Complex interactions reside between cardiac mechanical dysfunction and malignant arrhythmia generation. Sudden death is a common mode of death in patients with advanced heart failure. Arrhythmogenic substrates of SCD in HF patients occur at multiple levels, from molecular and subcellular changes to those occurring at the organ-system levels. Complex alterations in ion channels, ryanodine receptors, gap junction proteins, nerve sprouting and sympathetic nerve activities and trigger factors, all play their roles in predisposing to arrhythmias and sudden death in HF. HF-induced myocardiac substrate dysfunction could increase spatiotemporal gradients of repolarization, prolong the AP, promotes the vulnerability to arrhythmogenic triggers, and results in conduction abnormalities. The size of the heart failure patient population will continue to grow as the global population continues to get older and live longer as a result of advanced medical care. Understanding fundamental mechanisms of electrogenesis is a key to the development of novel and more effective device and pharmacotherapies for patients with HF globally.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Geriatric Cardiology|
|State||Published - Dec 1 2009|
ASJC Scopus subject areas
- Geriatrics and Gerontology
- Cardiology and Cardiovascular Medicine