Abstract
Objectives The aim of our study was to investigate the predictors of target lesion revascularization (TLR) and to compare the in-stent restenosis (ISR) progression rates of different 2nd-generation drug-eluting stents (DES). Background The predictors of early and late TLR after 2nd-generation DES implantation have not been fully evaluated. Methods We analyzed 944 stented lesions from 394 patients who had at least two serial follow-up angiograms, using quantitative coronary angiography (QCA) analysis. The study endpoints were TLR and the velocity of diameter stenosis (DS) progression. Results TLR occurred in 58 lesions (6.1%) during the first angiographic follow-up period and 23 de novo lesions (2.4%) during the following second interval. Independent predictors for early TLR were diabetes mellitus (DM) (HR 2.58, 95% CI 1.29–5.15, p=0.007), previous percutaneous coronary intervention (PCI) (HR 2.41, 95% CI 1.03–5.65, p=0.043), and postprocedure DS% (HR 1.08, 95% CI 1.05–1.11, p<0.001, per 1%), while predictors of late TLR were previous PCI (HR 9.43, 95% CI 2.58-34.52, p=0.001) and serum C-reactive protein (CRP) (HR 1.60, 95% CI 1.28-2.00, p<0.001). The ISR progression velocity (by DS%) was 12.1 ±21.0%/year and 3.7 ±10.1%/year during the first and second follow-up periods, respectively, which had no significant difference (p>0.05) between the four types of DESs. Conclusions Our data showed that predictors for TLR may be different at different time intervals. DM, pervious PCI, and postprocedure DS could predict early TLR, while previous PCI and CRP level could predict late TLR. Contemporary DESs had similar rates of ISR progression rates. Trial Registration This study was retrospectively registered and approved by the institutional review board of Seoul National University Hospital (no. 1801–138-918).
Highlights
In-stent restenosis (ISR), which is thought to be mostly caused by neointimal hyperplasia (NIH), was an important medical problem in the era of bare-metal stents (BMS) [1]
Subsequent intravascular ultrasound (IVUS) and quantitative coronary angiography (QCA) studies further strengthened the view that the main mechanism of ISR after BMS implantation was intrastent NIH [2, 3] with a biphasic change of lumen loss in the first 6 months and NIH regression between 6 months and 1–3 years after BMS implantation [4, 5]
The study flowchart is shown in Figure 1. 58 lesions in 40 patients were needed for target lesion revascularization (TLR) at the first angiographic follow-up
Summary
In-stent restenosis (ISR), which is thought to be mostly caused by neointimal hyperplasia (NIH), was an important medical problem in the era of bare-metal stents (BMS) [1]. Late TLR after BMS implantation was not a common phenomenon. Compared to BMS, DES significantly reduced the rates of ISR and TLR [6, 7]. Some studies mentioned a “late catch-up” phenomenon after the 1st generation DES implantation [8,9,10,11,12,13,14]. The “late catch-up” phenomenon suggests that the mechanism and rate of neointimal formation may be different at different time intervals. One clinical study suggested that the risk factors for late TLR were similar to those of early TLR [15]. There are few studies on predictors of both early and late TLR based on Journal of Interventional Cardiology contemporary 2nd generation DESs; the predictors are not consistent
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