The Potentially Direct Role of Intracellular Calcium Overload in the Electrophysiology of Cardiac Ischemia

  • William T. Clusin
  • Maurice Buchbinder
  • R. Hardwin Mead
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 39)


Sudden cardiac arrest in patients with coronary artery disease is responsible for approximately half of the 400,000 cardiovascular deaths that occur annually in the United States. A substantial fraction of these deaths result from immediate effects of ischemia on the electrophysiological properties of ventricular myocardium. Within the first minute after coronary occlusion, there is a reduction in the resting potential of ischemic cells, together with shortening of the action potential plateau. These changes in action potential characteristics lead to the flow of “injury” current across the ischemic border, which may produce the initiating beat of ventricular fibrillation (1,2). Moreover, early depolarization of ischemic myocardium causes slowing of conduction, which could, in turn, produce arrhythmias by permitting re-entrant conduction within or around the infarct zone.


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Copyright information

© Martinus Nijhoff Publishing, Boston 1984

Authors and Affiliations

  • William T. Clusin
    • 1
  • Maurice Buchbinder
    • 1
  • R. Hardwin Mead
    • 1
  1. 1.Cardiology DivisionStanford University School of MedicineStanfordUSA

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