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(Circulation. 2006;114:2309-2312.)
© 2006 American Heart Association, Inc.

Editorial

Cardiac Nociception

Paolo G. Camici, MD, FESC, FRCP; Massimo Pagani, MD

From MRC Clinical Sciences Centre and National Heart and Lung Institute, Imperial College, London, United Kingdom (P.G.C.), and CTNV, Department of Clinical Sciences L Sacco, University Milano, Milano, Italy (M.P.).

Correspondence to Paolo G. Camici, MRC, Clinical Sciences Centre, Imperial College, Hammersmith Campus, Ducane Road, London W12 0NN, United Kingdom. Email Paolo.camici@csc.mrc.ac.uk

Key Words: Editorials • angina • nervous system • molecularbiology

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Modern cardiovascular medicine, following Harvey’s inspiration, positions the heart indisputably at the center of a hemodynamic model. More deeply rooted in our cultural heritage are chronicles, such as Seneca’s own description of anginal attacks, or the account of Anania’s and Sapphira’s sudden death for fear of God’s punishment, clearly hinting at some less visible, more subtle, yet critical functions coupling the heart with life and death. These functions are now recognized as attained by the autonomic nervous system.

Article p 2351

A relationship between anginal pain and the heart was first described by Heberden more than 200 years ago.¹ The role of sympathetic afferents² in cardiac nociception was recognized a century later, and the causal contribution of reversible myocardial ischemia was suggested by Keefer and Resnik³ in 1928. Subsequent patient studies have demonstrated that the sensation of pain is not directly related to the degree of disease in the coronary artery subtending the ischemic territory or to the severity and duration of myocardial ischemia.

Most visceral pain research has been invasive and has used animal models. This research has established that adequate peripheral painful stimuli are transmitted through sympathetic afferents⁴ to the dorsal root ganglia and then, principally via the spinothalamic tracts and medial pain pathway, to the posterior thalamus. A significant number of vagal fibers connecting to the nucleus of the tractus solitarius and from there to the posterior thalamus are also involved in the afferent conduction of painful stimuli.⁴ Beyond this, the central connections mediating visceral pain perception . . . [Full Text of this Article]

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