doi: 10.1161/01.CIR.0000088001.59265.EE
(Circulation. 2003;108:1263.)
© 2003 American Heart Association, Inc.
Review: Clinical Cardiology: New Frontiers |
Silent Myocardial Ischemia
From the State University of New York Health Sciences Center, Stony Brook, NY (P.F.C.), and the Royal Brompton and Harefield NHS Trust, London (K.M.F., C.D.).
Correspondence to Prof K. Fox, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK (E-mail k.fox@rbh.nthames.nhs.uk), and Peter F. Cohn, MD, SUNY Health Sciences Center, Stony Brook NY 11794-8171 (E-mail pcohn@notes.cc.sunysb.edu).
Key Words: ischemia • myocardial infarction • angina • prognosis
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Silent myocardial ischemia is defined as objective documentation of myocardial ischemia in the absence of angina or anginal equivalents. Since its original description in the 1970s, it has undergone intensive investigation, and its clinical significance is now well established. This review will serve as an update on the pathophysiology, detection, prevalence, prognosis, and treatment of silent ischemia in both asymptomatic patients and those with angina, whether stable or unstable.
Pathophysiology
Pain Studies
No discussion of silent ischemia is complete without consideration of the cardiac pain mechanism. Although much has been learned about this subject, much is still uncertain. The afferent fibers that run in the cardiac sympathetic nerves are usually thought of as the essential pathway for the transmission of cardiac pain (Figure 1). The atria and ventricles are abundantly supplied with sympathetic sensory innervation; from the heart, the sensory nerve endings connect to afferent fibers in cardiac nerve bundles, which in turn connect to the upper 5 thoracic sympathetic ganglia and the upper 5 thoracic dorsal roots of the spinal cord. Within the spinal cord, impulses mediated by this sympathetic afferent route probably converge with impulses from somatic thoracic structures onto the same ascending spinal neurons. This would be the basis for cardiac pain referred to the chest, wall, arm, back etc. In addition to this "convergence-projection theory," the contribution of vagal afferent fibers must be acknowledged for an explanation of cardiac pain referred to the jaw and neck. How these vagal fibers are activated remains unclear. Furthermore, somatic localization
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