Department of Cardiovascular Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli, 1, 00168, Rome, Italy.
Department of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy.
Curr Cardiol Rep. 2022 Oct;24(10):1505-1515. doi: 10.1007/s11886-022-01766-6. Epub 2022 Aug 16.
Ischemic cardiomyopathy refers to systolic left ventricular dysfunction in the setting of obstructive coronary artery disease and represents the most common cause of heart failure worldwide. It is often the combination of an irreversible loss of viable mass following an acute myocardial infarction (AMI) with a dysfunctional, but still viable, myocardium in the context of a chronically reduced myocardial blood flow and reduced coronary reserve. Medical treatments aiming at modulating neurohumoral response and restoring blood flow to the ischemic cardiomyocytes were shown to dramatically abate the occurrence of ventricular dysfunction and adverse remodeling in ischemic cardiomyopathy.
Novel therapeutic approaches, such as mechanical unloading and modulation of the inflammatory response, appear to be promising. Furthermore, the understanding of the mechanisms by which, despite optimal treatment, heart failure ensues after AMI, with or without adverse remodeling and systolic dysfunction, is a critical step in the search for novel ways to tackle heart failure risk beyond preservation of left ventricular volumes and systolic function. In this review article, we explore the principal pathophysiological mechanisms and pathways of heart failure in ischemic cardiomyopathy, therapeutic opportunities, and knowledge gaps in this area.
缺血性心肌病是指在阻塞性冠状动脉疾病情况下出现的收缩性左心室功能障碍，是全球范围内心力衰竭最常见的病因。它通常是急性心肌梗死（AMI）后大量存活心肌不可逆丧失与慢性心肌血流减少和冠状动脉储备功能降低情况下的功能失调但仍存活的心肌的组合。旨在调节神经激素反应和恢复缺血性心肌细胞血流的药物治疗已被证明可显著减少缺血性心肌病中心室功能障碍和不良重构的发生。
机械卸载和炎症反应调节等新的治疗方法似乎很有前途。此外，尽管进行了最佳治疗，但在 AMI 后仍会发生心力衰竭，无论是否存在不良重构和收缩功能障碍，了解其机制是寻找除了保留左心室容积和收缩功能以外解决心力衰竭风险的新方法的关键步骤。在这篇综述文章中，我们探讨了缺血性心肌病心力衰竭的主要病理生理机制和途径、治疗机会以及该领域的知识空白。
