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At least 19 recordsLinked to original sources
PubMed2005

Recent insights into the mechanisms, predisposing factors, and racial differences of coronary vasospasm.

Coronary vasospasm is currently considered to be an exaggerated contractile nonspecific response of the vascular smooth muscle in the large coronary artery to various agonists or stimulation, that is established after the process of inflammation and fibrocellular proliferation. Endothelial dysfunction with reduced nitric oxide bioavailability has been reported in angiographically normal coronary arteries in Japanese patients with coronary spastic angina. Recently, several interesting findings concerning the exact mechanism of calcium hypersensitivity of spastic vascular smooth muscle have been reported. In animal models with coronary spasm Rho-kinase is upregulated at the spastic site and plays a key role in inducing vascular smooth muscle hypercontraction by inhibiting myosin light chain phosphatase, resulting in enhancement of its phosphorylation. Also, oxidative stress has been given attention as an important mediator of the spastic conversion of vascular smooth muscle cell "phenotype." The incidence of coronary spastic angina in the Japanese population is reported to be remarkably high compared with that in Caucasians. Clinical and pathophysiological differences between Japanese and Caucasian patients with respect to coronary vasospasm are characterized by a lower prevalence of fixed coronary artery stenoses and diffuse coronary hyperreactivity in the Japanese patients. Recently, several distinct characteristics have been recognized to be associated with coronary vasospasm in studies analyzing data obtained from Japanese patients. In the present review, we will discuss our point of view on the mechanisms and predisposing factors in coronary vasospasm. Predisposing factors include smoking, lipid metabolic disorders, and gene expression, all of which may be interrelated issues.

Asian People↗
PubMed1996

[The relation between coronary vasospasm and coronary obstructive lesions in patients with variant angina].

A series of 38 patients with variant angina in whom coronary arteriography was performed was reviewed to investigate the relation between coronary vasospasm and coronary obstructive lesions. 10 of the 38 (26.3%) patients had completely normal coronary arteriograms; 4 (10.5%) had insignificant coronary artery disease (< 50% stenosis); 24 (63.2%) had significant (> or = 50% stenosis) coronary artery disease, including single vessel disease in 12 cases, multiple vessel disease in 11 cases and left main trunk disease in one case. The results of this study showed that the incidence of coronary vasospasm increased with the severity of coronary stenosis and was highest at 75%-90% stenosis of the ischemia-related artery in those patients with significant coronary disease. In this study of 38 patients, coronary vasospasm involved the left anterior descending artery (LAD) in 25 patients (65.8%), right coronary artery (RCA) in 10 (26.3%) and left circumflex artery (LCX) in 2 (5.3%), but in patients with in significant stenosis (< 50%), LAD was involved in 50.0%, RCA in 42.9% and LCX in 7.1%. These results indicate that coronary vasospasm occurs frequently in patients with severe stenosis of the LAD.

Adult↗
PubMed1982

Pathogenetic mechanisms of coronary vasospasm.

Coronary vasospasm plays a role in several manifestations of coronary heart disease, though its causes still remain to be established. Among suggestions made to account for it are normal increases in vasomotor tone, particularly in stenosed arteries, and local vascular hypersensitivity reactions. Stimuli known to precipitate spasm are discussed, particularly the role of the sympathetic nervous system and the possible involvement of platelet aggregation. Coronary vasospasm is stimulated by a number of different triggering mechanisms which vary between patients and even within patients at different times. However, it is concluded that vasospasm is the result of an interaction between hypersensitive vascular smooth muscle and a number of specific constrictor stimuli.

Coronary Disease↗
PubMed1986

Role of autonomic nerves and endothelium in coronary vasospasm.

Coronary vasospasm may result from exaggerated contraction of the smooth muscle composing the arterial wall. An imbalance of the autonomic or humoral control of the smooth muscle might serve to initiate a pathological arterial contraction. Abnormal adrenergic or cholinergic nervous function might explain vasospasm of otherwise normal coronaries. Intimal damage due to disease leaves the smooth muscle deficient in the protective metabolic and vasodilator properties of the endothelium. The vasoactive substances released by the platelets aggregating at such a site could cause vasospasm by acting directly on the smooth muscle or by inhibiting the function of dilator nerves.

Animals↗
PubMed1993

Coronary vasospasm, multiple coronary thrombosis, unstable angina and essential thrombocytosis.

Rarely, essential thrombocythemia has led to coronary artery occlusion. Only one patient has been described, in whom coronary angiography demonstrated multiple coronary thrombosis. We report a case of coronary vasospasm, multiple coronary thrombosis involving right and left coronary artery and possibly leading to myocardial infarction and unstable angina pectoris in a woman with migraine, Raynaud's phenomenon, and essential thrombocytosis.

Angina, Unstable↗
PubMed1980

Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis.

This study explores the relation between coronary arterial spasm and the development of coronary atherosclerosis. The clinical history and coronary angiographic and electrocardiographic data in 212 consecutive patients with ischemic heart disease were correlated. These patients were classified into four groups: Group 1, patients without angiographic evidence of atherosclerosis; Group 2, patients with single vessel disease; Group 3, patients with double vessel disease; and Group 4, patients with significant narrowing of major coronary arteries. Although spontaneous angina occurred in all four groups, it was more common (55 percent) in the patients in Group 1, who were predominantly female and young. Spontaneous angina was confirmed in Group 1 with several techniques, including thallium-201 scintigraphy, ergonovine administration and electrocardiography during attacks of pain. Prior myocardial infarction was present with similar frequency in all four groups. A patient is discussed whose spontaneously occurring coronary arterial spasm later progressed to fixed arteriosclerotic narrowing requiring coronary bypass surgery. These observations and a review of the literature lend support to the hypothesis that coronary arterial spasm can be a possible antecedent leading to the later development of fixed atherosclerotic coronary arterial obstruction.

Adult↗
PubMed1984

Acute transmural myocardial infarction--coronary vasospasm, thrombosis or coronary embolus? A case report.

A very fit 28-year-old Coloured athlete presented with an acute transmural anteroseptal and non-transmural anterolateral myocardial infarction (MI). He had no significant risk factors for coronary artery disease apart from moderate cigarette smoking. Cardiac catheterization 2 months later demonstrated a significant area of myocardial damage as well as a large mural thrombus, but the coronary arteries appeared normal apart from a large irregular filling defect in the proximal left anterior descending (LAD) branch, apparently due to a thrombus. Cardiac catheterization a further 4 months later documented no further filling defect in the LAD branch and the coronary arteries appeared free of disease. Ergometrine maleate provocation on this occasion failed to demonstrate any coronary vasospasm. Possible pathophysiological mechanisms for the unexpected MI are outlined.

Adult↗
PubMed1999

Frequency of provoked coronary vasospasm in patients undergoing coronary arteriography with spasm provocation test of acetylcholine.

This study examines the incidence of spasm by intracoronary injection of acetylcholine in Japanese patients who underwent coronary angiography. The subjects were 685 consecutive patients (477 men, mean age 63.2 +/- 7.5 years) who were studied with an acetylcholine test. Acetylcholine was injected in incremental doses of 20, 50, and 80 microg into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Spasm was defined as total or subtotal occlusion. Coronary vasospasm was determined in 221 patients (32.3%). Spasm occurred often during effort and rest in patients with angina (25 of 51, 49.0%), exertional angina (25 of 74, 33.8%), recent myocardial infarction (30 of 80, 37.5%), healed myocardial infarction (14 of 37, 37.8%), and especially in patients with rest angina (83 of 124, 66.9%), whereas spasm was relatively uncommon in patients with nonischemic heart disease (23 of 252, 9.1%). Spasm was superimposed on significant atherosclerotic lesions in 35.9% of patients as well as on nonfixed atherosclerotic lesions in 30.8% of patients. We conclude that >9% of Japanese patients may have coronary vasospasm with intracoronary injection of acetylcholine and recommend the provocation test for evaluating coronary vasospasm if coronary angiography is undertaken.

Acetylcholine↗
PubMed2006

Comparison of serum levels of inflammatory markers in patients with coronary vasospasm without significant fixed coronary artery disease versus patients with stable angina pectoris and acute coronary syndromes with significant fixed coronary artery disease.

Serum levels of inflammatory markers (interleukin-6, monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, and C-reactive protein) were measured at baseline in serum samples from 189 patients who were admitted for coronary angiography because of suspected ischemic heart disease. Median duration of follow-up was 28 months. Patients in our sample were enrolled in 4 diagnostic groups: no hemodynamically significant coronary artery disease (CAD) and no coronary vasospasm (control group, n = 32), hemodynamically significant CAD and stable angina pectoris (SAP group, n = 34), coronary vasospastic angina pectoris without hemodynamically significant CAD (vasospasm group, n = 31), and acute coronary syndrome (ACS) and hemodynamically significant CAD (ACS group, n = 92). Overall, the level of serum inflammatory markers was highest in the ACS group and lowest in the control group, with intermediate values observed in the SAP and vasospasm groups, with the exception of soluble intercellular adhesion molecule-1, the level of which was highest in the vasospasm group. Multivariate analysis showed that log (interleukin-6) was independently associated with a diagnosis of coronary vasospastic angina pectoris in patients without hemodynamically significant CAD (odds ratio 8.48, p = 0.027). Patients in the ACS group had a significantly lower survival rate compared with the other 3 groups but without an independent predictor that could be identified in this patient cohort. Recurrent angina pectoris occurred with similar rates in the SAP, vasospasm, and ACS groups. The independent predictor for recurrent angina pectoris was treatment that did not include clopidogrel (odds ratio 3.88, p = 0.007). In conclusion, the results of this study suggest that inflammation can exist in coronary vasospasm without hemodynamically significant CAD.

Aged↗
PubMed1999

Hypoxia-reoxygenation triggers coronary vasospasm in isolated bovine coronary arteries via tyrosine nitration of prostacyclin synthase.

The role of peroxynitrite in hypoxia-reoxygenation-induced coronary vasospasm was investigated in isolated bovine coronary arteries. Hypoxia-reoxygenation selectively blunted prostacyclin (PGI2)-dependent vasorelaxation and elicited a sustained vasoconstriction that was blocked by a cyclooxygenase inhibitor, indomethacin, and SQ29548, a thromboxane (Tx)A2/prostaglandin H2 receptor antagonist, but not by CGS13080, a TxA2 synthase blocker. The inactivation of PGI2 synthase, as evidenced by suppressed 6-keto-PGF1 alpha release and a decreased conversion of 14C-prostaglandin H2 into 6-keto-PGF1 alpha, was paralleled by an increased nitration in both vascular endothelium and smooth muscle of hypoxia-reoxygenation-exposed vessels. The administration of the nitric oxide (NO) synthase inhibitors as well as polyethylene-glycolated superoxide dismutase abolished the vasospasm by preventing the inactivation and nitration of PGI2 synthase, suggesting that peroxynitrite was implicated. Moreover, concomitant administration to the organ baths of the two precursors of peroxynitrite, superoxide, and NO mimicked the effects of hypoxia-reoxygenation, although none of them were effective when given separately. We conclude that hypoxia-reoxygenation elicits the formation of superoxide, which causes loss of the vasodilatory action of NO and at the same time yields peroxynitrite. Subsequently, peroxynitrite nitrates and inactivates PGI2 synthase, leaving unmetabolized prostaglandin H2, which causes vasospasm, platelet aggregation, and thrombus formation via the TxA2/prostaglandin H2 receptor.

Angiotensin II↗
PubMed1986

Late symptomatic exercise-induced coronary vasospasm after percutaneous transluminal coronary angioplasty. A case report and review.

A patient who underwent a successful double-vessel percutaneous transluminal coronary angioplasty (PTCA) had suffered from exercise-induced ST-segment elevation associated with angina pectoris (AP). This ECG pattern was present both before and 12 months after PTCA while nifedipine (Adalat; Bayer-Miles) therapy was electively discontinued. Reintroduction of calcium blockade with this drug eliminated the chest pain and resulted in normalization of the stress ECG. Cardiac catheterization at 6 and 12 months after PTCA demonstrated continuing angiographic improvement of the coronary stenoses of the left anterior descending and left circumflex (LCx) coronary arteries previously subjected to PTCA. It is believed that coronary artery spasm at the PTCA site on the LCx coronary artery was responsible for the AP and exercise-induced ST-segment elevation. Likely pathogenetic mechanisms of coronary vasospasm during and after the performance of PTCA, as well as the interrelationship with re-stenosis and the clinical implications of drug therapy, are discussed.

Angina Pectoris↗
PubMed2003

[Coronary vasospasm during off-pump coronary artery bypass grafting; report of two cases].

Coronary vasospasm is one of the most dangerous and fatal complications of coronary artery bypass grafting (CABG) operation. Our experiences in recent 2 cases happened during off-pump CABG (OPCAB) are presented. Case 1: A 63-year-old male who had 3 vessels disease underwent OPCAB using left internal thoracic artery (LITA) and the radial artery. When the sternotomy was going to be closed, ST elevation of electrocardiogram (ECG) occurred and was followed by ventricular fibrillation. Intra-aortic balloon pumping (IABP) and percutaneous cardiopulmonary support (PCPS) were applied immediately and an additional grafting to first diagonal artery (D 1) was carried out using a saphenous vein. Case 2: A 67-year-old male underwent OPCAB using LITA and the radial artery. ST elevation of ECG suddenly occurred and was followed by complete atrio-ventricular (AV) block when the sternum was closed. IABP and the ventricular pacing were applied immediately. While OPCAB may be less invasive operating method than conventional CABG, we should pay more attention to the coronary vasospasm.

Aged↗
PubMed2002

Treatment of refractory coronary vasospasm during cardiopulmonary bypass with compulsory coronary perfusion.

Coronary vasospasm is still a devastating complication during cardiac surgery. We report on a case of intractable coronary vasospasm in a 45-year-old male during coronary bypass surgery refractory to drugs and intra-aortic balloon pumping (IABP). Under cardiopulmonary bypass (CPB) support, the aorta was again cross-clamped and the aortic root was compulsorily perfused with pump blood using a small pump for infusion of cardioplegia. Vasodilators were administered through the perfusion line. Coronary vasospasm was dramatically resolved. He was then successfully weaned from CPB and recovered without further incidents.

Cardiopulmonary Bypass↗
PubMedDate not supplied

Coronary vasospasm and the regulation of coronary blood flow.

Under physiologic conditions, epicardial arteries contribute minimally to coronary vascular resistance. However, in the presence of endothelial dysfunction, stimuli that normally produce vasodilation may instead cause constriction. Examples include neural release of acetylcholine or norepinephrine, platelet activation and production of serotonin and thrombin, and release of local factors such as bradykinin. This shift from a primary endothelial-mediated vasodilator influence to one of endothelial dysfunction and unchecked vasoconstriction is precisely the milieu in which coronary vasospasm is observed. This condition, which typically occurs during periods of relatively sedentary activity, is associated with focal and transient obstruction of an epicardial arterial segment resulting in characteristic echocardiographic changes and symptoms of myocardial ischemia. This review highlights the current understanding of mechanisms regulating the coronary circulation during health and examines the pathophysiologic changes that occur with coronary spasm. Genetic and other predisposing conditions are addressed, as well as novel therapies based on recent mechanistic insights of the coronary contractile dysfunction associated with coronary spasm.

Adrenergic Agonists↗