Postkondisjonering, en usannsynlig beskyttelse av hjertet?

Abstract

Coronary heart disease is one of the most important causes of death in the world. And it causes the death of about 8 million people every year. Methods of revascularization as thrombolysis, percutan coronary intervention (PCI), open heart surgery or combinations of these has improved the prognosis of ischemic hearth disease the last decades. Medical treatment with beta-blockers, ACE inhibitors, statins and antiplatelet agents has significantly reduced the morbidity and mortality of acute myocardial infarction (AMI). Despite that the restoration of blood flow is absolutely necessary treatment of myocardial ischemia, reoxygenation will cause further damage of the heart. Studies show that the damage by reoxygenation can be reduced with postconditioning wich is an intervention best described by brief periods of ischemia and reperfusion by restoration of blod flow. We have therefore studied postconditioning and examined the experiments and mechanisms of this phenomenon. Studies have so far showed that adenosine reseptors, Ca-overload, reactive oxygen species (ROS), protein kinases and mitochondrial permeability transition pore (mPTP) are important in the understanding of the mechanisms behind postconditioning. Postconditioning seems to be a fairly simple strategy to apply during coronary angioplasty in patients with ongoing AMI. It is still unknown whether postconditioning is feasible, safe and efficient in those patients. And we still lack clear evidence for the existence of lethal myocardial reperfusion injury in human. The potential of postconditioning (i.e limitation of infarct size, improvement in prognosis) should be tested in clinical trials. Further studies are still important to find the optimal algorythm for perfusion-occlusion sequences, just as much as for other mechanisms in postconditioning.