(Circulation. 1997;96:1696-1700.)
© 1997 American Heart Association, Inc.
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From the World Health Organization Cardiovascular Center and the Departments of Medicine and Pathology at the University of Texas Medical Branch, Galveston.
Correspondence to Thomas N. James, MD, Office of the President, The University of Texas Medical Branch, Galveston, TX 77555-0129.
Abstract It is too often deduced that myocardial infarction is due to coronary occlusion and that subsequent death needs no other explanation. But the great majority of myocardial infarctions are not fatal, whether treated or untreated. There is, of course, some relation to the size of the infarct and the presence or absence of complicating conditions such as diabetes mellitus or hypertension, but little attention has been directed at the myriad of other events and processes influencing the clinical course. Examples include the exact anatomic territory infarcted and whether it includes the sinus node or AV node or important neuroreceptors; whether many small arteries are occluded (especially downstream of narrowed main coronary branches); whether the heart is hypertrophied, dilated, infected, or infiltrated; and whether there may be intracardiac, extracardiac, or intracranial neuropathological conditions that could destabilize cardiac electrical activity. It is now known that apoptosis plays a major role in myocardial infarction or ischemia, but it also occurs within the heart completely independently of infarction. There is also the vexing dilemma that an effective coronary collateral circulation, which is determined primarily by transanastomotic pressure gradient, is made less effective by exactly those treatments that reestablish flow in an occluded coronary artery. Since thrombolysis and angioplasty are automatically considered urgent treatment for an occluded coronary artery, it is prudent to remember the complex causes that determine whether the patient lives or dies.
Key Words: reperfusion apoptosis conduction
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