This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bolli, R. Articles by Abdel-Latif, A. Search for Related Content PubMed PubMed Citation Articles by Bolli, R. Articles by Abdel-Latif, A. Related Collections Ischemic biology - basic studies Related Article

(Circulation. 2005;112:3541-3543.)
© 2005 American Heart Association, Inc.

Editorial

No Pain, No Gain

The Useful Function of Angina

Roberto Bolli, MD; Ahmed Abdel-Latif, MD

From the Institute of Molecular Cardiology, Division of Cardiology, University of Louisville, Louisville, Ky.

Correspondence to Roberto Bolli, MD, Chief, Division of Cardiology, Vice Chairman for Research, Department of Medicine, Director, Institute of Molecular Cardiology, University of Louisville, Louisville, KY 40292. E-mail rbolli@louisville.edu

Key Words: Editorials • angina • nervous system, sympathetic • reperfusion • ischemia

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

Myocardial ischemia, the major cause of mortality and morbidity in the United States, accounts for nearly 20% of all deaths.¹ The prognosis of patients with acute myocardial infarction is strongly related to the amount of tissue destroyed during ischemia/reperfusion; hence, limiting this injury is of paramount importance for reducing the morbidity and mortality associated with ischemic heart disease.^2,3 Over the past 40 years, several hundred pharmacological or nonpharmacological therapies have been reported to alleviate ischemia/reperfusion injury in experimental animal models; unfortunately, few of these results have been reproducible, and, with the exception of early reperfusion, none have been translated into clinical therapies.⁴ These sobering facts provide a cogent rationale for a reassessment of the models and methodologies that have been used heretofore to test the efficacy of putative cardioprotective interventions. The obvious translational failure in this field calls for a new paradigm in which preclinical studies must be done as rigorously as their clinical counterparts, that is, using clinically relevant animal models, appropriate statistical methods, and a multicenter, randomized, blinded design using centralized core laboratories for data analysis.⁴ This paradigm would also improve our understanding of the mechanism of cardiomyocyte death during ischemia/reperfusion.

Article p 3617

One facet of ischemic biology that has received relatively little attention is the role of cardiac sensory nerves. Myocardial ischemia/reperfusion is known to cause the release of bradykinin and protons, both of which activate the vanilloid receptor 1 (VR1, also known as transient receptor potential vanilloid type 1 [TRPV1]) on the capsaicin-sensitive cardiac sensory . . . [Full Text of this Article]

Related Article:

TRPV1 Gene Knockout Impairs Postischemic Recovery in Isolated Perfused Heart in Mice

Lihong Wang and Donna H. Wang
Circulation 2005 112: 3617-3623. [Abstract] [Full Text]

This article has been cited by other articles:

				W. Huang, J. Rubinstein, A. R. Prieto, L. V. Thang, and D. H. Wang Transient Receptor Potential Vanilloid Gene Deletion Exacerbates Inflammation and Atypical Cardiac Remodeling After Myocardial Infarction Hypertension, February 1, 2009; 53(2): 243 - 250. [Abstract] [Full Text] [PDF]

				R. Huang, A. Karve, I. Shah, M. C. Bowers, D. J. DiPette, S. C. Supowit, and G. S. Abela Deletion of the mouse {alpha}-calcitonin gene-related peptide gene increases the vulnerability of the heart to ischemia-reperfusion injury Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1291 - H1297. [Abstract] [Full Text] [PDF]