Cardioprotective therapy and sodium-hydrogen exchange inhibition: current concepts and future goals.

نویسندگان

  • I B Menown
  • A A Adgey
چکیده

Following acute myocardial infarction (MI), limitation of infarct size is central to long-term outcome (1). Successful reperfusion results in smaller infarct size and a marked reduction in mortality (1,2). However, following fibrinolytic therapy, ischemic myocardial injury continues during the process of clot lysis. Although reperfusion arrests the acute ischemic injury, it may cause further injury (3) and lead to cell death (4). In addition, successful epicardial reperfusion may still be associated with a “no reflow” phenomenon at the myocardial level (5). Hence the need for effective cardioprotective strategies against ischemic-reperfusion injury. Such strategies may be employed during three key time intervals—prior to onset of ischemia, following onset of ischemic injury but prior to reperfusion, and following reperfusion.

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عنوان ژورنال:
  • Journal of the American College of Cardiology

دوره 38 6  شماره 

صفحات  -

تاریخ انتشار 2001