Incidence Of Coronary Artery Spasm Research Articles

TCT-223 Incidence of Coronary Artery Spasm According to the Stratified 10-Year Atherosclerotic Cardiovascular Disease Risk Score in Patients With Chest Pain With Near Normal Coronary Artery Stenosis

TCT-223 Incidence of Coronary Artery Spasm According to the Stratified 10-Year Atherosclerotic Cardiovascular Disease Risk Score in Patients With Chest Pain With Near Normal Coronary Artery Stenosis

TCT-489 Impact of Left Ventricular Hypertrophy on Coronary Artery Spasm as assessed by Acetylcholine Provocation Test

In our previous study, hypertensive patients with uncontrolled blood pressure had a significantly lower incidence of coronary artery spasm (CAS) than those with controlled blood pressure. However, it is unknown whether hypertensive patients with target-organ damage have a lower incidence of CAS than

ACETYLCHOLINE INJECTION CAUSES CORONARY ARTERY SPASM AND CORONARY ARTERY MICROCIRCULATION DYSFUNCTION—A CLINICAL RESEARCH

ObjectivesObserving the patients with angina during the procedure acetylcholine causes coronary artery spasm, whether coronary artery microcirculation dysfunction is existed and surveying the influencing factor.MethodsWe studied the patients with doubtful...

PP-230: KOUNIS SYNDROME SECONDARY TO IBUPROFEN USE

Objective: Catheter-induced coronary artery spasm may ocur during coronary angiography. The incidence of coronary artery spasm during coronary angiography has been reported between 0.26% and 0.93%. it is generally ascribed to mechanical irritation of the vessel by the catheter tip. We report an unusual case of catheter-induced vasospasm of right coronary artery, mimicking atherosclerotic stenosis. Methods: A 40-year-old man patient was admitted to our hospital with a 6-months history of atypical chest pain and dyspnea on exertion. The patient had no cardiovascular disease risk factors. On cardiac auscultation, heart sounds were soft and 1–2/6 systolic murmur was heard in the mezocardiac area. The respiratory sounds on auscultation were normal. The electrocardiogram showed

PP-229: CATHETER-INDUCED VASOSPASM OF THE RIGHT CORONARY ARTERY MIMICKING CORONARY LESION

Objective: Catheter-induced coronary artery spasm may ocur during coronary angiography. The incidence of coronary artery spasm during coronary angiography has been reported between 0.26% and 0.93%. it is generally ascribed to mechanical irritation of the vessel by the catheter tip. We report an unusual case of catheter-induced vasospasm of right coronary artery, mimicking atherosclerotic stenosis. Methods: A 40-year-old man patient was admitted to our hospital with a 6-months history of atypical chest pain and dyspnea on exertion. The patient had no cardiovascular disease risk factors. On cardiac auscultation, heart sounds were soft and 1–2/6 systolic murmur was heard in the mezocardiac area. The respiratory sounds on auscultation were normal. The electrocardiogram showed

Variant Angina and Coronary Artery Spasm: The Clinical Spectrum, Pathophysiology, and Management

Variant angina is a form of angina pectoris that shows transient ST-segment elevation on electrocardiogram during an attack of chest pain. Ischemic episodes of variant angina show circadian variation and often occur at rest from midnight to early morning. Ischemic episodes also occur during mild exercise in the early morning. However, they are not usually induced by strenuous exercise in the afternoon. Other important clinical features of variant angina include the high frequency of asymptomatic ischemic episodes and the syncope that sometimes occur during the ischemic episodes. Syncope is due to severe arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high-degree atrioventricular block. Coronary artery spasm is the mechanism of ischemic episodes in variant angina. The incidence of coronary artery spasm shows a racial difference and is higher in Japanese than in Caucasians. Coronary arteriograms are normal or near-normal in most Japanese patients with variant angina. Deficient basal release of nitric oxide (NO) due to endothelial dysfunction, and enhanced vascular smooth muscle contractility with the involvement of the Rho/Rho-kinase pathway are reported to play important roles in the pathogenesis of coronary artery spasm. Other precipitating factors of coronary artery spasm include imbalance in autonomic nervous activity, increased oxidative stress, chronic low-grade inflammation, magnesium deficiency, and genetic susceptibility. The genetic risk factors associated with coronary artery spasm include gene polymorphisms of endothelial NO synthase (NOS), paraoxonase, and other genes. Calcium channel blockers are extremely effective in preventing coronary spasm. The long-acting nitrate, nicorandil, and Rho-kinase inhibitor are also useful for inhibiting coronary artery spasm. Because variant angina can lead to acute myocardial infarction, fatal arrhythmias, and sudden death, early treatment is important. The prognosis of patients with variant angina is favorable, if early complications can be overcome. However, because coronary artery spasm cannot be suppressed in some patients, even with multiple medications, medications to suppress intractable coronary artery spasm must be developed.

AS-233: Impact of Obesity on Acetylcholine-Induced Coronary Artery Spasm

Obesity is known to be associated with endothelial dysfunction. Thus, a higher incidence of coronary artery spasm (CAS) would be expected in patients with obesity. We evaluated the impact of obesity on CAS with the intracoronary acetylcholine (Ach) provocation test.

Influence of atenolol on coronary artery spasm after acute myocardial infarction in a Japanese population

BackgroundJapanese patients with acute myocardial infarction (MI) have a greater incidence of coronary artery spasm than Caucasians. Some beta-blockers have been reported to aggravate coronary spasm. This study sought to assess the effects of beta-adrenoceptor blockade on coronary vasospasm in Japanese patients with acute MI who had been treated with primary angioplasty. MethodsIn 69 patients we analyzed the effect of atenolol 50 mg/day initiated the day after emergency primary angioplasty on the results of intracoronary ergonovine provocation test performed 4 weeks after onset. ResultsAmong 35 patients in the atenolol group, the drug was discontinued in 9 (26%) due to hemodynamic compromise. The remaining 26 in the atenolol group and 34 in the control group underwent the spasm provocation test. Atenolol did not significantly increase the incidence of coronary vasospasm (31% vs. 15% in the atenolol and control groups, respectively, p= 0.135). Multivariate analysis revealed that only the pre-provocation diameter of the distal segment of the infarct-related artery predicted coronary spasm whereas atenolol did not. ConclusionsThis study showed that atenolol 50 mg/day did not increase coronary spasm in Japanese acute MI patients. It is suggested that beta-blockers can be safely used soon after coronary intervention for acute MI without the risk of increasing coronary spasm; however, attention should be paid to hemodynamic change in the acute phase.

Does prevalence of migraine and Raynaud's phenomenon also increase in Korean patients with proven variant angina?

Background. The incidence of coronary artery spasm in oriental patients is higher than that in western patients. Oriental patients with variant angina (VA) frequently show normal or insignificant coronary artery stenosis by angiogram, compared with western patients. The prevalence of migraine and Raynaud's phenomenon in oriental patients with VA has not yet reported. Objective. We did a prospective study on the prevalence of migraine and Raynaud's phemonenon in patients with proven VA compared with those in two control groups using a radioisotope technique following ice water exposure. Simultaneously, we studied lipid profiles of each group. Methods and results. migraine was diagnosed if the score in part A totalled 7 or more of 26, and Raynaud's phemonenon was diagnosed if the score in part B totalled 4 or more of 11 by Miller et al. Technetium-99m-labeled red blood cells (99mTc-RBC) radionuclide angiography was performed in all patients. Patients were included in a prospective protocol. Patients were grouped as follows: Group I: 20 patients with proven VA; Group II: 30 patients with coronary artery disease; Group III: 31 patients without heart disease. Age and sex of patients were not statistically different among the three groups. Migraine was diagnosed in 8 patients (40.0%) of group I and in 6 patients (20.0%) of group II and in 12 patients (38.7%) of group III. Raynaud's phemonenon was reported in 2 (10.0%) of the patients in group I and in 5 (16.1%) of the patients of group III. The mean index ratio of the digital blood flow of right over left hand on static image was 0.85 ± 0.07 (mean ± S.E.M.) of the patients of group I, 0.73 ± 0.03 of the patients of group II and 0.74 ± 0.04 of the patients of group III. The mean flow index ratio of right over left hand of the digital blood flow on dynamic study was 0.51 of the patients of group I, 0.43 of the patients of group II and 0.43 of the patients of group III. The score of migraine did not differ significantly among the three groups. The score of Raynaud's phenomenon of patients with variant angina did not differ significantly from that of patients in the non-coronary control group, although it differed significantly from that of patients in the coronary control group. But, the prevalence of migraine and Raynaud's phemonenon (questionnaire and radionuclide angiography) in patients of group I did not differ significantly from that in groups II and III. In the end, more patients with variant angina than coronary or non-coronary control group did not reach the predetermined point level for the diagnosis of migraine and Raynaud's phenomenon. Lipid profiles were not significantly different among three groups. Conclusions. This result suggests that variant angina may not be a manifestation of a generalized vasospastic disorder in Korean patients.

Age related alteration in cholinergic but not alpha adrenergic response of rat coronary vasculature.

The aim was to determine whether aging alters coronary vascular responses to cholinergic and alpha adrenergic stimulation. Changes in coronary perfusion pressure and myocardial contractility in response to infusion of cholinergic and alpha adrenergic agonists and antagonists were determined in isolated Langendorff perfused hearts from adult (6-8 months old) and aged (28-30 months old) Fischer 344 rats. In electrically paced hearts (250 beats.min-1), perfused at constant perfusate flow rate, the cholinergic agonist carbachol (10(-10)-10(6)M) elicited concentration dependent coronary vasoconstriction. The maximum response and the sensitivity to carbachol were more than twofold greater in the aged than in the adult heart: concentration of carbachol producing 50% increase in coronary perfusion pressure: adult 916(SEM 210) nM; aged 21(7) nM; p < 0.01. Under these experimental conditions, the negative inotropic response elicited by carbachol was also relatively greater (approximately twofold) in the aged hearts. A similar age related difference in coronary vascular response to carbachol was also observed in potassium (18 mM KCl) arrested, non-beating, constant flow perfused hearts. In adult and aged hearts, the carbachol induced vasoconstriction was mediated by vascular (M3) muscarinic receptors as judged from blockade of the response by the non-selective muscarinic receptor antagonist atropine, but not by the cardioselective (M2) muscarinic receptor antagonist AFDX-116. The Ca2+ channel antagonist verapamil markedly attenuated the carbachol induced coronary vasoconstriction, indicating that a large component of the contractile Ca2+ mobilised by vascular muscarinic receptor activation is derived via influx of extracellular Ca2+. The alpha adrenergic agonist phenylephrine (10(-10)-10(6)M) produced concentration dependent coronary vasoconstriction; there was no age related difference in this alpha adrenergic response. There is striking enhancement of coronary vascular response to cholinergic but not alpha adrenergic stimuli with aging. Such age related cholinergic hypersensitivity may contribute to the high incidence of coronary artery spasm and impairment of coronary blood flow, cardiac energy metabolism, and contractile function that occurs with aging.

Incidence of spasm at the site of previous successful transluminal coronary angioplasty: effect of ergometrine maleate in consecutive patients.

The incidence of coronary artery spasm at the site of previous successful angioplasty and its importance in leading to subsequent restenosis or recurrence of symptoms are unknown. Fourteen consecutive patients with single vessel coronary artery disease who had undergone successful percutaneous transluminal angioplasty were studied. All patients were given ergometrine maleate (ergonovine maleate) intravenously during repeat cardiac catheterisation six weeks to three months after angioplasty. Five patients demonstrated excessive luminal reduction (spasm) at the site of previous angioplasty that led to luminal stenoses ranging from 50% to 79%. Two of these patients developed chest pain and ST segment changes during ergometrine maleate provocation and they also showed maximal vasoconstriction. The remaining nine patients did not develop important luminal change at the site of angioplasty after ergometrine maleate. Ergometrine maleate administration resulted in less than or equal to 20% reduction in lumen diameter of adjacent apparently normal sections of the coronary arteries in all but two patients. At the site of previous angioplasty in the five patients with spasm, however, the lumen was constricted by a mean (SD) of 51 (12)%, whereas in the nine patients not demonstrating spasm mean reduction was 12 (7)%. Thus hypersensitivity to ergometrine maleate at the site of previous successful angioplasty was demonstrated in over a third of consecutive patients with single vessel coronary artery disease. The importance of this finding to long term results of coronary angioplasty needs to be investigated further.

Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography.

We established the incidence of coronary artery spasm provoked by 0.4 mg of methergine in 1089 consecutive patients undergoing coronary angiography. The test was performed after routine coronary arteriography. Subjects included patients with angina, both typical and atypical, patients who had recently had myocardial infarction and patients with either valvular disease or congestive cardiomyopathy. Patients with spontaneous spasm, left main narrowing or severe three-vessel disease were excluded. One hundred thirty-four patients experienced focal spasm. Focal spasm was uncommon in patients with atypical precordial pain (1.2%), angina of effort (4.3%), valvular disease (1.95%) or cardiomyopathy (0%). It occurred most often in patients with angina at rest and less often in patients with angina both at rest and induced by exercise. Spasm was provoked in 20% of patients with recent transmural infarction, but in only 6.2% of patients studied later after infarction. Spasm was superimposed on fixed atherosclerotic lesions in 60% of the patients. No serious complications were encountered. Although the patients who underwent provocation tests in this study are not representative of all patients with coronary artery disease, spasm occurred in 20% of patients who experienced a coronary event and in 15% of patients who complained of chest pain.

Coronary artery spasm: Prevalence, clinical significance, and provocative testing

Recent clinical and laboratory observations indicate that coronary artery spasm may play a role in the pathophysiology of ischemic heart disease. The majority of patients with ischemic heart disease have coronary atherosclerosis. The prevalence of coronary artery spasm in these patients is unknown. However, current evidence suggests that patients with rest angina have a higher incidence of coronary artery spasm than do patients with reproducible effort angina. Coronary artery spasm may initiate or contribute to acute myocardial infarction, but recent evidence obtained in patients undergoing thrombolytic therapy during the early phases of myocardial infarction suggests that it is not a common occurrence. Although numerous examples of ventricular tachycardia and ventricular fibrillation occur during eplsodes of coronary artery spasm, the incidence of coronary artery spasm in association with sudden death is unknown. Provocative testing with ergonovine maleate reveals that the highest incidence of provocable coronary artery spasm is found in patients with rest angina. In patients with the syndrome of variant angina, coronary artery spasm is nearly always provocable.