Pathophysiology of Myocardial Infarction

  1. KENNETH I. SHINE, M.D.;
  2. ALAN M. FOGELMAN, M.D.;
  3. ALBERT A. KATTUS, M.D., F.A.C.P.;
  4. GERALD D. BUCKBERG, M.D.; and
  5. JAN H. TILLISCH, M.D., F.A.C.P.
  1. Los Angeles, California

    Abstract

    Primary prevention of death from ischemic heart disease requires further understanding of the pathogenesis of this disorder. Cellular defects of cholesterol metabolism may be more significant markers than serum lipid levels for the identification and treatment of atherosclerotic risk. Coronary spasm has been shown to be an important cause of ischemia in the presence and absence of atherosclerotic lesions. Careful manipulation of physiologic variables with vasodilator agents during cardiopulmonary bypass can substantially alter the myocardial oxygen supply-demand relation, thereby minimizing ischemic injury. The cellular basis for loss of mechanical function during ischemia and the factors that determine irreversible injury are yet unknown.

    Article and Author Information

    • *Division of Cardiology, Department of Medicine, UCLA School of Medicine.

    • ▸An edited transcription of an Interdepartmental Clinical Case Conference arranged by the Department of Medicine of the UCLA School of Medicine; Los Angeles, California.

    • ▸Authors who wish to cite a section of this conference and specifically indicate its authors can use this example for the form of reference:

      Fogelman AM: Remarks in Shine KI (moderator): Pathophysiology of myocardial infarction. Ann Intern Med 87:75-85, 1977

    • ▸Requests for reprints should be addressed to Kenneth I. Shine, M.D.; Department of Medicine, UCLA School of Medicine; Los Angeles, CA 90024.

      • Received April 24, 1977.
      • Accepted April 25, 1977.
    « Previous | Next Article »Table of Contents