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Percutaneous Coronary Intervention (PCI) is associated with 5% to 30% incidence of elevation of serum Creatine Kinase MB fraction (CK-MB) reflect the periprocedural myonecrosis,’Appearance of Creatine Kinase MB (CKMB) in the circulation is the strongest predictor of long term clinical outcome of PCI 2-5 , correlating the deleterious consequences of myonecrosis on Left Ventricular function or Electrophysiological stability 6 . Pathophysiology of myonecrosis during PCI has been related to side branch closure or compression, major intimal dissection, intramural thrombus formation, coronary spasm, distal atheroembolization. The first four causes may be clinically apparent and measures can be taken during the procedure, the latter may be entirely asymptomatic and occur even Angiographically uneventful procedure. Contrast enhanced Magnetic Resonance Imaging suggest that distal embolization of atherogenic materials from plaque disruption 7 , causing micro infarction by obstructing the blood flow at capillary level 8,9 . Studies show that intra venous Adenosine infusion as an adjunct to reperfusion in the treatment of acute myocardial infarction associated with reduction of heart muscle damage 10,11 . Adenosine is a naturally occurring nucleoside with a half life in blood of less than 10 seconds. Adenosine may be administered via intravenous or Intracoronary route, produce hyperemic effect that is commonly used to measure the coronary flow reserve during PCI. The

university heart journal

Intracoronary Adenosine Induced hyperaemia reduces the incidence of myonecrosis due to micro infraction after elective Percutaneous Coronary Intervention