Heart failure results from damage and stress to the myocardium whatever the aetiology. An increase in stress by cardiac overload is initially overcome by compensatory mechanisms that maintain blood pressure through a combination of the sympathetic nervous system and the renin-angiotensin-aldosterone system. These mechanisms may also alter myocyte function and induce progressive cell death and replacement by fibrous tissue. Disease therapy must reduce cardiac loading and avoid blood pressure control by mechanisms that have deleterious effects. Therapy includes diuretics, vasodilators and alpha-and beta-adrenergic blockade. Complete blockade of all receptors involved in the adverse effects of neurohormonal stimulation might represent an ultimate therapy objective, and improve subsequent prognosis. Large clinical trials are in progress to determine the therapy of choice in the prevention of progression of heart failure.
机构:
Ahmanson-UCLA Cardiomyopathy Center, Division of Cardiology, Los Angeles, CA 90095-1679, 47-123 CHSAhmanson-UCLA Cardiomyopathy Center, Division of Cardiology, Los Angeles, CA 90095-1679, 47-123 CHS
Horwich T.B.
Fonarow G.C.
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机构:
Ahmanson-UCLA Cardiomyopathy Center, Division of Cardiology, Los Angeles, CA 90095-1679, 47-123 CHSAhmanson-UCLA Cardiomyopathy Center, Division of Cardiology, Los Angeles, CA 90095-1679, 47-123 CHS