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Heart Fail Clin. 2017 Jan;13(1):29-41. doi: 10.1016/j.hfc.2016.07.003.

Cellular and Molecular Aspects of Dyssynchrony and Resynchronization.

Author information

1
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.
2
Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Research Building, Room 858, 720 Rutland Avenue, Baltimore, MD 21205, USA.

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.

KEYWORDS:

Animal models; Cardiac resynchronization therapy; Dyssynchrony; Myocyte; Myofilament

PMID:
27886930
DOI:
10.1016/j.hfc.2016.07.003
[Indexed for MEDLINE]

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