Volume 6, Number 57;  December 4, 2006 - Coronary Vasospasm

 

Clinical Question: 

1) What is coronary vasospasm?

 

Recommended reading:

Patient:

Session Handout:

 

Readings:

 

Link Directly to Fulltext Article at Science Direct

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Unique Identifier [PMID]: 14961457

Authors: Konidala S. Gutterman DD.

Institution: Department of Medicine, Cardiovascular Center, General Clinical Research Center, Milwaukee, WI 53226, USA.

Title: Coronary vasospasm and the regulation of coronary blood flow. [Review] [276 refs]

 

Source: Progress in Cardiovascular Diseases. 46(4):349-73, 2004 Jan-Feb.

Abstract: 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. [References: 276]

Publication Type: Journal Article. Review.

 

 

Link Directly to Fulltext Article at Publisher

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Unique Identifier [PMID]: 9392345

Authors: Yasue H. Kugiyama K.

Institution: Division of Cardiology, Kumamoto University School of Medicine.

Title: Coronary spasm: clinical features and pathogenesis. [Review] [59 refs]

 

Source: Internal Medicine. 36(11):760-5, 1997 Nov.

Abstract: Coronary artery spasm (coronary spasm) is an abnormal contraction of an epicardial coronary artery resulting in myocardial ischemia and its incidence is relatively high in Japanese as compared with Caucasians. Coronary spasm occurs most often from midnight to early morning when the patient is at rest and it is usually not induced by exercise in the daytime. Coronary spasm can be induced by acetylcholine, an endothelium-dependent vasodilator which causes vasodilatation in the normal coronary artery. Spasm artery is hyperresponsive to the vasodilator effect of nitroglycerin, an nitric oxide (NO) donor and is deficient in NO activity. The major risk factor for coronary spasm is cigarette smoking. Coronary spasm can be a cause of not only variant angina but also ischemic heart disease in general, including unstable angina, acute myocardial infarction and sudden ischemic death. [References: 59]

Publication Type: Journal Article. Review.

 

 

Link Directly to Fulltext Article at Publisher

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Unique Identifier [PMID]: 15700195

Authors: Miwa K. Fujita M. Sasayama S.

Institution: Division of Medicine, Hamamatsu Rosai Hospital, 25 Shogen-cho, Hamamatsu, Shizuoka 430-8525, Japan. ku-miwa@hamamatsuh.rofuku.go.jp

Title: Recent insights into the mechanisms, predisposing factors, and racial differences of coronary vasospasm. [Review] [69 refs]

 

Source: Heart & Vessels. 20(1):1-7, 2005 Feb.

Abstract: 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. [References: 69]

Publication Type: Journal Article. Review.

 

 

 

Resident Report / Department of Medicine & Grady Branch Library

Emory University School of Medicine

2006 Edition

Participating Faculty:  Carlos Del Rio MD  / Joyce Doyle MD / Lorenzo Difrancesco MD / Joel Mermis MD / Maunank Shah MD

Contact: Karl Woodworth 

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