Immaturity of smooth muscle cells in the neointima is associated with acute coronary syndrome.

Abstract

Acute coronary syndrome (ACS) is mostly caused by ruptured plaques. The characteristics of rupture-prone vulnerable plaques include thin fibrous cap, large lipid core, and lower number of smooth muscle cells. Smooth muscle cells appearing in neointimal plaques are currently thought to have a uniformly synthetic phenotype, and their sub-classification has not been performed by h-caldesmon, which is supposed to be expressed in vascular smooth muscle cells that are beyond intermediately differentiated. Stenotic coronary arteries were obtained from autopsy material of 51 adults. Cases were divided into three groups: those who died from ACS, those with a past history of ACS but died from other causes, and those without ACS history. Histological data including fibrous cap and lipid core were measured in each specimen. Immunohistochemistry for alpha-smooth muscle actin (α-SMA), h-caldesmon, and smoothelin was performed. The ratio of h-caldesmon(+) cells to α-SMA(+) cells was counted in the neointima. The positivity ratio of neointimal h-caldesmon decreased in a step-wise manner from cases without history of ACS through cases with past history of ACS to cases with ACS with statistical significance (P<.001). The correlation between h-caldesmon expression and progression of ACS among the different groups was more prominent than the differences in the extent of fibrous cap and lipid core. Smoothelin(+) cells were rarely observed in the neointima. Decreased positivity of h-caldesmon in neointimal smooth muscle cells is indicative of a more immature phenotype, thus may be associated with plaque vulnerability that will promote ACS.