Carvedilol for Prevention of Restenosis After Directional Coronary Atherectomy

Serruys, Patrick W.; Foley, David P.; Höfling, B.; Puel, Jacques; Glogar, Helmut D.; Seabra-Gomes, R; Goicolea, Javier; Coste, Pierre; Rutsch, Wolfgang; Katus, Hugo A.; Bonnier, Hans; Wijns, William; Betriu, Amadeo; Hauf-Zachariou, U.; Swijndregt, Eline Montauban van; Melkert, Rein; Simon, R.

doi:10.1161/01.cir.101.13.1512

Cited by 34 publications

(10 citation statements)

References 27 publications

(48 reference statements)

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“…45 However, it was recently shown that carvedilol treatment failed to reduce restenosis after directional coronary arthrectomy in patients with coronary artery disease. 46 In that study, carvedilol was given orally 24 hours before the procedure. Such duration might not be enough for a full vascular protection of carvedilol in vivo.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol Inhibits Tumor Necrosis Factor-α–Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells

Chen

Lin

Chen

et al. 2004

ATVB

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Objective-We tested the hypothesis that carvedilol, a ␤-adrenoceptor and ␣-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-␣ (TNF-␣)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results-Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 mol/L for 18 hours) or probucol (5 mol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-␣-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-␣-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0Ϯ2.0% and 55.60Ϯ1.0% of control, PϽ0.05, respectively) expression, whereas probucol inhibited only VCAM-1 expression (79.0Ϯ5.0% of control, PϽ0.05). Propanolol, prazosin, or both did not alter the expression of adhesion molecules. Further, pretreatment with carvedilol significantly inhibited TNF-␣-stimulated intracellular reactive oxygen species (ROS) production and the activation of redox sensitive nuclear factor kappa B and activator protein-1 transcription pathways. Conclusions-Carvedilol reduced TNF-␣-stimulated endothelial adhesiveness to human MNCs by inhibiting intracellular ROS production, transcription factor activation, and VCAM-1 as well as E-selectin expression, suggesting its potential role in clinical atherosclerosis disease. Key Words: antioxidant Ⅲ atherosclerosis Ⅲ carvedilol Ⅲ cell adhesion molecules Ⅲ endothelium I n the early phase of atherogenesis, cell surface adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and endothelial cell selectin (E-selectin) could express on endothelial cells to recruit circulating mononuclear cells (MNCs), mainly monocytes, and facilitate their binding to endothelium and migrating to subendothelial space. 1-3 Reactive oxygen species (ROS) may serve as a common intracellular messenger for various redox-sensitive transcription pathways that lead to adhesion molecule expression in vascular endothelial cells. 1,4,5 Accumulating in vitro and in vivo evidence showed that substances with antioxidant activity such as probucol and ginkgo biloba extract could scavenge intracellular ROS and inhibit endothelial adhesiveness to monocytes by reducing the expression of various adhesion molecules. 6,7 However, because of the presence of significant side effects or lack of clinical evidence, these drugs are rarely used for human atherosclerosis disease. 8 Carvedilol, 1-[carbazolyl-4-oxy]-3-[(2-methoxyphenoxyethyl)-amino]-propanol-2, a nonselective ␤-adrenoceptor antagonist with ␣1 adrenoceptor blocking and potent antioxidant activity, is currently used for treatment of hypertension or symptomatic heart failure. 9,10 Previous in vitro evidence showed that carvedilol, as an oxidant scavenger, could inhibit cardiomyocyte membrane lipid perox...

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Section: Discussionmentioning

confidence: 99%

Carvedilol Inhibits Tumor Necrosis Factor-α–Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells

Chen

Lin

Chen

et al. 2004

ATVB

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“…Embora alguns pequenos ensaios tenham apresentado resultados promissores, não existem dados convincentes de que fármacos hipolipemiantes 35,36 , agentes antitrombóticos 37 , inibidores da angiotensina 38 ou betabloqueadores 39 sejam eficazes em prevenir o crescimento neointimal. Seu insucesso foi atribuído à baixa potência antiproliferativa desses agentes associada à inadequada concentração local da droga para inibir os estágios iniciais do processo de reestenose.…”

Section: Discussionunclassified

Aplicação intracoronária de nanopartículas de paclitaxel durante intervenção percutânea para supressão da hiperplasia intimal após implante de stents não-farmacológicos

Chamié¹,

Abizaid²,

Costa³

et al. 2010

Rev. Bras. Cardiol. Invasiva

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Background: Although drug-eluting stents have proven to be highly effective in decreasing neointimal hyperplasia and its direct clinical consequence, restenosis, concerns regarding their long-term safety have led to the development of new technologies. The systemic use of antiproliferative drugs may resolve restenosis while minimizing the longterm safety issues inherent to synthetic polymers. Recently, a study investigating the intravenous administration of albumin-bound paclitaxel (ABI-007) showed that it produced a mild effect on the reduction of neointimal tissue formation. The present study was aimed at investigating, by means of serial angiography and intravascular ultrasound (IVUS), the efficacy of intracoronary ABI-007 administration in the suppression of neointimal hyperplasia after bare-metal stent implantation. Method: From November 2006 and May 2007, patients with de novo coronary lesions < 18 mm were submitted to percutaneous coronary intervention using bare-metal stents, followed by a 70 mg/m² intracoronary injection of ABI-007. Angiography and IVUS assessment was planned for all of the patients immediately after the procedure and at the six-month follow-up. The primary end-point was late lumen loss (LL) and percent neointimal volume obstruction caused by neointimal hyperplasia (IVUS) at 6 months. Results: 11 patients were included, with mean age of 58.4 ± 7.3 years, 54% were female and 18.2% diabetics. Left anterior descending artery was the most frequent vessel treated (45.5%) and most of the lesions were type A/B1 (63.7%). ABI-007 administration was well tolerated by all patients. At the 6-month follow-up, LL was

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“…Although most experimental studies and some small initial clinical studies showed promise, subsequent large randomized trials have been disappointing {Faxon, 1995, Bertrand et al, 1997, Boccuzzi et al, 1998, Serruys et al, 2000. Failure to achieve significant reduction in ISR with systemic drug therapy led to the exploration of the concept of local drug delivery.…”

Section: Treatment Of Restenosismentioning

confidence: 99%