Novel adjunctive treatments of myocardial infarction

Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve clinical outcome,but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic and pharmacological conditioning,but despite decades of research,the translation into clinical effects has been challenging. Recently published clinical studies,however,prompt optimism as novel techniques allow for improved clinical applicability. Cyclosporine A,the GLP-1 analogue exenatide and rapid cooling by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising,three follow-up studies of the effect of remote ischemic conditioning(RIC) show clinical prognostic benefit in patients undergoing coronary surgery and percutaneous coronary intervention. The discovery that RIC canbe performed noninvasively using a blood pressure cuff on the upper arm to induce brief episodes of limb ischemia and reperfusion has facilitated the translation of RIC into the clinical arena. This review focus on novel advances in adjunctive therapies in relation to acute and elective coronary procedures.

Extract of Paris polyphylla Simth Protects Cardiomyocytes from Anoxia-Reoxia Injury through Inhibition of Calcium Overload

Objective：To assess any direct effect of extract of Paris polyphylla Simth（EPPS）,a Chinese plant,on a cardiomyocyte subject to ischemia-reperfusion injury and to further elucidate its protective effect against myocardium ischemia on the cellular level.Methods：Neonatal rat cardiomyocytes were isolated and subjected to an anoxia-reoxia injury simulating the ischemia-reperfusion injury in vivo in the presence or absence of EPPS or diltizem,a positive control.The lactate dehydrogenase（LDH） activities in culture supematants and cell viabilities were analyzed using the enzymatic reaction kinetics monitoring-method and MTT method, respectively.Free intracellular calcium concentrations and activities of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase in cells were also measured with laser confocal microscopy and the inorganic phosphorus-transformation method,respectively.Results：In cardiomyocytes subject to anoxia-reoxia injury,EPPS at 50-400 mg/L showed a concentration-dependent inhibition on LDH leakage and maintenance of cell viability,and the effect was significant at 275 and 400 mg/L（both P0.01）.In addition,EPPS at 275 and 400 mg/L significantly inhibited the increase in intracellular free calcium（both P0.01） as well as decreased the activities of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase（P0.01,P0.05）.Conclusions：EPPS prevents anoxia-reoxia injury in neonatal rat cardiomyocytes in vitro by preservation of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase activities and inhibition of calcium overload.The direct protective effect on cardiomyocytes may be one of the key mechanisms that underlie the potential therapeutic benefit of EPPS against myocardium ischemia.