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Heart failure and ventricular hypertrophy

Altered cardiac contractility and compensatory mechanisms
  • James F. Spann Jr.
    Correspondence
    Address for reprints: James F. Spann Jr., M.D., Cardiopulmonary Section, School of Medicine, University of California at Davis, Davis, Calif. 95616.
    Affiliations
    From the Cardiopulmonary Section, School of Medicine, University of California at Davis, Davis, Calif., USA
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      Abstract

      It would appear that when the ventricle is chronically stressed by an abnormal pressure load, its initial response is to increase the total muscle mass. This increase in muscle mass, operating in conjunction with the Frank-Starling mechanism and increased sympathetic stimulation,15 maintains over-all circulatory compensation despite depression of the intrinsic contractile state of each unit of myocardium. This depression is expressed as a reduction in the intrinsic velocity of shortening and tension development of each myocardial fiber. The marked reduction of cardiac norepinephrine stores, which occurs in the failing heart,5, 15, 16 impairs the potential support available to the myocardium from sympathetic stimulation,17 although it is not responsible for the intrinsic depression of myocardial contractile state.2 Although an improvement in function in response to positive inotropic stimuli can occur in failing muscles, the augmentation is decreased and the resultant level of contractility remains less than normal. As the intrinsic contractile state of each unit of myocardium becomes more severely depressed, there is a more extensive fall in the maximal velocity of shortening (Vmax), a decrease in maximal isometric force and a decrease in the rate of force development. At this point, circulatory compensation can no longer be maintained despite maximal utilization of the compensatory mechanisms provided by the Frank-Starling mechanism and the increases in muscle mass; overt congestive heart failure then occurs.
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