[Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: effect of ACE inhibitors and other vasodilators].
A decrease in cardiac output in patients with congestive heart failure due to dilated cardiomyopathy is compensated by stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. The increase in plasma norepinephrine and depletion of norepinephrine in the myocardium as well as the disturbance of beta-adrenal and baroreceptor function reflect the limits of the sympathetic nervous stimulation. Together with augmented levels of angiotensin II and vasopressin, this stimulation leads to a significant increase in systemic vascular resistance. Sustained stimulation of at least one of these mechanisms can cause further impairment of the left ventricular function. The severity and prognosis of congestive heart failure due to dilated cardiomyopathy is expressed by the plasma norepinephrine concentration and by its myocardial depletion. Ultimately, activation of the compensatory mechanisms provides the basis for therapeutic approaches: 1. reduction of afterload and systemic vascular resistance and/or 2. diminution of the sympathetic nervous activity. For about the last ten years, ACE inhibitors have been used as pharmacological treatment in addition to positive inotropic and vasodilating substances. Captopril, one of the first orally applicable drugs, reduces left ventricular filling pressure, pulmonary capillary pressure, systemic vascular resistance and increases the cardiac output. Beside the hemodynamic improvement, a decrease in plasma norepinephrine and aldosterone can be observed. Vasodilators and alpha-blocking agents can also reduce afterload and systemic vascular resistance in patients with congestive heart failure due to dilated cardiomyopathy, and may lead to hemodynamic improvement. The main limitations of their long-term application are relatively short duration of action, reflex activation of the renin-angiotensin system due to vasodilation and induction of tolerance.
Langes
K
K
Medizinische Klinik, Universitätskrankenhaus Hamburg-Eppendorf.
Bleifeld
W
W
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy*; D006333:Heart Failure / Q000188:drug therapy*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D013564:Sympathetic Nervous System / Q000187:drug effects*; D014665:Vasodilator Agents / Q000627:therapeutic use*
D000806:Angiotensin-Converting Enzyme Inhibitors; D014665:Vasodilator Agents
Sympathische Aktivität bei Patienten mit Herzinsuffizienz auf dem Boden einer idiopathischen dilatativen Kardiomyopathie: Einfluss von ACE-Hemmern und anderen Vasodilatatoren.