title: Cellular and Molecular Aspects of Dyssynchrony and Resynchronization.
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.
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Research Building, Room 858, 720 Rutland Avenue, Baltimore, MD 21205, USA. Electronic address: jkirk2@luc.edu.
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Kirk
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Research Building, Room 858, 720 Rutland Avenue, Baltimore, MD 21205, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000818:Animals; D058406:Cardiac Resynchronization Therapy / Q000379:methods*; D056966:Excitation Contraction Coupling; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control; D006801:Humans; D008955:Models, Cardiovascular; D032342:Muscle Cells; D009200:Myocardial Contraction; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control
keywords: Animal models; Cardiac resynchronization therapy; Dyssynchrony; Myocyte; Myofilament