ARN extracelular – un predictor nou şi un eventual mecanism al restenozei intrastent

Abstract

Background: The evaluation of new predictors of negative coronary remodeling after angioplasty remains an adequate approach of interventional cardiology in the diagnosis and prognosis of in-stent restenosis (ISR). Previously we have demonstrated on a murine model of atherosclerosis that extracellular RNA (eRNA) increases proportionally to vascular injury progression, and a first activation of the blood RNAase is changed by its steady quantitative decline, a reason that suggests a plausible role of eRNA in coronary neointima hyperplasia. Material and methods: This article is aimed at the study of eRNA amount in a tissue pattern of a stent with restenosis as well as its correlation with such inflammatory predictors as macrophage number and TNF-alpha expression. Using the techniques of confocal microscopy and immunohistochemistry we have first proved that eRNA level significantly increases in the coronary wall of segments with ISR (the specimens have been taken postmortem from 19 patients exposed to angioplasty). Results: The rise in the assay has been closely correlated to restenosis degree, and in muscular media it has been 2-4 times beyond the control range estimated in the adjacent coronary segment without negative vascular remodeling. In the restenosis zone eRNA has risen by about 130% from minimal to severe ISR. Moreover, its level has been found markedly increased earlier also comparatively to the control pattern: by 62% in moderate and 128% in severe ISR. A key disclosed evidence is that eRNA is positively correlated with TNF-alpha level (r = +0.88) and the number of macrophages (r = +0.84), whereas the last is notably enhanced depending on ISR progression. Conclusions: The obtained outcomes result in 2 opportunities: 1. eRNA may be a feasible predictor of negative coronary remodeling, facilitating the prognosis of ISR risk; 2. eRNA may be singled out as a factor involved in the pathogenesis of neointima formation and hyperplasia due to its relation to the inflammatory process.