Serial Follow-up After Optimized Ultrasound-Guided Deployment of Palmaz-Schatz Stents

Mudra, Harald; Regar, Evelyn; Klauß, Volker; Werner, F.; Henneke, Karl‐Heinz; Sbarouni, Efthia; Theisen, K.

doi:10.1161/01.cir.95.2.363

Cited by 176 publications

(45 citation statements)

References 22 publications

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“…Intravascular ultrasound has shown that the stent area remains constant during follow-up and that stents can prevent constrictive vessel remodeling. 20,21 It has been recognized that almost all stent implantations cause some tissue proliferation and neointimal hyperplasia at the stented lesion 22 and this tissue proliferation seems to be associated with genetically controlled ACE activity. 11 The increase in the late loss mainly indicates inward tissue proliferation within stented lesion and the progression of this inward remodeling in patients with the DD genotype may be associated with the higher ACE activity.…”

Section: Discussionmentioning

confidence: 99%

The DD Genotype of Angiotensin Converting Enzyme Polymorphism is a Risk Factor for Coronary Artery Disease and Coronary Stent Restenosis in Japanese Patients.

et al. 2001

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Section: Discussionmentioning

confidence: 99%

The DD Genotype of Angiotensin Converting Enzyme Polymorphism is a Risk Factor for Coronary Artery Disease and Coronary Stent Restenosis in Japanese Patients.

et al. 2001

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“…1,2 Over the past decade, both systemic pharmacological and novel mechanical treatment strategies to prevent in-stent neointimal hyperplasia have been unsuccessful. [3][4][5] Only intracoronary radiation therapy has emerged as a promising modality to attenuate the neointimal hyperplasia after stent placement.…”

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confidence: 99%

Vascular Responses at Proximal and Distal Edges of Paclitaxel-Eluting Stents

et al. 2004

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MD; for the TAXUS II Study GroupBackground-On the basis of brachytherapy experience, edge stenosis has been raised as a potential limitation for drug-eluting stents. We used serial intravascular ultrasound (IVUS) to prospectively analyze vessel responses in adjacent reference segments after implantation of polymer-controlled paclitaxel-eluting stents. Methods and Results-TAXUS II was a randomized, double-blind trial with 2 consecutive patient cohorts that compared slow-release (SR) and moderate-release (MR) paclitaxel-eluting stents with control bare metal stents (BMS). By protocol, all patients had postprocedure and 6-month follow-up IVUS. Quantitative IVUS analysis was performed by an independent core laboratory, blinded to treatment allocation, in 5-mm vessel segments immediately proximal and distal to the stent. Serial IVUS was available for 106 SR, 107 MR, and 214 BMS patients. For all 3 groups, a significant decrease in proximal-edge lumen area was observed at 6 months. The decrease was comparable (by ANOVA, Pϭ0.194) for patients in the SR (Ϫ0.54Ϯ2.1 mm 2 ) and MR (Ϫ0.88Ϯ1.9 mm 2 ) groups compared with the BMS (Ϫ1.02Ϯ1.9 mm 2 ) group. For the distal edge, a significant decrease in lumen area was only observed with BMS (Ϫ0.91Ϯ2.0 mm 2 , PϽ0.0001); this decrease was significantly attenuated with SR (0.08Ϯ2.0 mm 2 ) and MR (Ϫ0.19Ϯ1.7 mm 2 ) stents (PϽ0.0001 by ANOVA). Negative vessel remodeling was observed at the proximal (Ϫ0.48Ϯ2.2 mm 2 , Pϭ0.011) but not the distal edges of BMS and at neither edge of SR or MR stents. Conclusions-The marked reduction in in-stent restenosis with SR or MR stents is not associated with increased edge stenosis at 6-month follow-up IVUS. In fact, compared with BMS, there is instead a significant reduction in late lumen loss at the distal edge with TAXUS stents.

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“…In general, a small RVD has been shown to be an independent predictor of in-stent restenosis. 21,[36][37][38] In-stent restenosis is almost entirely due to intimal proliferation 39,40) and the amount of intimal hyperplasia and thus late loss is relatively constant and independent of stent size, 41) and this has been held responsible for the increased rate of restenosis in stented small vessels by Elezi, et al 32) who, in a large series of 2602 stented patients, found small vessel size, DM, previous PTCA, complex lesion morphology, multiple stents, DS before intervention, and a lower balloonto-vessel ratio to be independent predictors of in-stent restenosis. In an analysis by Akiyama, et al 18) baseline RVD, lesion length, and final intrastent cross-sectional area irrespective of vessel size were demonstrated to be independent predictors of in-stent restenosis.…”

Section: Discussionmentioning

confidence: 99%

<b>Early and Late Outcome of Stenting in a Consecutive Series of Patients With Coronary Lesions in Vessels Less Than 2.8 mm in Diameter</b>

et al. 2003

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SUMMARYIn an attempt to determine the early and late outcomes of small vessel stenting, we retrospectively evaluated our database on 51 consecutive patients (41 males, mean age, 57.1 ± 10.1 years) who underwent stenting of at least one significant lesion in a coronary artery with a reference vessel diameter (RVD) < 2.8 mm between March 1999 and March 2001.Sixty balloon expandable tubular stents were implanted in 57 lesions (29 Type B2/C, mean RVD: 2.54 ± 0.16 mm) without intravascular ultrasound guidance under a heparinaspirin-ticlopidine regimen. The mean diameter stenosis (DS) decreased from 75.8 ± 13.6% to 4.2 ± 1.9% (P < 0.0001) with stenting at a mean deployment pressure of 13.6 ± 1.7 atm and a final balloon to RVD ratio (FB/RVD) of 1.08 ± 0.03. All stents were deployed successfully. Acute stent thrombosis occurred in 3 patients (6%), one died, and 2 developed non-Q-wave myocardial infarction (procedural success 94%). Clinical follow-up, available in 48 patients, revealed a 29% target lesion revascularization rate, a 2% myocardial infarction rate, and a 71% event-free survival at a mean of 11.6 months. Angiographic follow-up, available in 40 patients, showed a DS of 48.8 ± 31.3% and a binary restenosis rate of 50% at a mean of 7.7 months. The FB/RVD ratio was significantly lower in the group with restenosis than in the group without (1.06 ± 0.02 vs 1.1± 0.05, P = 0.04). Subgroup analysis yielded a significantly greater rate of restenosis in diabetics with complex (Type B2/C) lesion morphology compared to nondiabetics with simple (Type A/B1) lesions (75% vs 21%, P < 0.05).In conclusion, stenting in vessels < 2.8 mm was found to be associated with a high rate of acute stent thrombosis and in-stent restenosis. Further analysis detected a subgroup of patients without diabetes or complex lesions who could be stented with an acceptable in-stent restenosis rate. (Jpn Heart J 2003; 44: 163-177)

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Serial Follow-up After Optimized Ultrasound-Guided Deployment of Palmaz-Schatz Stents

Cited by 176 publications

References 22 publications

The DD Genotype of Angiotensin Converting Enzyme Polymorphism is a Risk Factor for Coronary Artery Disease and Coronary Stent Restenosis in Japanese Patients.

The DD Genotype of Angiotensin Converting Enzyme Polymorphism is a Risk Factor for Coronary Artery Disease and Coronary Stent Restenosis in Japanese Patients.

Vascular Responses at Proximal and Distal Edges of Paclitaxel-Eluting Stents

<b>Early and Late Outcome of Stenting in a Consecutive Series of Patients With Coronary Lesions in Vessels Less Than 2.8 mm in Diameter</b>

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