title: [The endogenous cardioprotection during reperfusion in acute myocardial infarction].
abstract: A prompt primary percutaneous coronary intervention with aspiration thrombectomy and subsequent stent implantation at  the culprit lesion combined with optimal anti-platelet and anti-thrombotic pharmacotherapy is the safest and most effective  reperfusion strategy. Unfortunately, this therapy does not guarantee always a good, long-term clinical outcome and left  ventricular function recovery. Despite the unquestionable benefit of reperfusion, we have evidence that its initial phase leads  to additional damage at the area at risk, so the final effect is the compromise between benefits and destruction, which come  with the reperfusion wavefront. Experimental studies suggest that postconditioning with several very brief cycles of ischaemia  alternating with reperfusion applied immediately after relief of a prolonged epicardial occlusion is associated with the infarct  size limitation. The cellular protective effect of postconditioning seems to be related to prevention of mitochondrial permeability  transition pore activation. We have still to wait for confirmation of the clinical effectiveness of both postconditionig as  well as pharmacotherapy that mimics postconditioning effects (e.g. with cyclosporine) in a randomised, multicenter clinical  trial with properly designed endpoint. To date, most clinically tested agents that induced endogenous cardioprotection such  as adenosine, erythropoietin, protein kinase C-δ inhibitor, atrial natriuretic peptide, atorvastatin and nicorandil were failed to  reduce infarct size. Time will tell whether postconditioning and therapy that it mimics meet expectation and find place in the  recommendations concerning management of acute myocardial infarction.   Kardiol Pol 2011; 69, supl. III: 67-74.
authors: Krakowski Szpital Specjalistyczny im. Jana Pawła II, Kraków. jzalewski@szpitaljp2.krakow.pl
authors: Jarosław
authors: J
authors: Zalewski
authors: Jadwiga
authors: J
authors: Nessler
mesh_terms: D000208:Acute Disease; D006801:Humans; D057775:Ischemic Postconditioning / Q000379:methods*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D009203:Myocardial Infarction / Q000517:prevention & control*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore