title: The neuroendocrine and sympathetic nervous system in congestive heart failure.
abstract: A review of recent randomized clinical trials has shown that neurohormonal activation starts early in the natural history of left ventricular dysfunction and levels of the circulating hormones increase in proportion to the severity of heart failure. Most studies suggest that high levels of neurohormones predict a poor prognosis. Among the several neurohormones, the sympathetic system is the one which is activated earlier, it increases in proportion to the severity of the disease and has a negative prognostic implication. These concepts have been also proven in untreated patients. Augmented sympathetic activity in the syndrome of heart failure is initially beneficial, appears to be adaptive and helps support blood pressure and cardiac output. Prolonged and excessive sympathetic activation has deleterious effects with adverse consequences at both cardiac and vascular levels which aggravates the clinical status of the syndrome and negatively affects its prognosis. Evidence is accumulating that, contrary to popular belief, beta-blockers may be beneficial in heart failure by inhibiting sympathetic activation. In addition to neuroendocrine activation, another class of biologically active molecules, termed cytokines, are excessively secreted by cells in heart failure. Important among these cytokines are tumour necrosis factor-alpha and interleukin-6. They appear to exert deleterious effects on the heart and circulation which may be also involved in the progression of heart failure.
authors.affiliation: Cardiovascular Research Center, S. Maugeri Foundation, Gussago, Brescia, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Ferrari
authors.forename: C
authors.initials: C
authors.lastname: Ceconi
authors.forename: S
authors.initials: S
authors.lastname: Curello
authors.forename: O
authors.initials: O
authors.lastname: Visioli
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000009:adverse effects / Q000627:therapeutic use; D016207:Cytokines / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009490:Neurosecretory Systems / Q000187:drug effects / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D016207:Cytokines; D018377:Neurotransmitter Agents; D009638:Norepinephrine