Kirk Jonathan A, Kass David A
Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Research Building, Room 858, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Research Building, Room 858, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Card Electrophysiol Clin. 2015 Dec;7(4):585-97. doi: 10.1016/j.ccep.2015.08.011.
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.
心室不同步收缩会显著加重心力衰竭（HF）患者的发病率和死亡率。约三分之一的HF患者存在心脏不同步，是心脏再同步治疗（CRT）的适用对象。对不同步和CRT的最初认识是基于整体力学和血流动力学，但在相当一部分表面上适合治疗的接受者中缺乏临床获益，这对这种模式提出了挑战。本文回顾了目前对这些细胞和亚细胞机制的认识，认为这些方面是改善CRT应用以及将其益处扩展到更广泛HF人群的关键。
