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Myocardial Reverse Remodeling

机译：心肌逆重塑

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Despite an extensive literature defining the mechanisms and significance of pathological myocardial remodeling, there has been no comprehensive review of the inverse process, often labeled reverse remodeling. Accordingly, the goal of this review is to overview the varied settings in which clinically significant reverse remodeling has been well documented. When available, we reviewed relevant randomized, controlled clinical trials, and meta-analyses with sufficient cardiac imaging data to permit conclusions about reverse remodeling. When these types of studies were not available, relevant case-control studies and case series that employed appropriate methodology were reviewed. Regression of pathological myocardial hypertrophy, chamber shape distortions, and dysfunction occurs in a wide variety of settings. Although reverse remodeling occurs spontaneously in some etiologies of myocardial dysfunction and failure, remodeling is more commonly observed in response to medical, device-based, or surgical therapies, including β-blockers, revascularization, cardiac resynchronization therapy, and valve surgery. Indeed, reverse remodeling following pathophysiologically targeted interventions helps validate that the targeted mechanisms are propelling and/or sustaining pathological remodeling. The diverse clinical settings in which reverse remodeling has been observed demonstrates that myocardial remodeling is bidirectional and occurs across the full spectrum of myocardial disease severity, duration, and etiology. Observations in several settings suggest that recovered hearts are not truly normal despite parallel improvements at organ, tissue, and cellular level. Nevertheless, the link between reverse remodeling and improved outcomes should inspire further research to better understand the mechanisms responsible for both reverse remodeling and persistent deviations from normalcy.
机译：尽管有大量文献定义了病理性心肌重塑的机制和意义，但尚未对逆过程进行全面的综述，通常将其标记为逆重塑。因此，本综述的目的是概述临床已被充分证明具有重大临床意义的反向重塑的各种环境。如果可用，我们将回顾相关的随机对照临床试验，并进行荟萃分析，并提供充足的心脏成像数据，以得出关于逆向重构的结论。当这些类型的研究不可用时，将审查采用适当方法的相关病例对照研究和病例系列。在多种情况下都会发生病理性心肌肥大，房形变形和功能障碍的退化。尽管在心肌功能障碍和衰竭的某些病因中会自发发生逆重塑，但对药物，基于器械或外科疗法（包括β受体阻滞剂，血运重建，心脏再同步化治疗和瓣膜手术）的反应更为常见。实际上，在进行病理生理学靶向干预后进行逆向重塑有助于验证靶向机制是否在推动和/或维持病理性重塑。观察到反向重塑的各种临床情况表明，心肌重塑是双向的，并且发生在整个心肌疾病严重程度，病程和病因学方面。在几种情况下的观察结果表明，尽管器官，组织和细胞水平有所改善，但恢复的心脏并不是真正正常的。然而，逆向重构与改善结果之间的联系应该激发进一步的研究，以便更好地理解逆向重构和持续偏离正常状态的机制。

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