doi: 10.1161/CIRCULATIONAHA.105.594358
(Circulation. 2006;113:e665.)
© 2006 American Heart Association, Inc.
Correspondence |
Letter Regarding Article by Staat et al, "Postconditioning the Human Heart"
University of New Mexico, School of Medicine, Albuquerque, NM
I read with great interest the recent report by Staat et al1 and the accompanying editorial by Vinten-Johansen and colleagues2 on the topic of "postconditioning" of the heart. I would like to compliment Dr Staat and colleagues on the conduct of a most timely and elegant trial. Although clinical medicine has struggled with finding the proper role for ischemic preconditioning of the myocardium,3 the concept of postconditioning was not on anyone’s radar screen until the seminal studies of Vinten-Johansen (in Zhao et al4). The idea that myocardial protection might be conferred by manipulations after the lethal ischemic insult, for example, acute myocardial infarction, was inconceivable to all but the most ardent believers in preconditioning. In fact, several years ago, my colleagues and I embarked on a somewhat lengthy pilot study of the feasibility of evoking postconditioning during the throes of acute myocardial infarction by using a classic preconditioning stimulus. These results were recently reported5 and are in agreement with the findings and conclusions of Staat et al.1 I would take issue, however, with the claim made by Vinten-Johansen and colleagues that postconditioning is a "simple" clinically applicable procedure. Not only did it take several years for us to complete our study, but in approximately 50% of the initial population, the "simple" protocol had to be abandoned consequent to the vicissitudes of events that occur during reperfusion for acute myocardial infarction.5 This is not to mitigate the inherent value of postconditioning but to caution those embarking on the systematic application of this technique in real-world scenarios. Being a passionate believer in the benefit of preconditioning and now postconditioning in the treatment of ischemic heart disease, I lend my voice to those of others seeking to expand the knowledge base in this area. A larger-scale randomized trial with "hard" clinical end points is in the planning stages and may finally convince skeptics of the clinical value of this powerful endogenous cardioprotective mechanism.
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Disclosures
None.
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 Top References Acknowledgments References |
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1. Staat P, Rioufol G, Piot C, Cottin Y, Cing TT, L’Huillier I, Aupetit J-F, Bonnefoy E, Finet G, Fouet X, Ovize M. Postconditioning the human heart. Circulation. 2005; 112: 2143–2148.
2. Vinten-Johansen J, Yellon D, Opie LH. Postconditioning: a simple, clinically applicable procedure to improve revascularization in acute myocardial infarction. Circulation. 2005; 112: 2085–2088.
3. Kloner RA, Yellon D. Does ischemic preconditioning occur in patients? J Am Coll Cardiol. 1994; 24: 1133–1142.[Abstract]
4. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, Vinten-Johansen J. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003; 285: H579–H588.
5. Laskey WK. Brief, repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction. Catheter Cardiovasc Interv. 2005; 65: 361–367.[CrossRef][Medline] [Order article via Infotrieve]
Hôpital Cardiologique et Pneumologique Louis Pradel, Lyon, France
Hôpital Arnaud de Villeneuve, Montpellier, France
Hôpital du Bocage, Dijon, France
Hôpital Saint Luc-Saint Joseph, Lyon, France
Response
We thank Dr Laskey for his comments regarding our paper, "Postconditioning the human heart."1 Murry et al2 and Zhao et al3 demonstrated that applying a preconditioning-type regimen in early reperfusion reduces infarct size in animals. Besides proving that lethal reperfusion injury does exist, their work suggested that infarct size reduction becomes a realistic goal in patients with acute myocardial infarction (AMI). The feasibility of ischemic postconditioning in humans is not a major issue. For years, cardiologists have performed repeated balloon inflations after reopening of an occluded coronary artery to "predilate" before stent implantation, dilate multiple lesions, improve stent expansion, or break thrombi. Modifying the first minutes of reperfusion to protect the heart is not a new idea. In the early 1980s, Buckberg et al4 controlled the conditions of reperfusion to protect the heart after cardiac surgery, and recent evidence suggests that controlled reperfusion and postconditioning share common mechanisms.5 The key question was whether postconditioning might reduce infarct size in humans. We1 performed a "proof of concept" study and demonstrated that the postconditioning machinery can be activated in the human heart. We agree with Dr Laskey that percutaneous transluminal coronary angioplasty postconditioning is not the easiest, and probably not the best, solution for all patients with AMI, and several questions remain to be addressed, including whether postconditioning protects the hearts of patients with comorbidities (diabetes, hyperlipidemia, age), what the time window is in humans, and whether it improves functional recovery and clinical outcome. Rather, we believe that pharmacological postconditioning is the issue. Administration, at the time of reperfusion, of a given drug that will mimic ischemic postconditioning will make this protection available to all patients with AMI, including those who undergo thrombolysis instead of percutaneous transluminal coronary angioplasty.
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TopReferencesAcknowledgments References |
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Disclosures
None.
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References |
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TopReferencesAcknowledgments References |
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1. Staat P, Rioufol G, Piot C, Cottin Y, Tri Cung T, L’Huillier I, Aupetit JF, Bonnefoy E, Finet G, Andre-Fouet X, Ovize M. Postconditioning the human heart. Circulation. 2005; 112: 2143–2148.
2. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74: 1124–1136.
3. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, Vinten-Johansen J. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003; 285: H579–H588.
4. Buckberg GD. Myocardial protection: an overview. Semin Thorac Cardiovasc Surg. 1993; 5: 98–106.[Medline] [Order article via Infotrieve]
5. Bopassa JC, Ferrera R, Gateau-Roesch O, Couture-Lepetit E, Ovize M. PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning. Cardiovasc Res. 2006; 69: 178–185.
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