Curbing Inflammation in the Ischemic Heart Disease

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. 1. Introduction Inflammatory response following acute myocardial infarction (AMI) has been documented since the 1940s and 1950s, including increased erythrocyte sedimentation rate (ESR), the C-reactive protein analysis (CRP), and the determination of serum complement ( ). Boltax and Fischel (1956) using serial assay of the ESR, , and CRP in sixty-one AMI episodes observed that such tests were positive in over 90% of patients by the third day from the onset of the disease [1]. In 1943, Lofstrom reported that patients with myocardial infarction also presented the “non-specific capsular swelling in pneumococci,” later associated with the presence of the “C-reactive protein” [2]. Since then, a number of studies have confirmed the occurrence of CRP in myocardial infarction and other noninfectious inflammatory conditions [3, 4]. Surprisingly, an extensive literature overview including publications from 1960s to the 1980s revealed that the role of the inflammation in the AMI lost relevance, virtually disappearing from the literature reports. The reversal of this historical process occurred in the 1990s with the upsurge of investigations involving cytokines (Figure 1). Figure 1: Web of Science timespan references (1940–2012). Therefore, considering the importance of inflammation in the pathophysiology of ischemic heart disease (IHD), the aim of this review is to present an overview of concepts in order to explore the possibilities for curbing the inflammatory process associated with myocardial