title: Heart failure in 2001: a prophecy.
abstract: Understanding of heart failure has developed through 3 paradigms involving organ, cell, and gene. The first views heart failure as an abnormality of organ (pump) function leading to salt and water retention and vasoconstriction. Therapy to correct these circulatory abnormalities is well accepted and effective. The second considers heart failure as a disordered cellular function, mainly impaired contraction and relaxation. Efforts to correct the biochemical and biophysical abnormalities responsible for these disorders of myocardial performance have, however, been less successful. Recent emphasis on efforts to improve prognosis as well as symptoms in patients with chronic heart failure demonstrates that it is a lethal disease with problems of survival similar to those in malignancies. The third paradigm of abnormal gene expression, which in the failing heart represents a cardiomyopathy of overload, appears to be a major cause of poor prognosis in these patients. Evidence that the angiotensin-converting enzyme inhibitors have important effects on cell growth, as well as on vascular tone, suggests that their ability to prolong survival in patients with heart failure may be due largely to the inhibition of detrimental effects of angiotensin II on cardiac gene expression. Thus, it seems likely that work focused on the third paradigm will uncover specific abnormalities of gene expression that are responsible for poor survival of patients with heart failure. By 2001, I predict that heart failure will be viewed as an abnormality of cell growth and this will lead to the development of therapies to retard, if not reverse, the clinical deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, University of Connecticut, Farmington 06030.
authors.forename: A M
authors.initials: AM
authors.lastname: Katz
mesh_terms: D015870:Gene Expression; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D009206:Myocardium / Q000473:pathology