How does the atheromatous plaque responsible for acute myocardial infarction (MI, heart attack) develop, and what is its role in acute coronary syndrome (ACS)?

Updated: May 07, 2019
  • Author: A Maziar Zafari, MD, PhD, FACC, FAHA; Chief Editor: Eric H Yang, MD  more...
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The atheromatous plaque responsible for acute MI develops in a dynamic process in multiple stages. Starting with arterial intimal thickening, which consists of vascular smooth muscles with very minimal or no inflammatory cells, this process can be observed soon after birth. Subsequently, the formation of fibrous cap atheroma occurs, which has a lipid-rich necrotic core that is surrounded by fibrous tissue. Eventually, a thin-cap fibroatheroma develops, this is also known as a vulnerable plaque which is composed mainly of a large necrotic core separated from the vascular lumen by a thin fibrous cap that is infiltrated by inflammatory cells and is deficient of smooth muscle cells, making it vulnerable to rupture. [14, 15]

The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of plaque rupture, and less frequently plaque erosion.

The Brasilia Heart Study Group indicates that changes in high-density lipoprotein (HDL) during an MI may alter the antiatherogenic function of HDL to transport lipids from arterial walls. [16]  The investigators noted a simultaneous decrease in lipid transfer to HDL and in the capacity of HDL to efflux cholesterol from cells occurs in the acute period after an MI.

In a nested case-control study that evaluated the associations of plasma metabolic markers with the risks of incident MI, ischemic stroke, and intracerebral hemorrhage, investigators found positive associations of lipoproteins and lipids with MI and ischemic stroke but not with intracerebral hemorrohage, as well as positive associations between triglyceride concentrations and MI. [17] Except for small HDL, there was also an inverse association of HDL particles with MI, and an inverse association of cholesterol in large HDL with MI and ischemic stroke. The study cohort included 912 patients with MI, 1146 with ischemic stroke, 1138 with intracerebral hemorrhage, and 1466 control subjects. [17]

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