title: Compensatory and maladaptive responses to cardiac dysfunction.
abstract: The field of congestive heart failure continues to be vigorously investigated at both the basic science level and in the clinic. As we move from the "hemodynamic" to the "neurohormonal" model of heart failure, more emphasis is being placed on interruption of neurohormone activity as a therapeutic strategy. A number of important clinical trials have been reported in the past year that underscore the potential of using drugs to inhibit neuroendocrine activity. The ultimate neuroendocrine inhibitors are perhaps the beta-adrenergic blocking drugs. They have yet to be adequately studied in a statistically powerful, randomized, placebo-controlled multicenter trial. Such a trial is about to begin in North America. In the meantime, numerous studies continue to confirm manifestations of neurohormone imbalance in clinical heart failure. Reduced heart rate variation has been under intensive investigation. A great variety of animal models of heart failure are also currently being studied. Perhaps more important advances have been made in the treatment of patients with heart failure than in any other field in internal medicine in recent years. However, improved patient survival tends to further increase the overall cost of patient care. Perhaps we are simply shifting the patient population, extending survival by 9 to 18 months. More advanced heart failure is more expensive to care for. It is only through understanding the basic biology and pathophysiology of heart failure that fresh new ideas will emerge leading to earlier therapy and, ultimately, prevention of this important disorder.
authors.affiliation: Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.
authors.forename: G S
authors.initials: GS
authors.lastname: Francis
authors.forename: C
authors.initials: C
authors.lastname: Chu
mesh_terms: D000818:Animals; D002986:Clinical Trials as Topic; D004195:Disease Models, Animal; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009490:Neurosecretory Systems / Q000503:physiopathology