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      Vasospastic Angina and Role of Cardiac Catheterization

      case-report

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          Abstract

          Prinzmetal angina, also known as vasospastic or variant angina, is defined as an intermittent focal coronary artery spasm often associated with an atherosclerotic lesion near the site of spasm. It is caused by a focal or diffuse spasm of the smooth layer of the arterial wall of an epicardial coronary artery. Acute infarctions or malignant arrhythmias may develop during spasm-induced ischemia. Evaluation includes observation of echocardiogram (EKG) for transient ST elevations during discomfort; diagnosis is confirmed with coronary angiography using provocative testing. We describe two cases of patients who presented for non-cardiac complaints, but had episodes of vasospastic angina during their hospitalization. Both underwent cardiac catheterization with differing results, demonstrating the importance of catheterization in patients who experience vasospastic angina.

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          International standardization of diagnostic criteria for vasospastic angina.

          The Coronary Vasomotion Disorders International Study Group (COVADIS) was established to develop international standards for the diagnostic criteria of coronary vasomotor disorders. The first symposium held on the 4-5 September 2013 addressed the criteria for vasospastic angina, which included the following (i) nitrate-responsive angina, (ii) transient ischaemic electrocardiogram changes, and (iii) documented coronary artery spasm. Adoption of these diagnostic criteria will improve the clinical diagnosis of this condition and facilitate research in this field.
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            Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina.

            It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers and pharmacologic agents. It is not known, however, to what extent different stimuli can induce spasm in the same patient. To investigate whether coronary arterial spasm results from specific abnormal agonist-receptor interactions or from a local nonspecific coronary supersensitivity to different stimuli, 28 patients with vasospastic angina were submitted to a series of diverse vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine, hyperventilation, handgrip, cold pressor, and exercise-tests, were carried out in all 28 patients. In the last 15 patients histamine was also administered. Spasm was provoked by ergonovine in 96% of patients, by hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by the cold pressor and handgrip tests in 11% and 7%, respectively. No significant differences were found in the responses to provocative tests of patients with normal coronary arteries or nonsignificant stenoses and those with significant lesions. In the same individual, spasm was induced by at least two vasoconstrictive stimuli, although with a different mechanism of action, in 82% of patients and spasm was induced by three or more stimuli in 39%. Tests were repeated in at least 23 patients and short-term reproducibility paralleled sensitivity. These results suggest that in patients with variant angina, a local nonspecific supersensitivity rather than an abnormal specific agonist-receptor interaction plays a major role in the genesis of coronary arterial spasm.
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              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.
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                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                6 September 2019
                September 2019
                : 11
                : 9
                : e5588
                Affiliations
                [1 ] Internal Medicine, Graduate Medical Education, Regional Medical Center Bayonet Point, Hudson, USA
                [2 ] Cardiology, Graduate Medical Education, Regional Medical Center Bayonet Point, Hudson, USA
                Author notes
                Article
                10.7759/cureus.5588
                6820897
                6dd12359-6f94-4edf-8fb9-a911be1e56ca
                Copyright © 2019, Kleyman et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 26 August 2019
                : 6 September 2019
                Categories
                Cardiology

                prinzmetal,angina,st-elevation,coronary occlusion,transient ischemia,catheterization,percutaneous intervention,ventricular arrhythmias

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