Evora Paulo Roberto B, Nather Julio, Tubino Paulo Victor, Albuquerque Agnes Afrodite S, Celotto Andrea Carla, Rodrigues Alfredo J
Department of Surgery and Anatomy, Ribeirão Preto Faculty of Medicine, University of São Paulo, Avenida Bandeirantes 3900, 14048-900 Ribeirão Preto, SP, Brazil.
Int J Inflam. 2013;2013:183061. doi: 10.1155/2013/183061. Epub 2013 May 30.
A modern concept considers acute coronary syndrome as an autoinflammatory disorder. From the onset to the healing stage, an endless inflammation has been presented with complex, multiple cross-talk mechanisms at the molecular, cellular, and organ levels. Inflammatory response following acute myocardial infarction has been well documented since the 1940s and 1950s, including increased erythrocyte sedimentation rate, the C-reactive protein analysis, and the determination of serum complement. It is surprising to note, based on a wide literature overview including the following 30 years (decades of 1960, 1970, and 1980), that the inflammatory acute myocardium infarction lost its focus, virtually disappearing from the literature reports. The reversal of this historical process occurs in the 1990s with the explosion of studies involving cytokines. Considering the importance of inflammation in the pathophysiology of ischemic heart disease, the aim of this paper is to present a conceptual overview in order to explore the possibility of curbing this inflammatory process.
一种现代观念认为急性冠脉综合征是一种自身炎症性疾病。从发病到愈合阶段，炎症持续不断，在分子、细胞和器官水平存在复杂的多重相互作用机制。自20世纪40年代和50年代以来，急性心肌梗死后的炎症反应已有充分记录，包括红细胞沉降率升高、C反应蛋白分析以及血清补体测定。令人惊讶的是，基于包括接下来30年（20世纪60年代、70年代和80年代）的广泛文献综述，炎症性急性心肌梗死失去了关注焦点，几乎从文献报道中消失。这一历史进程的逆转发生在20世纪90年代，随着涉及细胞因子的研究激增。鉴于炎症在缺血性心脏病病理生理学中的重要性，本文旨在进行概念性概述，以探讨抑制这一炎症过程的可能性。
