Effect of short-term prostacyclin administration on restenosis after percutaneous transluminal coronary angioplasty

Knudtson, Merril L.; Flintoft, Virginia; Roth, David L.; Hansen, James L.; Duff, Henry J.

doi:10.1016/0735-1097(90)90648-9

Cited by 91 publications

(12 citation statements)

References 35 publications

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“…Several therapeutic strategies aimed to enhance PGI 2 production and successfully reduced restenosis in different animal models [31–33]. However, available data from clinical trials are conflicting and currently do not support the concept that PGI 2 or stable mimetics may be successfully used to suppress restenosis after PTCA [34,35]. These findings may be explained, at least partly, by IP‐R long‐term desensitization.…”

Section: Resultsmentioning

confidence: 99%

Agonist‐induced long‐term desensitization of the human prostacyclin receptor

et al. 2000

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Phosphorylation of the human prostacyclin (PGI 2 ) receptor (hIP-R) by diacylglycerol-regulated protein kinase C (PKC) has been reported to be responsible for its rapid desensitization in HEK293 cells. In this study we demonstrate, that human fibroblasts reveal a much slower hIP-R desensitization kinetics, which was neither affected by stimulation nor inhibition of PKC by either phorbol 12-myristate-13-acetate or GF-109203X suggesting a different cellular mechanism. Although agonist-promoted sequestration of a C-terminally green fluorescent protein-tagged hIP-R was demonstrated, it did not account for the long-term desensitization. Concanavalin A did not abolish, but accelerated receptor desensitization kinetics. Resensitization of hIP-R involved receptor recycling and/or de novo synthesis of receptor protein, depending on the duration of prior desensitization. This is the first study investigating the mechanisms of hIP-R desensitization in intact human cells naturally expressing hIP-R. Our data suggest, that a hitherto unknown mechanism of hIP-R long-term desensitization, which is independent of receptor phosphorylation by conventional and novel type PKC isoforms or endocytosis, is a key event in regulating the cellular responsiveness to PGI 2 . ß

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Section: Resultsmentioning

confidence: 99%

Agonist‐induced long‐term desensitization of the human prostacyclin receptor

et al. 2000

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“…16,17) In addition to its antiplatelet effect, aspirin has anti-inflammatory activity that may contribute to its clinical effectiveness in preventing serious vascular events, and also reduces the frequency of ischemic complication after PCI. 12,13,18,19) Moreover, in experimental studies, other mechanisms have been proposed to explain the long-term reduction in mortality due to coronary artery disease. One of the mechanisms is that aspirin improves endothelial dysfunction in artherosclerotic vessels.…”

Section: Discussionmentioning

confidence: 99%

Impact of Aspirin Treatment on Long-Term Outcome (Over 10Years) After Percutaneous Coronary Intervention

et al. 2006

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SUMMARYAspirin has been shown to reduce cardiovascular morbidity and mortality following percutaneous coronary intervention (PCI). However, its effects on long-term (over 10years) mortality have not been fully elucidated.This retrospective study recorded the patient characteristics and admission medication for all patients undergoing PCI over an 8-year period from 1984 to 1992. Follow-up information was available for 748 patients (100%) for a mean of 143.6 ± 43.4 months. A propensity analysis was performed to adjust for presumed selection biases in the administration of aspirin.The baseline clinical characteristics were similar between the group that received aspirin and the group that did not, except for the administration of statins and PCI procedural success rate. Of the 748 patients, 535 (71.5%) received aspirin treatment at the time of PCI. During the 12-year follow-up, 54 patients died from any cause and 20 patients from cardiac death. Kaplan-Meier analysis showed that aspirin treatment led to a significant reduction in all cause mortality (10% versus 16.4%; P = 0.01) and cardiac death (3.7% versus 8.0%; P = 0.02) compared to other antiplatelet drugs. The hazard ratio (HR) for the total mortality and cardiac mortality rates was adjusted using the Cox-proportional hazard model for confounding variables and propensity score. The all cause (HR, 0.49;, P = 0.005) and cardiac mortality rates (HR, 0.32;, P = 0.006) for patients receiving aspirin remained lower than for those not receiving aspirin.Aspirin treatment at the time of PCI significantly reduced the risk of death from any cause and cardiac death. The administration of aspirin had a positive impact on the over 10-year long-term outcomes of patients who underwent PCI. (Int Heart J 2006; 47: 37-45)

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“…Numerous pharmacological strategies have been tested in the prevention of restenosis mainly after conventional PTCA but also after stent implantation, and these include the following: antiproliferative drugs (colchicine, lanreotide) [21][22][23] calcium channel antagonists (nifedipine, diltiazem) [24,25] fish oil, [26][27][28] heparin, [29] low molecular weight heparin (enoxaparin sodium), [30] lipidlowering drugs (lovastatin), [31,32] prostacyclin analogs (epoprostenol, ciprostene), [33,34] serotonin (5-HT 2 ) receptor antagonists (ketanserin) [35] and thromboxane inhibitors (aspirin) [acetylsalicylic acid], sulotroban, vapiprost. [36,37] In the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) trial the positive effect of abciximab, a platelet glycoprotein IIb/IIIa antagonist, was restricted to patients with diabetes mellitus.…”

Section: Concepts For Preventing Restenosismentioning

confidence: 99%

Can Angiotensin Receptor Antagonists Prevent Restenosis After Stent Placement?

Peters

2002

American Journal of Cardiovascular Drugs

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Restenosis rates after coronary stent implantation in complex lesions are between 30 and 50%. Neointimal hyperplasia promoted by complex interaction between cellular and acellular elements, such as cytokines and growth factors, is thought to be the primary process responsible for restenosis. The risk of in-stent restenosis is increased in patients with a history of restenosis after percutaneous transluminal coronary angioplasty, in long lesions, in total occlusions, in patients with diabetes mellitus, in small vessels, in the proximal parts of the left anterior descending coronary artery and in cases of stent oversizing. In-stent restenosis represents a serious economic burden on society because treatment strategies include expensive approaches such as cutting-balloon angioplasty, rotational atherectomy and brachytherapy. A number of pharmacological agents, including ACE inhibitors, have been unsuccessful in preventing restenosis. Alternative procedures such as brachytherapy, radioactive stents and drug-eluting stents are under evaluation. Although sirolimus- or paclitaxel-eluting stents have been associated with very low restenosis rates over durations of 6 to 12 months, the long-term efficacy and tolerability of this approach is currently being investigated. Although ACE inhibitors have failed in reducing restenosis rates, the selective angiotensin II type 1 (AT(1)) receptor antagonist valsartan has shown encouraging results in the single-center Valsartan for Prevention of Restenosis after Stenting of Type B2/C lesions trial (ValPREST). The ValPREST trial is the first randomized, placebo-controlled study to have evaluated the effect of an angiotensin receptor antagonist on in-stent restenosis in a moderate number of patients. Compared with ACE inhibitors, angiotensin receptor blockers exert additional effects on the pathophysiological processes which lead to restenosis. Angiotensin receptor antagonists may affect several mechanisms involved in neointimal hyperplasia such as decreasing circulating cytokine and growth factor levels and reducing neutrophil activation, especially after stenting in acute coronary syndromes, but the results need to be confirmed in a large multicenter trial. The question whether long-term therapy, with an oral angiotensin receptor antagonist, is cost-effective and whether angiotensin receptor antagonists should be used as an add-on therapy to drug-eluting stents, requires clarification.

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Effect of short-term prostacyclin administration on restenosis after percutaneous transluminal coronary angioplasty

Cited by 91 publications

References 35 publications

Agonist‐induced long‐term desensitization of the human prostacyclin receptor

Agonist‐induced long‐term desensitization of the human prostacyclin receptor

Impact of Aspirin Treatment on Long-Term Outcome (Over 10Years) After Percutaneous Coronary Intervention

Can Angiotensin Receptor Antagonists Prevent Restenosis After Stent Placement?

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