Effect of ACE inhibitors on angiographic restenosis after coronary stenting (PARIS): a randomised, double-blind, placebo-controlled trial

Meurice, Thibaud; Bauters, Christophe; Hermant, Xavier; Codron, Valérie; VanBelle, Eric; Fadden, Eugène P. Mc; Lablanche, Jean‐Marc; Bertrand, Michel E.; Amouyel, Philippe

doi:10.1016/s0140-6736(00)04518-9

Cited by 91 publications

(52 citation statements)

References 18 publications

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“…Therapeutic success is also dependent on achieving adequate delivery of the therapy at the site of interest. Many drugs, which have shown promising results in in vitro and preclinical animal trials, have proved to be ineffective for decreasing restenosis rates after PCI in humans, largely due to the requirement for systemic administration (84)(85)(86)(87)(88)(89)(90)(91)(92)(93). Discrepancies in efficacy between animal studies and human trials may also be due to species differences in the response to vascular injury or the inability to achieve adequate drug concentrations at the target vascular site in human patients.…”

Section: Targeting the Cell Cycle To Inhibit Vascular Proliferative Dmentioning

confidence: 99%

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

Charron

Nili

Strauss

2006

Canadian Journal of Cardiology

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Section: Targeting the Cell Cycle To Inhibit Vascular Proliferative Dmentioning

confidence: 99%

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

Charron

Nili

Strauss

2006

Canadian Journal of Cardiology

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“…4 -6 Many therapies to prevent or treat restenosis after stent implantation have been evaluated, [7][8][9][10][11][12] including systemic pharmacological approaches that have failed, possibly because of insufficient local drug concentration. [13][14][15][16] …”

mentioning

confidence: 99%

Non–Polymer-Based Paclitaxel-Coated Coronary Stents for the Treatment of Patients With De Novo Coronary Lesions

et al. 2004

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; for the DELIVER Clinical Trial InvestigatorsBackground-Paclitaxel, a microtubule-stabilizing compound with potent antitumor activity, has been shown to inhibit smooth muscle cell proliferation and migration. The DELIVER trial was a prospective, randomized, blinded, multicenter clinical evaluation of the non-polymer-based paclitaxel-coated ACHIEVE stent compared with the stainless steel Multi-Link (ML) PENTA stent. Methods and Results-A total of 1043 patients with focal de novo coronary lesions, Ͻ25 mm in length, in 2.5-to 4.0-mm vessels were randomized (ACHIEVE nϭ524; ML PENTA nϭ519). Angiographic follow-up was performed in a subset of 442 patients (ACHIEVE nϭ228; ML PENTA nϭ214). Prespecified end points were a 40% reduction in target-vessel failure at 9 months (primary clinical end point) and a 50% reduction in binary restenosis at 8 months (major secondary end point). Baseline clinical characteristics were comparable between the groups. Patients in ACHIEVE had more type C lesions and a larger reference diameter. At follow-up, stent late loss was 0.81 versus 0.98 mm (Pϭ0.003), stent binary restenosis was 14.9% versus 20.6% (Pϭ0.076), and target-vessel failure was 11.9% versus 14.5% (Pϭ0.12) for ACHIEVE and ML PENTA, respectively. Conclusions-The ACHIEVE paclitaxel-coated stent decreased neointimal proliferation compared with the bare-metal PENTA stent; however, this reduction was insufficient to meet the prespecified primary end point of target-vessel failure and the secondary end point of binary restenosis.

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“…23) In contrast, another study reported that ACE inhibitors worsened in-stent restenosis in patients with the DD genotype of ACE polymorphism. 7) Thus, it remains controversial whether ACE inhibitors reduce in-stent restenosis in clinical situations, though our results suggested that they may have exacerbated it, apparently irrespective of the type of ACE gene polymorphism. The precise mechanism(s) by which the ACE inhibitors promoted in-stent restenosis was beyond the scope of this study.…”

Section: Effect Of Basal Antiplatelet Treatmentmentioning

confidence: 65%

“…It is also possible that ACE inhibitors actually promote tissue inflammation through the inhibition of kinin degradation. 7) An increase in tissue chymase activity is another possible mechanism. In human atherosclerotic tissue, the major angiotensin II-forming enzyme may be chymase rather than ACE.…”

Section: Effect Of Basal Antiplatelet Treatmentmentioning

confidence: 99%

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Effects of Angiotensin-Converting Enzyme Inhibitors or an Angiotensin Receptor Blocker in Combination With Aspirin and Cilostazol on In-stent Restenosis

et al. 2006

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SUMMARYIt remains to be determined whether adding an angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin II receptor blocker (ARB) to antiplatelet therapy has a therapeutic benefit on in-stent restenosis.After successful coronary stenting, 165 patients (167 lesions) were randomly assigned to a basal (aspirin 162 mg + cilostazol 200 mg/day), ACEI (basal treatment + quinapril 10 mg or perindopril 4 mg/day), or ARB (basal treatment + losartan 50 mg/day) treatment group. Quantitative coronary angiography was performed before, immediately following, and 6 months after stenting. Follow-up coronary angiography was completed in 126 patients (128 lesions). Restenosis rates tended to be higher (12, 26, and 12% for the basal, ACEI, and ARB groups, respectively), and target lesion revascularization rates were higher in the ACEI group than in the other groups (9, 23,* and 5%, respectively, *P < 0.05 versus basal group). Moreover, late lumen loss was higher in the ACEI group than in the basal group (0.60 ± 0.55, 0.98 ± 0.61* and 0.73 ± 0.64 mm in the basal, ACEI, and ARB groups, respectively).The combinations of an ACEI or ARB with aspirin and cilostazol are ineffective for the prevention of in-stent restenosis, and an ACEI may even promote intimal proliferation after stent implantation. (Int Heart J 2006; 47: 173-184)

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Effect of ACE inhibitors on angiographic restenosis after coronary stenting (PARIS): a randomised, double-blind, placebo-controlled trial

Cited by 91 publications

References 18 publications

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

Non–Polymer-Based Paclitaxel-Coated Coronary Stents for the Treatment of Patients With De Novo Coronary Lesions

Effects of Angiotensin-Converting Enzyme Inhibitors or an Angiotensin Receptor Blocker in Combination With Aspirin and Cilostazol on In-stent Restenosis

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