Assessment Of The Effect Of Myocardial Post Conditioning On MBG In STEMI Patients

Abstract

ST-elevation myocardial infarction is a leading cause of mortality and morbidity. Infarct size is an important determinant of outcome. Hence reduction of myocardial injury is a therapeutic mainstay, best achieved by early reperfusion through primary percutaneous coronary intervention. (Anderson et al, 2003) Patients receiving such treatment will achieve infarct-related vessel patency and reperfusion, but risk sustaining clinically significant myocardial infarction, even when the procedure is done soon after symptom onset. (Kaltoft et al, 2009) Reperfusion contributes to lethal injury following prolonged periods of ischaemia. The idea of reperfusion injury was first introduced by Jennings et al as significant morphological alterations appearing after the onset of reperfusion, including cardiomyocyte swelling, mitochondrial clarification, and amorphous/flocculent densities representing calcium phosphate deposits, hypercontracture, and loss of sarcomere organization. Attempts to improve outcomes with adjuvant mechanical treatments such as thrombectomy and distal protection devices show inconsistent benefit. (Kaltoft et al, 2006) & (Sardella et al, 2009) Zhao et al.were the first to report in 2003 the application of postconditioning to limit lethal reperfusion injury in experimental AMI. Later studies by Zhao et al. and others ( Halkos et al , 2004) revealed that postconditioning also reduced cardiomyocyte apoptosis and contracture, coronary endothelial dysfunction, microvascular injury, tissue oedema, and organelle dysfunction. Remote ischaemic preconditioning induced by repeated brief periods of limb ischaemia before index ischaemia,( Kharbanda et al,2002) reduces myocardial injury in patients exposed to predictable ischaemia.(Cheung et al, 2006)& (Hausenloy et al, 2007) Furthermore, remote ischaemic postconditioning, applied in the early reperfusion phase after prolonged ischaemia, seems to be more effective than local postconditioning in experimental myocardial infarction. (Gritsopoulos et al, 2009).