Systemic inflammatory response following acute myocardial infarction

Lu Fang, Xiao-Lei Moore, Anthony M Dart, Le-Min Wang, Lu Fang, Xiao-Lei Moore, Anthony M Dart, Le-Min Wang

Abstract

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.

Keywords: Acute myocardial infarction; Inflammatory markers; Leukocytes; Systemic inflammatory response.

Figures

Figure 1.. Initiation of inflammatory response following…
Figure 1.. Initiation of inflammatory response following AMI.
AMI triggers an intense inflammatory response including elevation of inflammatory mediators, and recruitment of inflammatory cells via DAMPs/TLR/IL-1signaling. Inflammasomes also recognize danger signals and activate caspase-1, and release active IL-1β. Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse LV remodeling and heart failure. AMI is also associated with bone marrow activation via SNS activation and spleen monocytopoiesis, resulting in increased leukocyte influx which aggravates atherosclerosis and contributes to recurrent MI. Spleen monocytopoiesis is also regulated by IL-1β. AMI: acute myocardial infarciton; DAMPs: damage-associated molecular patterns; IL-1: interleukin-1; LV: left ventricular; TLR: toll-like receptor; SNS: sympathetic nervous system.

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