The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions

Pons, Douwe; Monraats, Pascalle S.; Maat, Moniek P.M. de; Pires, Nuno; Quax, Paul H.A.; Vlijmen, Bart J.M. van; Rosendaal, Frits R.; Zwinderman, Aeilko H.; Doevendans, Pieter A.; Waltenberger, Johannes; Winter, Robbert J. de; Tio, René A.; Frants, Rune R.; Laarse, Arnoud van der; Wall, Ernst E. van der; Jukema, J. Wouter

doi:10.1160/th07-04-0301

Cited by 11 publications

(4 citation statements)

References 39 publications

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“…Among other prothrombotic polymorphisms, factor V G1691A and PAI-1 4G5G may also play a role in the process of restenosis after PTCA. The PAI-1 4G variant was associated with an increased risk of restenosis after this procedure in contrast to factor V G1691A, which decreased the risk [42]. As far as we know, there has been no studies on the association of GPIIIa T1565C, factor II G20210A, factor XII C46T, and PAI-1 4G5G polymorphism with restenosis/reocclusion after PTA.…”

Section: Hemostasismentioning

confidence: 89%

Is Restenosis/Reocclusion after Femoropopliteal Percutaneous Transluminal Angioplasty (PTA) the Consequence of Reduced Blood Flow, Inflammation, and/or Hemostasis Disturbances?

Mijovski¹,

Boc²,

Salapura³

et al. 2015

Thrombosis, Atherosclerosis and Atherothrombosis - New Insights and Experimental Protocols

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Percutaneous transluminal angioplasty PTA is an established method for treatment of peripheral artery disease PAD of the femoropopliteal artery. However, in up to % of patients restenosis and/or reocclusion remain a frequent complication occurring in the first year after the procedure. In this study, we focused on the influence of compromised postprocedural infrapopliteal runoff of the affected limb, on the hypercoagulability as detected by a global hemostasis assay and on genetic predisposition to hypercoagulability and on the regulation of the inflammation through the nuclear receptor related protein NuRR . Consecutive PAD patients treated by femoropopliteal PTA because of disabling claudication or critical limb ischemia were followed up by vascular ultrasound imaging at , , and months after the procedure. Venous blood samples for hemostasis, inflammation, and gene analysis were obtained before and h after PTA. One month after femoropopliteal PTA, % of patients with compromised runoff developed the combined end point restenosis/reocclusion in comparison to % with good runoff p = . . After months, the differences were no longer significant. It was concluded that compromised postprocedural infrapopliteal runoff predisposes to early restenosis/reocclusion after femoropopliteal PTA and that the deterioration of infrapopliteal runoff in the year after femoropopliteal PTA is accompanied by worsening of long-term femoropopliteal patency. Patients were genotyped for the prothrombotic gene polymorphisms platelet receptor glycoprotein IIIa T C, coagulation factor V G A, coagulation factor II G A, coagulation factor XII C -T, and plasminogen activator inhibitor-G G. We were not able to show any association between these polymorphisms and the restenosis/reocclusion rate in patients treated with femoropopliteal PTA. Furthermore, no association between thrombin generation and reste-

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Section: Hemostasismentioning

confidence: 89%

Is Restenosis/Reocclusion after Femoropopliteal Percutaneous Transluminal Angioplasty (PTA) the Consequence of Reduced Blood Flow, Inflammation, and/or Hemostasis Disturbances?

Mijovski¹,

Boc²,

Salapura³

et al. 2015

Thrombosis, Atherosclerosis and Atherothrombosis - New Insights and Experimental Protocols

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“…Варіант PAI-1 4G був пов'язаний з підвищеним ризиком повторної реваскуляризації протягом року. Порівняно з гомозиготами 5G/5G, гетерозиготні пацієнти мали більший ризик розвитку рестенозу (ВШ 1,46; 95 % ДІ 1,05-2,03), тоді як пацієнти з генотипом 4G/4G мали ще більший ризик (ВШ 1,69; 95 % ДІ 1, 41). На відміну від цього, амінокислотна заміна фактора V 506Gln (фактор V Лейдена) була пов'язана зі зниженим ризиком розвитку рестенозу (ВШ 0,41; 95 % ДІ 0,19-0,86) протягом періоду спостереження [41].…”

Section: роль внутрішньосудинних зображеньunclassified

Causes and risk factors for stent restenosis in patients after percutaneous coronary interventions

Kopytsya¹,

Kutya²,

Rodionova³

et al. 2023

CSIC

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Percutaneous coronary intervention (PCI) is one of the main components in the treatment of the coronary artery disease (CAD) and especially its acute forms. Nevertheless, restenosis of stented coronary arteries, which significantly worsens the course of CAD, remains a significant clinical problem of this technology. Prevention of this complication requires a modern understanding of the complex pathogenetic mechanisms of restenosis. Based on the literature data, the frequency of restenosis development in stents with medical coatings is in the range from 3 to 20 %. The mechanism of restenosis is multifactorial and includes biological, mechanical, and genetic factors. The main mechanical causes are insufficient expansion of the stent or its destruction, and biological factors include local inflammation, leading to aggressive neointimal proliferation and late neoatherosclerosis. The search for genetic factors and possibilities of influence on the development of this complication is still ongoing. Intracoronary imaging is crucial for identifying mechanisms of restenosis and selecting individual therapy.

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“…Despite the introduction of (drug-eluting) stents, this problem remains in part of the patients. Endothelial injury during PCI promotes leukocyte attachment and extravasation [ 1 , 3 , 5 ]. Subsequently, leukocytes and vascular smooth muscle cells (vSMCs) produce pro-inflammatory cytokines which lead to vSMC migration, proliferation and extracellular matrix formation [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

The epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia development

et al. 2017

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ObjectiveGenetic P300/CBP-associated factor (PCAF) variation affects restenosis-risk in patients. PCAF has lysine acetyltransferase activity and promotes nuclear factor kappa-beta (NFκB)-mediated inflammation, which drives post-interventional intimal hyperplasia development. We studied the contributing role of PCAF in post-interventional intimal hyperplasia.Methods and resultsPCAF contribution to inflammation and intimal hyperplasia was assessed in leukocytes, macrophages and vascular smooth muscle cells (vSMCs) in vitro and in a mouse model for intimal hyperplasia, in which a cuff is placed around the femoral artery. PCAF deficiency downregulate CCL2, IL-6 and TNF-alpha expression, as demonstrated on cultured vSMCs, leukocytes and macrophages. PCAF KO mice showed a 71.8% reduction of vSMC-rich intimal hyperplasia, a 73.4% reduction of intima/media ratio and a 63.7% reduction of luminal stenosis after femoral artery cuff placement compared to wild type (WT) mice. The association of PCAF and vascular inflammation was further investigated using the potent natural PCAF inhibitor garcinol. Garcinol treatment reduced CCL2 and TNF-alpha expression, as demonstrated on cultured vSMCs and leukocytes.To assess the effect of garcinol treatment on vascular inflammation we used hypercholesterolemic ApoE*3-Leiden mice. After cuff placement, garcinol treatment resulted in reduced arterial leukocyte and macrophage adherence and infiltration after three days compared to untreated animals.ConclusionsThese results identify a vital role for the lysine acetyltransferase PCAF in the regulation of local inflammation after arterial injury and likely the subsequent vSMC proliferation, responsible for intimal hyperplasia.

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The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions

Cited by 11 publications

References 39 publications

Is Restenosis/Reocclusion after Femoropopliteal Percutaneous Transluminal Angioplasty (PTA) the Consequence of Reduced Blood Flow, Inflammation, and/or Hemostasis Disturbances?

Is Restenosis/Reocclusion after Femoropopliteal Percutaneous Transluminal Angioplasty (PTA) the Consequence of Reduced Blood Flow, Inflammation, and/or Hemostasis Disturbances?

Causes and risk factors for stent restenosis in patients after percutaneous coronary interventions

The epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia development

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