Division of Cardiovascular Sciences, Centre of Applied Medical Research, University of Navarra, Pamplona, Spain.
J Am Coll Cardiol. 2011 Oct 25;58(18):1833-43. doi: 10.1016/j.jacc.2011.06.058.
Classical therapy of heart failure is based on treatment of its pre-disposing/triggering factors and of the neurohumoral activation secondary to the deterioration of cardiac function. A new view is emerging that proposes the direct intervention on the pathological structural remodeling of the myocardium as part of heart failure therapy. In fact, in conditions of chronic injury, the cardiomyocytic and the noncardiomyocytic components of the myocardium undergo a series of structural lesions (i.e., cardiomyocyte growth and death, inflammation, alterations of collagen matrix, and microvascular rarefaction) that are governed by a complex interplay of mechanisms. Our increasing knowledge of the role of these mechanisms in remodeling enables us not only to better understand how our more successful therapies work but also to explore novel therapies for the future. In this paper, we will examine recent insights from experimental and pilot clinical studies that have provided new targets for interventions to prevent or reverse inflammation, alterations of collagen matrix, and cardiomyocyte death.
心力衰竭的传统治疗基于对其诱发因素和心功能恶化继发的神经体液激活的治疗。一种新的观点正在出现，即提出直接干预心肌的病理性结构重塑作为心力衰竭治疗的一部分。事实上，在慢性损伤的情况下，心肌细胞和非心肌细胞成分经历一系列结构损伤（即心肌细胞生长和死亡、炎症、胶原基质改变和微血管稀疏），这些损伤受一系列机制的复杂相互作用控制。我们对这些机制在重塑中的作用的认识不断增加，不仅使我们能够更好地理解我们更成功的治疗方法的工作原理，还为未来探索新的治疗方法提供了依据。在本文中，我们将研究来自实验和初步临床研究的最新见解，这些研究为干预炎症、胶原基质改变和心肌细胞死亡提供了新的靶点。
