Sympathetic activation in heart failure and its treatment with β- blockade

Gregory S. Pepper, Richard W. Lee

Research output: Contribution to journalReview articlepeer-review

79 Scopus citations


Multiple models explaining the pathogenesis of heart failure have been put forth during the past 5 decades. These models were modified as clinical evidence supported or refuted their assumptions. During the past 2 decades, heart failure models emphasized the importance of neurohormonal systems in heart failure progression. The positive impact that angiotensin-converting enzyme inhibitors have had on mortality from heart failure has bolstered the neurohormonal theory. Attention recently has turned to the sympathetic nervous system and its potential deleterious effects on the cardiovascular system in heart failure. The sympathetic nervous system can negatively impact the cardiovascular system in heart failure in several ways, including down- regulating β1-receptors, exerting direct toxic effects on the myocardium, and contributing to myocardial remodeling and life-threatening arrhythmias. β-Adrenergic blockers have shown promise for reducing morbidity and mortality in heart failure, but definitive reductions in mortality remain to be shown by future investigations.

Original languageEnglish (US)
Pages (from-to)225-234
Number of pages10
JournalArchives of internal medicine
Issue number3
StatePublished - Feb 8 1999

ASJC Scopus subject areas

  • Internal Medicine


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