Acute myocardial infarction leads to acceleration of atherosclerosis

Abstract

Patients who experience acute myocardial infarction (AMI) are at increased risk of recurrent events in the weeks to months following the initial event. The underlying etiology for this vulnerable period following MI is unclear but could be related to the same underlying triggers responsible for the initial MI. Alternatively, the recurrent cardiac event could be promoted by the incident event. For example, several biomarkers reflecting inflammatory activity have been shown to be elevated for weeks to months following MI and this inflammatory response could aggravate existing atherosclerotic lesions by accelerating their growth and/or promoting plaque instability. The purpose of this review is to highlight recent preclinical and clinical studies supporting links between AMI and atherosclerosis and to consider potential therapeutic interventions.

Figure 1. Acute myocardial infarction (AMI) triggers atherosclerosis and recurrent MI

Systemic inflammatory cytokines (i.e. TNFα, IL-1β) are elevated following AMI, promoting leukocyte recruitment to atherosclerotic lesions characterized by increased leukocyte-endothelial (L–E) interactions. Haematopoietic stem/progenitor cells are released from bone marrow via activation of sympathetic nervous system (SNS) following AMI and hosted in spleen. Spleen-derived leukocytosis and activation of leukocytes by inflammatory cytokines contribute to the acceleration of atherosclerosis and recurrent MI.