Electrophysiological remodeling in hypertrophy and heart failure
Design
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Discussion
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Implication
Highlights remodeling-driven arrhythmia risk in HF; leaves open targeted therapies pending prospective trials.
Key Points
- To review the cellular, molecular, and neurohumoral mechanisms of electrophysiological and structural remodeling in hypertrophy and heart failure that provoke lethal cardiac arrhythmias.
- Synthesized epidemiological data, clinical trial outcomes including the Veterans Administration Heart Failure Trial (V-HeFT), and pathophysiological mechanisms of neurohumoral activation and ventricular remodeling.
- Compensatory activation of the sympathetic nervous and renin-angiotensin-aldosterone systems drives maladaptive gene expression, myocyte hypertrophy, and progressive ventricular dysfunction.
- Electrophysiological remodeling increases the frequency and complexity of ventricular ectopy, predisposing patients to sudden cardiac death, which accounts for up to 50% of heart failure mortality.
Cite This Study
Gordon F. Tomaselli (1999) studied this question.