| Literature DB >> 26596804 |
Jonathan A Kirk1, David A Kass2.
Abstract
Dyssynchronous contraction of the ventricle significantly worsens morbidity and mortality in patients with heart failure (HF). Approximately one-third of patients with HF have cardiac dyssynchrony and are candidates for cardiac resynchronization therapy (CRT). The initial understanding of dyssynchrony and CRT was in terms of global mechanics and hemodynamics, but lack of clinical benefit in a sizable subgroup of recipients who appear otherwise appropriate has challenged this paradigm. This article reviews current understanding of these cellular and subcellular mechanisms, arguing that these aspects are key to improving CRT use, as well as translating its benefits to a wider HF population.Entities:
Keywords: Animal models; Cardiac resynchronization therapy; Dyssynchrony; Myocyte; Myofilament
Mesh:
Year: 2015 PMID: 26596804 PMCID: PMC4660268 DOI: 10.1016/j.ccep.2015.08.011
Source DB: PubMed Journal: Card Electrophysiol Clin ISSN: 1877-9182