Abstract 17404: The Impact of Drug-eluting Stent Induced Coronary Endothelial Dysfunction on Neointimal Hyperplasia 9 Months After Stent Implantation
Background: Recent studies reported that drug-eluting stent (DES) induced epicardial endothelial dysfunction (ED). However, it is unclear whether DES induced ED is associated with the degree of neointimal hyperplasia.
Methods: Consecutive series of 18 patients who underwent DES implantation in the left anterior descending artery were prospectively enrolled. Patients who had vasoconstriction by intracoronary acetylcholine (Ach) infusion at the end of initial procedure were excluded. Coronary angiography and coronary blood flow (CBF) measurement with a Doppler guidewire were performed 9 months after DES implantation. Average peak velocity (APV) was measured at the position of 5 to 10mm distal to DES and CBF was calculated as π(coronary artery diameter/2)2х(APV/2). Epicardial ED was evaluated by the degree of reference segments vasoconstriction in response to Ach (10-7&10-6mol/L). Epicardial ED was defined as >20% decrease of %diameter stenosis (DS), and entire coronary ED as <50% increase of CBF in response to 10-6mol/L Ach.
Results: Vasoconstriction to 10-6mol/L Ach was more prominent in distal stent segments than in proximal segments (-7.5±15.1% and -4.5±16.6%). No correlation was identified between the degree of epicaldial ED and coronary risk factor, ACC/AHA Lesion Classification or stent type. There was no linear relationship between in-stent %DS and epicardial endothelial function. Percent change of CBF in response to Ach varied between individuals (-41.5% to 371%). In-stent %DS at 9-month follow-up was significantly lower in patients with entire coronary ED than in patients without (10.9% versus 21.3%, P=0.04, figure).
Conclusion: The degree of neointimal hyperplasia after DES negatively correlated to the degree of ED in entire coronary artery including both epicardial artery and coronary microvasculature. Our results suggest that DES impaired endothelial function of entire coronary vasculature that may lead to stent thrombosis.
- © 2013 by American Heart Association, Inc.