Electromechanical dyssynchrony and resynchronization of the failing heart.
Electromechanical dyssynchrony and resynchronization of the failing heart.
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DOI：
10.1161/circresaha.113.300270
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发表时间：
2013-08-30
影响因子：
20.1
通讯作者：
Kass DA
中科院分区：
文献类型：
--
作者：
Kirk JA;Kass DA
心力衰竭和功能低下的患者经常因电激活延迟而出现收缩不协调。通常被称为不同步，这进一步抑制收缩功能和心室效率，并恶化发病率和死亡率。 20 世纪 90 年代中期，开发了一种基于起搏器的治疗方法，称为心脏再同步治疗 (CRT)，通过电激活心脏的左右两侧来恢复机械同步。这是新千年的重大治疗进展。CRT 的急性心室效应包括增加心输出量和机械效率，并减少二尖瓣反流，而心室容积的减少会长期发生。 CRT 候选者的 QRS 持续时间延长且室壁运动不协调，但其他因素也可能很重要，因为约 30% 的选定受试者对治疗没有反应。与现有的药理学正性肌力药物相比，CRT 可以急性和长期地增加心脏收缩功能和工作，同时还可以降低长期死亡率。最近的研究揭示了 CRT 带来的独特的分子/细胞变化，这也可能有助于这一成功。不同步性心力衰竭表现出肌细胞和肌丝功能、钙处理、β-肾上腺素能反应性、线粒体 ATP 合酶活性、细胞存活信号传导和其他变化降低。 CRT 通常通过触发全新的途径来逆转许多这些异常。在这篇综述中，我们讨论了不同步和 CRT 对衰竭心脏的心室、循环和基本心肌影响，并重点介绍了旨在更好地瞄准和实施 CRT 以及利用其分子效应的新研究。
Patients with heart failure and depressed function frequently develop discoordinate contraction due to electrical activation delay. Often termed dyssynchrony, this further depresses systolic function and chamber efficiency, and worsens morbidity and mortality. In the mid-1990s, a pacemaker-based treatment termed cardiac resynchronization therapy (CRT) was developed to restore mechanical synchrony by electrically activating both right and left sides of the heart. It is a major therapeutic advance for the new millennium.. Acute chamber-effects of CRT include increased cardiac output and mechanical efficiency, and reduced mitral regurgitation, while reduction in chamber volumes ensues more chronically. Patient candidates for CRT have a prolonged QRS duration and discoordinate wall-motion, although other factors may also be important as ∼30% of such selected subjects fail to respond to the treatment. In contrast to existing pharmacological inotropes, CRT both acutely and chronically increases cardiac systolic function and work yet it also reduces long-term mortality. Recent studies reveal unique molecular/cellular changes from CRT that may also contribute to this success. Heart failure with dyssynchrony displays depressed myocyte and myofilament function, calcium handling, beta-adrenergic responsiveness, mitochondrial ATP-synthase activity, cell survival signaling, and other changes. CRT reverses many of these abnormalities often by triggering entirely new pathways. In this review, we discuss chamber, circulatory, and basic myocardial effects of dyssynchrony and CRT in the failing heart, and highlight new research aiming to better target and implement CRT as well as leverage its molecular effects.