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(Circulation. 2005;112:2085-2088.)
© 2005 American Heart Association, Inc.

Editorial

Postconditioning

A Simple, Clinically Applicable Procedure to Improve Revascularization in Acute Myocardial Infarction

Jakob Vinten-Johansen, MS, PhD; Derek M. Yellon, DSc, FRCP; Lionel H. Opie, MD, DPhil, FRCP

From the Carlyle Fraser Heart Center, Emory University, Atlanta, Ga (J.V.-J.); the Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, London, United Kingdom (D.M.Y.), and the Hatter Institute for Heart Research, Cape Heart Centre, University of Cape Town, Cape Town, South Africa (L.H.O.).

Correspondence to Dr Jakob Vinten-Johansen, Carlyle Fraser Heart Center, Emory University, 550 Peachtree St NE, Atlanta, GA 30308-2225. E-mail jvinten@emory.edu

Key Words: Editorials • myocardial infarction • reperfusion • stents • ischemia

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

	Introduction

 
"From bench to bedside" is a favorite aphorism for the scientifically inclined cardiologist. When the powerful antiischemic effects of preconditioning were discovered in 1996, it was a revolutionary concept: Repetitive brief ischemia could beget protection instead of the logically anticipated increased myocardial damage. The 75% reduction in histological infarct size was truly astounding.¹ Early laboratory and clinical studies with concordant mechanisms strongly suggested that this powerful tool would soon have practical application.^2,3 It has been a long road (Table) to clinical application, and consistently an elusive goal until the landmark study by Staat et al in this issue of Circulation.⁴ The major problem has been that the protection provided by preconditioning is a relatively short-lived phenomenon, so that to reduce infarct size it would have to be instituted just before the patient experienced an unannounced myocardial infarction. Furthermore, the recent experimental emphasis on reperfusion-induced cell death⁵ seems a far cry from clinical reality because there has been no convincing demonstration of major reperfusion injury after revascularization for acute myocardial infarction. The animal experiments show extensive reperfusion damage resulting in large infarcts of up to half of the area at risk after only a relatively short period of ischemia.^2,5 Clinicians argue that if such large infarcts were produced by reperfusion, then why does early reperfusion within 1 hour afford such good clinical recovery?

View this table: [in this window] [in a new window]   Some Key Events in Evolution of Postconditioning From Preconditioning

Article p 2143

These reservations are more than vanquished by the study of Staat et al.⁴ . . . [Full Text of this Article]

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