Restenosis after coronary angioplasty

CD40-CD40 ligand interaction is involved in the inflammatory pathogenesis of atherosclerosis but clinical data about its role in stent restenosis are still limited. We investigated the effect of preprocedural CD40 ligand (sCD40L) on stent restenosis. We enrolled 36 patients (mean age 61.4 ± 8.5 years) with stable angina who underwent successful stent implantation. Control angiograms were performed in all patients after 6 months. Plasma sCD40L and high-sensitive C-reactive protein levels were measured before stent implantation and at 1 and 6 months after the procedure. Angiographically proven restenosis rate was 27.8%. Plasma sCD40L levels were significantly higher (preprocedural 0.74 ± 0.79) and more prolonged in patients with stent restenosis compared with patients without stent restenosis (0.02 ± 0.22 ng/ml, p <0.001). According to receiver-operator characteristic analysis, sCD40L >0.41 ng/ml was the best distinguished parameter between patients with and without restenosis. At the multivariate logistic regression analysis, preprocedural sCD40L was an independent predictor (RR 39.4, 95% confidence interval 4.05 to 383.8, p = 0.002) of stent restenosis after adjusting for confounding variables, including diabetes, reference vessel diameter, lesion length, stent diameter, stent length, and baseline high-sensitive C-reactive protein. Sensitivity, specificity, and positive and negative predictive values and likelihood ratio of preprocedural sCD40L levels in stent restenosis were 78%, 92%, 78%, 92%, and 9.37%, respectively. In conclusion, enhanced inflammation of plaque (increased sCD40L) before percutaneous coronary intervention may increase the rate of stent restenosis. Increased preprocedural sCD40L level is an independent predictor of stent restenosis. We can use this marker for the assessment of risk stratification before planning stent implantation.

Restenosis is a major health care problem, with approximately 40% of angioplasties resulting in restenosis. Mechanisms related to elastic recoil, cell proliferation, and extracellular matrix (ECM) synthesis are implicated. In vivo studies have demonstrated the potential for cryotherapy to combat the process of restenosis, but the mechanisms whereby freezing and/or cooling can reduce or eliminate smooth muscle cell (SMC) proliferation and ECM synthesis are not well known. While in vivo testing is ultimately necessary, in vitro models can provide important information on thermal parameters and mechanisms of injury. However, it is important to carefully choose the model system for in vitro work on cryoinjury characterization to adequately reflect the clinical situation. In this study, we examined the differences in response to cryoinjury by SMCs from different species (rat, pig, and human) and in different cellular environments (suspension vs. tissue equivalent). Tissue equivalents, composed of cells embedded in collagen or fibrin gel, provide a 3-D tissue-like environment, while allowing for controlled composition. As reported here, all SMCs showed similar trends, but rat cells appeared less sensitive to cooling at faster cooling rates in suspension, while human SMCs were less sensitive to temperatures just above freezing when embedded in collagen. In addition, the SMCs were less sensitive in suspension than they were in collagen. Cells in suspension exhibited 70% viability at −11 °C, whereas cells in the tissue equivalent model showed only 30% survival. Future studies will aim to more adequately represent the conditions in restenosis by providing inflammatory and proliferative cues to the cells.

Background: E-Selectin is expressed only on activated endothelial cells, and may be used as a marker of endothelial activation. The relationship between soluble form of E-selectin (sE-selectin) and development of restenosis after balloon angioplasty (PTCA) is controversial, and there are no data for after stent implantation. We evaluated the role of serially measured sE-selectin levels in predicting the development of restenosis after PTCA and stent implantation. Methods: In sixty-one patients with stable angina pectoris who underwent PTCA (n=20) or stent implantation (n=41), peripheral blood samples were taken just before (baseline), at 3 and at 24 h after the intervention. sE-Selectin levels were measured by ELISA. Coronary angiography was repeated at 4–6 months after the intervention, and ≥50% stenosis at the site of the intervention was regarded as restenosis. Levels and time course of sE-selectin after the intervention were compared in patients with and those without restenosis. Results: sE-Selectin levels of the patients with and those without restenosis were similar at each of the three measurements, and significantly increased after the intervention both in the PTCA and stent groups (P<0.001 for both groups). Posthoc analysis showed that sE-selectin levels increased significantly at 3 h after PTCA (P=0.024) and stent implantation (P=0.018), and did not change thereafter in patients with restenosis. In the nonrestenotic group, sE-selectin did not change significantly in the 24 h following PTCA, however, a significant difference was observed only by comparing the values at baseline with those at 24 h after stent implantation (P=0.021). Conclusions: A substantial increase in sE-selectin levels early (at 3 h) after PTCA and stent implantation may predict development of restenosis.

OBJECTIVES

To evaluate a quantitative model of restenosis in patients with vein graft disease undergoing percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA).

BACKGROUND

A quantitative relationship between acute gain and late loss has been developed to describe the late changes in lumen dimension after native vessel coronary intervention. This same relationship may also be seen after treatment of saphenous vein graft disease.

METHODS

Patients with native coronary artery stenoses (CAVEAT-I) or saphenous vein graft lesions (CAVEAT-II) were randomized to either DCA or PTCA, and data from these trials were analyzed retrospectively. Angiographic results of the target lesions were reviewed, and each lesion was assessed for vessel caliber and reference diameter, absolute minimal lumen diameter, percent diameter stenosis, percent stenosis of the cross-sectional area, acute gain and late loss. Linear regression models were used to determine late loss and to detect differences in angiographic outcomes.

RESULTS

Vein grafts had significantly larger reference vessel diameters than native coronary arteries; they also had significantly more acute gain and more late loss. Directional coronary atherectomy was associated with a larger acute gain in both studies. Patients undergoing DCA also experienced greater late loss although the effect was statistically significant only in the CAVEAT-I study. After adjusting for the acute gain, the treatment effect on late loss became nonsignificant in both studies.

CONCLUSIONS

In patients undergoing DCA or PTCA of saphenous vein graft narrowings, the relationship between late loss and acute gain is also demonstrated, similar to the device-independent relationships seen in native coronary lesions. In CAVEAT-II, larger degrees of acute gain were also associated with higher degrees of late lumen loss.