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on February 11, 2008

A more recent version of this article appeared on February 26, 2008

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Submitted on July 24, 2007
Accepted on December 24, 2007

Long-Term Benefit of Postconditioning

Hélène Thibault MD, Christophe Piot MD, PhD, Patrick Staat MD, Laurence Bontemps MD, Catherine Sportouch MD, Gilles Rioufol MD, PhD, Thien Tri Cung MD, Eric Bonnefoy MD, PhD, Denis Angoulvant MD, Jean-François Aupetit MD, PhD, Gérard Finet MD, PhD, Xavier André-Fouët MD, Jean Christophe Macia MD, Franck Raczka MD, Rolland Rossi MD, Rolland Itti MD, PhD, Gilbert Kirkorian MD, PhD, Geneviève Derumeaux MD, PhD, and Michel Ovize MD, PhD^*

From the Hospices Civils de Lyon, Université Claude Bernard Lyon 1, Lyon, France (H.T., P.S., L.B., G.R., E.B., D.A., G.F., X.A.-F., R.R., R.I., G.K., G.D., M.O.); Hôpital Arnaud de Villeneuve, Montpellier, France (C.P., C.S., T.T.C., J.C.M., F.R.); Hôpital Saint Luc–Saint Joseph, Lyon, France (J.A.); and INSERM U886, Lyon, France (H.T., G.R., D.A., G.F., G.D., M.O.).

^* To whom correspondence should be addressed. E-mail: ovize{at}sante.univ-lyon1.fr.

Background—We previously demonstrated that ischemic postconditioning decreases creatine kinase release, a surrogate marker for infarct size, in patients with acute myocardial infarction. Our objective was to determine whether ischemic postconditioning could afford (1) a persistent infarct size limitation and (2) an improved recovery of myocardial contractile function several months after infarction.

Methods and Results—Patients presenting within 6 hours of the onset of chest pain, with suspicion for a first ST-segment–elevation myocardial infarction, and for whom the clinical decision was made to treat with percutaneous coronary intervention, were eligible for enrollment. After reperfusion by direct stenting, 38 patients were randomly assigned to a control (no intervention; n=21) or postconditioned group (repeated inflation and deflation of the angioplasty balloon; n=17). Infarct size was assessed both by cardiac enzyme release during early reperfusion and by ²⁰¹thallium single photon emission computed tomography at 6 months after acute myocardial infarction. At 1 year, global and regional contractile function was evaluated by echocardiography. At 6 months after acute myocardial infarction, single photon emission computed tomography rest-redistribution index (a surrogate for infarct size) averaged 11.8±10.3% versus 19.5±13.3% in the postconditioned versus control group (P=0.04), in agreement with the significant reduction in creatine kinase and troponin I release observed in the postconditioned versus control group (-40% and -47%, respectively). At 1 year, the postconditioned group exhibited a 7% increase in left ventricular ejection fraction compared with control (P=0.04).

Conclusions—Postconditioning affords persistent infarct size reduction and improves long-term functional recovery in patients with acute myocardial infarction.

Key words: infarction • ischemia • myocardial infarction • postconditioning • reperfusion

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