Curbing Inflammation in the Ischemic Heart Disease

Table 1

Ischemic heart disease and inflammation—key physiopathology concepts.

(i) A modern concept considers ACS as an autoinflammatory disorder.
(ii) Inflammatory response following AMI has been well documented since the 1940s and 1950s.
(iii) It is surprising to note, based on extensive literature overview including the following 30 years (decades of 1960, 1970, and 1980), that the inflammatory AMI lost its focus, virtually disappearing from the literature reports.
(iv) There are two different inflammatory processes in patients with AMI: the coronary arterial inflammation that leads to the pathogenesis of AMI, followed by myocardial inflammation that leads to ventricular remodeling.
(v) Systemic inflammatory response (SIRS), complement activation, release of inflammatory cytokines, iNOS expression, and vasodilatation cannot only play a pivotal role in the genesis and evolution of shock.
(vi) The most frequent biomarkers used in humans and experimental protocols are (1) plasma levels of cytokines IL-6, IL-8, and TNF-𝛼; (2) membrane expression of Toll-like receptor; (3) CD11b, CD62L, and CD14 on monocytes and granulocytes as markers of inflammation.
(vii) Curiously, increased erythrocyte sedimentation rate (ESR) and the C-reactive protein analysis (CRP) are the oldest markers of AMI and still are the most useful on the clinical practice.