-adrenergic stimulation underlying either of these two clinical entities. The left main stem was narrowed significantly less than the three main branches of the coronary artery tree. The degree of diffuse coronary artery narrowing was not influenced by the presence or absence of minor (less than or equal to 50%) fixed stenotic lesions, nor by the initial calibre of the arteries. Ergometrine did not alter arterial lactate concentration or lactate extraction in the absence of coronary spasm.

Adult↗
PubMed1981

Prinzmetal's angina with documented coronary artery spasm. Treatment and follow-up.

Eighteen patients with Prinzmetal's angina were studied angiographically and 17 were followed for an average of 27 months. The were 12 men and six women, with a mean age of 46.3 years. The mean duration of symptoms before clinical diagnosis was 4.1 weeks. Four had had a previous myocardial infarction. Six patients had spontaneous cardiac arrests within 48 hours of diagnosis and hospital admission. At coronary arteriography, 10 patients had significant coronary artery disease; two of these had coronary artery spasm. The remaining eight patients had normal cornary arteries with significant coronary artery spasm at arteriography. Angiographic mitral valve prolapse was found in eight patients; seven of these had inferior ST segment elevation with pain. Six of the 10 patients with significant coronary artery disease had aortocoronary bypasses performed with good results. Ten of the remaining 11 patients who were treated medically had their symptoms controlled with oral isosorbide dinitrate alone or in combination with propranolol, nifedipine or perhexiline but propranolol may have an adverse effect. Though the initial clinical course in untreated patients was unfavourable, progress after starting treatment was good, with no further cardiac arrests, myocardial infarctions, or deaths.

Angina Pectoris↗
PubMed1988

Short term reproducibility of exercise testing in patients with ST segment elevation and different responses to the dipyridamole test.

The short term reproducibility of exercise testing in 25 patients who had exercise induced ST segment elevation without baseline regional asynergy or a previous myocardial infarction, who had different responses to the dipyridamole test, was assessed. The patients performed a dipyridamole echocardiography test and a second exercise stress test. All underwent coronary arteriography. Seventeen patients had transient regional asynergy after dipyridamole (group 1) and either ST segment elevation (14 patients) or depression (three patients); a second group of eight had no asynergy and no electrocardiographic changes (group 2). The repeated exercise stress test was positive in 16 of the 17 patients of group 1 (11 with ST elevation and five with ST depression) and in two patients of group 2 (both had ST depression and one had coronary artery disease). The dipyridamole echocardiography test was positive in 17 of the 19 patients with coronary artery disease and was negative in all six patients without coronary artery disease. The repeated exercise stress test was positive in 17 of the 19 patients with coronary artery disease and in one patient without. The dipyridamole echocardiography test and a repeated exercise stress test, but not a single exercise stress test, identified coronary artery disease causing exercise induced ST segment elevation.

Adult↗
PubMed1992

Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms.

OBJECTIVE: A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms. MATHEMATICAL MODEL: The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism. CLINICAL OBSERVATION: To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (> 1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability < 200 ms) over a wide range of RR intervals (> 700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39.3%) in whom coupling interval/RR diagrams were not definitive. CONCLUSION: These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.

Adolescent↗