Circulation. 2005;112:2143-2148
Published online before print September 26, 2005, doi: 10.1161/CIRCULATIONAHA.105.558122
Published online before print September 26, 2005, doi: 10.1161/CIRCULATIONAHA.105.558122
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(Circulation. 2005;112:2143-2148.)
© 2005 American Heart Association, Inc.
Heart Failure |
Postconditioning the Human Heart
From Hôpital Cardiologique et Pneumologique Louis Pradel, Lyon (P.S., G.R., E.B., G.F., X.A.-F., M.O.); Hôpital Arnaud de Villeneuve, Montpellier (C.P., T.T.C.); Hôpital du Bocage, Dijon (Y.C., I.L.); Hôpital Saint Luc–Saint Joseph, Lyon (J.-F.A.); and Inserm E 0226, Lyon (G.R., G.F., M.O.), France.
Correspondence to Professor Michel Ovize, Hôpital L. Pradel, Hospices Civils de Lyon, 59, Bd Pinel, 69394 Lyon Cedex 03, France. E-mail ovize{at}sante.univ-lyon1.fr
Received April 25, 2005; revision received June 2, 2005; accepted June 17, 2005.
Background— In animal models, brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called postconditioning. In this prospective, randomized, controlled, multicenter study, we investigated whether postconditioning may protect the human heart during coronary angioplasty for acute myocardial infarction.
Methods and Results— Thirty patients, submitted to coronary angioplasty for ongoing acute myocardial infarction, contributed to the study. Patients were randomly assigned to either a control or a postconditioning group. After reperfusion by direct stenting, control subjects underwent no further intervention, whereas postconditioning was performed within 1 minute of reflow by 4 episodes of 1-minute inflation and 1-minute deflation of the angioplasty balloon. Infarct size was assessed by measuring total creatine kinase release over 72 hours. Area at risk and collateral blood flow were estimated on left ventricular and coronary angiograms. No adverse events occurred in the postconditioning group. Determinants of infarct size, including ischemia time, size of the area at risk, and collateral flow, were comparable between the 2 groups. Area under the curve of creatine kinase release was significantly reduced in the postconditioning compared with the control group, averaging 208 984±26 576 compared with 326 095±48 779 (arbitrary units) in control subjects, ie, a 36% reduction in infarct size. Blush grade, a marker of myocardial reperfusion, was significantly increased in postconditioned compared with control subjects: 2.44±0.17 versus 1.95±0.27, respectively (P<0.05).
Conclusions— This study suggests that postconditioning by coronary angioplasty protects the human heart during acute myocardial infarction.
Key Words: ischemia • myocardial infarction • postconditioning • reperfusion
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