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Society of University Surgeons| Volume 74, ISSUE 2, P276-283, August 1973

Response of the hypertrophied heart to stress

  • Alexander S. Geha
    Correspondence
    Reprint requests: Dr. Alexander S. Geha, Department of Surgery, Washington University School of Medicine, St. Louis, Mo. 63110.
    Affiliations
    From the Department of Surgery, Washington University School of Medicine, St. Louis, Mo., U.S.A.

    From the Division of Thoracic and Cardiovascular Surgery and Cardiopulmonary Research Laboratory, Department of Surgery, The Jewish Hospital of St. Louis, Mo., U.S.A.
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  • Asrar B. Malik
    Affiliations
    From the Department of Surgery, Washington University School of Medicine, St. Louis, Mo., U.S.A.

    From the Division of Thoracic and Cardiovascular Surgery and Cardiopulmonary Research Laboratory, Department of Surgery, The Jewish Hospital of St. Louis, Mo., U.S.A.
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  • Tomio Abe
    Affiliations
    From the Department of Surgery, Washington University School of Medicine, St. Louis, Mo., U.S.A.

    From the Division of Thoracic and Cardiovascular Surgery and Cardiopulmonary Research Laboratory, Department of Surgery, The Jewish Hospital of St. Louis, Mo., U.S.A.
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  • Hugh O. O'Kane
    Affiliations
    From the Department of Surgery, Washington University School of Medicine, St. Louis, Mo., U.S.A.

    From the Division of Thoracic and Cardiovascular Surgery and Cardiopulmonary Research Laboratory, Department of Surgery, The Jewish Hospital of St. Louis, Mo., U.S.A.
    Search for articles by this author
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      Abstract

      Stable compensated left ventricular lypertrophy (LVH) was produced in dogs, often leading to sudden death following bursts of physical activity. To investigate the mechanism of death, we measured in 10 dogs with LVH and 12 normal dogs the effects of stress by six-minute infusions of isoproterenol and norepinephrine. Contractility indices of the intact left ventricle (output, minute work, external mechanical efficiency, Vmax, and ratio of Math Eq to isovolumic pressure) were comparable in both groups in the unstressed state and increased similarly with stress. Mean QLV was significantly lower in LVH at rest, and increased in both groups with isoproterenol and norepinephrine. In the unstressed dogs, LV oxygen consumption was similar in LVH and normal, but oxygen extraction was 46 ± 3 percent in normal and 66 ± 5 percent in LVH. With stress, O2 Consumption increased to the same level in both groups, and oxygen extraction increased to 63 ± 5 percent in normal but did not change in LVH. Thus, the intact stable hypertrophied myocardium shows no functional impairment during catecholamine-induced stress, but the increased oxygen requirements of stress can be met only by an increase in coronary flow since oxygen extraction in hypertrophy is already maximal.
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