Middlekauff Holly R
David Geffen School of Medicine at UCLA, Department of Medicine (Cardiology), Los Angeles, California 90095, USA.
J Card Fail. 2005 Sep;11(7):534-41. doi: 10.1016/j.cardfail.2005.03.002.
Studies have shown that neither ejection fraction nor hemodynamic abnormalities during exercise in chronic heart failure (HF) correlate with symptoms of fatigue and exhaustion. The concept that exercise limitation in patients with chronic HF is due to abnormal hemodynamics during exercise has been revised to acknowledge that the skeletal myopathy of chronic HF contributes significantly to exercise dysfunction in heart failure. Why then does cardiac resynchronization therapy (CRT), a therapy that improves abnormalities of cardiac function, such as cardiac output and ejection fraction, produce a consistent, measurable, irrefutable increase in exercise capacity?
In this review I will (1) review the mechanisms of exercise dysfunction in chronic HF, with special attention to the concept of "coordinated adaptation"; (2) analyze the effects of CRT on autonomic dysfunction in HF; and (3) propose a unifying hypothesis to understand how a therapy that improves cardiac function can improve exercise dysfunction attributable to a skeletal myopathy. Specifically, I will review evidence that CRT improves exercise capacity by attenuating the chronic sympathetic activation of HF.
The decrease in sympathetic activation, and perhaps inflammation, during CRT likely reverses many features of the skeletal myopathy, leading to improved exercise capacity.
研究表明，慢性心力衰竭（HF）患者运动期间的射血分数和血流动力学异常均与疲劳和疲惫症状无关。慢性HF患者运动受限是由于运动期间血流动力学异常这一概念已被修正，以承认慢性HF的骨骼肌病在心力衰竭运动功能障碍中起重要作用。那么，为何心脏再同步治疗（CRT）这种可改善心功能异常（如心输出量和射血分数）的治疗方法，能使运动能力持续、可测量且无可辩驳地提高呢？
在本综述中，我将（1）回顾慢性HF运动功能障碍的机制，特别关注“协调适应”的概念；（2）分析CRT对HF自主神经功能障碍的影响；（3）提出一个统一的假设，以理解改善心功能的治疗方法如何改善由骨骼肌病引起的运动功能障碍。具体而言，我将回顾CRT通过减弱HF慢性交感神经激活来提高运动能力的证据。
CRT期间交感神经激活的降低以及可能的炎症减轻，可能会逆转骨骼肌病的许多特征，从而提高运动能力。
