Coronary vasospasm and the regulation of coronary blood flow. Prog Cardiovasc Dis 2004;46(4):349-73
Date
02/13/2004Pubmed ID
14961457DOI
10.1016/j.pcad.2003.10.001Scopus ID
2-s2.0-1042298991 (requires institutional sign-in at Scopus site) 68 CitationsAbstract
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.
Author List
Konidala S, Gutterman DDAuthor
David Gutterman MD Emeritus Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Adrenergic AgonistsAngina Pectoris
Animals
Coronary Circulation
Coronary Vasospasm
Coronary Vessels
Disease Models, Animal
Endothelium, Vascular
Humans
Microcirculation
Muscle, Smooth, Vascular
Platelet Adhesiveness
Platelet Aggregation
Prognosis
Reactive Oxygen Species
Regional Blood Flow
Vasodilation
