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Published on: May 22, 2018
Neurohumoral activation in congestive heart failure: a double-edged sword?
1Department of Medicine, Gazes Cardiac Research Institute Medical University of South Carolina, Charleston.
Insights
Excessive adrenergic stimulation initially aids failing hearts but can worsen function over time. This review suggests it plays a key role in congestive heart failure development.
Area of Science:
- Cardiology
- Pathophysiology
- Pharmacology
Background:
- Congestive heart failure involves progressive left ventricular dysfunction.
- The exact mechanisms driving this deterioration remain incompletely understood.
- A single cause for congestive heart failure is unlikely due to its complexity.
Purpose of the Study:
- To review evidence on the dual role of adrenergic stimulation in heart failure.
- To explore how excessive adrenergic signaling impacts myocardial function.
Main Methods:
- Review of recent experimental data.
- Analysis of clinical evidence.
Main Results:
- Adrenergic stimulation can initially support failing myocardium.
- Prolonged excessive adrenergic stimulation may cause myopathic effects.
- This can lead to worsening left ventricular function and intractable heart failure.
Conclusions:
- Excessive adrenergic stimulation appears to be a double-edged sword in heart failure.
- While not the sole cause, it may play a primary role in the pathogenesis of congestive heart failure.
Abstract:
The search for the basic mechanism(s) responsible for the progressive and frequently irreversible deterioration of left ventricular pump function in congestive heart failure has been quite extensive; nonetheless, no single explanation has been forthcoming. Indeed, given the complexity of this disease process, it is becoming increasingly unlikely that a single pathogenetic mechanism will ever be uncovered for congestive heart failure. This review will examine recent experimental and clinical evidence which suggests that excessive adrenergic stimulation of the heart is double-edged. That is, while increased adrenergic input to the heart may initially enable the failing myocardium to function adequately for a period of months to years, continued excessive adrenergic stimulation of the heart through both local neural and circulating catecholamines may lead to frank myopathic effects on the heart, with resultant worsening of left ventricular function and the development of intractable congestive heart failure. While we do not mean to suggest that excessive sympathetic stimulation of the heart is the only, or even the major mechanism responsible for the development of irreversible congestive heart failure, the data reviewed herein do suggest that adrenergic stimulation may play a primary role in the pathogenesis of congestive heart failure.
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