Abstract 2571: Long-Term Endothelial Dysfunction after Coronary Artery Stenting with Drug-Eluting Stent Associated with Local Inflammatory Response

Abstract

Endothelial function remains chronically abnormal after vascular injury associated with coronary intervention. The long-term effects of drug-eluting stent (DES) on endothelial function are not known. We evaluated the endothelial-dependent vasomotor function and local release of pentraxin3 (PTX3) as a local inflammatory marker in nonrestenotic coronary arteries more than six months following DES and bare metal stent (BMS) implantation. Fifty-two patients treated six months earlier with a coronary stenting for isolated proximal left anterior descending (LAD) stenosis, with no evidence of restenosis, were studied. Twenty patients had been stented with BMS, and 32 had been with DES. Changes in diameter at distal site of the stented LAD in response to intracoronary acetylcholine (Ach) infusions (1,3,10,30 μg/min) were assessed by quantitative angiography. At the completion of the protocol, a 2mg bolus of isosorbide dinitrate (ISDN) was injected into the LAD. We also measured serum PTX3 levels sampled in coronary sinus (CS) and sinus of Valsalva (V). Results: The two groups had similar risk factors for endothelial dysfunction. The mean percent change in the diameter of the stented LAD by Ach injection was significantly more in the DES group than in the BMS group (−38.9±6.1 vs. −19.2±6.7 %, p<0.01). There was no significant difference in maximal dilation achieved by ISDN infusion between the two groups (34.6±6.6 vs. 31.2±4.6 %, NS). The translesional PTX3 gradient (CS-PTX3 minus V-PTX3) was higher in the DES group than in the BMS group (+0.11±0.05 vs. −0.01±0.05 ng/ml, p<0.01). More severe endothelial dysfunction was observed long term after DES implantation as compared to BMS. These findings were associated with an increased local inflammatory response to DES stenting.