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Acute myocardial infarction (AMI) is a leading cause of heart failure and premature death worldwide [1]. Immediate medical treatment is required and includes antiplatelet agents such as aspirin or thienopyridines [2]. Rapid reperfusion to limit myocardial damage is also strongly recommended [2,3]. However, reperfusion has the potential to initiate additional lethal injury, known as “ischemia-reperfusion (IR) injury” and could result in increased cardiomyocyte death [4]. New therapeutic strategies that directly target the reperfusion-mediated damage have been proven to reduce infarct size in experimental animal models. These approaches include 1) ischemic postconditioning [5] (which has been shown to be effective in animals evenwhen the postconditioning stimulus is delayed [6]); 2) pharmacological postconditioning with cyclosporine [7] or other molecules such as erythropoietin (EPO) (unpublished information); and 3) genetic perturbation in animal models of critical proapoptotic pathways involved in reperfusion injury [8,9]. Some of these new approaches have been shown to improve ventricular remodeling and clinical outcomes after AMI [10–13]. It is difficult to dissect the molecular mechanisms mediating the beneficial effects of these promising approaches because of several confounding factors (see Fig. 1). Antiplatelet agents could be among the most powerful cardioprotective drugs. Yang et al. now provide one of the first basic studies shedding light on the role of anti-platelet agents in cardioprotection. Recently, the same authors described their initial findings in a rabbit model (in press) [14], providing mechanistic insights into the action of these anti-platelet agents. Based on the rabbit model, they proposed that the cardioprotective effects of these anti-platelet agents are not mediated by a reduction of microvascular obstruction. In this issue of Cardiovascular Drugs and Therapy, they confirmed and report for the first time similar results in a primate model, providing convincing evidence of the cardioprotective benefits provided by antiplatelet agents following MI [15]. This is an important finding as most studies in clinical settings are hampered by the systematic use of these agents. The authors demonstrate, in a rarely used IR monkey model, a cardioprotective effect of two different classes of antiplatelet therapies: cangrelor, a powerful P2Y12 receptor inhibitor and a novel murine antibody against the collagen receptor glycoprotein VI (OM2). The antibody against the collagen receptor glycoprotein VI reacts only with the primate protein. Although the primate model has technical limitations (for example, it is difficult to dissect the molecular mechanisms mediating these beneficial effects) it also provides a reliable model for clinical translation. Both drugs provided efficient cardioprotective effects with a reduction of the infarct size/area at risk ratio between 23 % and 41 %. This benefit is most likely mediated through the effect of the drugs on platelets, which could limit IR injury. The drugs could prevent platelet activation [16] and release of deleterious cytokines, which otherwise could have enhanced inflammation [17] or activated other cell types including F. Roubille : J.-C. Tardif Montreal Heart Institute, Universite de Montreal, Montreal, QC, Canada

Cardioprotection—Time to Take Into Account Clinical Complexity: The Case of Antiplatelet Agents