Late Lumen Loss After Coronary Angioplasty Is Associated With the Activation Status of Circulating Phagocytes Before Treatment

Pietersma, Anneke; Kofflard, Marcel; Wit, L. Elly A. de; Stijnen, Theo; Koster, J.F.; Serruys, Patrick W.; Sluiter, Wim J.

doi:10.1161/01.cir.91.5.1320

Cited by 131 publications

(79 citation statements)

References 25 publications

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“…Most systemic pharmacological therapies have been unsuccessful in preventing arterial restenosis in humans, and the preliminary results of drug-eluting stents are remarkable in reducing in-stent restenosis. Nevertheless, LBPs offer a systemic therapy to a systemic process, 4,32 regardless of the procedure and the device(s) used. If effective in a clinical setting, it may be an easily adminis-tered, cost-effective modality that allows flexibility in choosing the type and number of stents to be deployed, may serve as an adjunct therapy in high-risk patients, and may even reduce the need for stenting altogether.…”

Section: Danenberg Et Al Liposomal Alendronate Inhibits In-stent Restmentioning

confidence: 99%

“…1,2 Macrophage content in atherectomy tissue and activation status of blood monocytes correlate with an increased rate of restenosis in humans. 3,4 We recently showed that transient macrophage depletion reduces experimental neointimal formation after balloon injury in rats and rabbits. 5 Stent deployment profoundly alters vascular repair, and the role of innate immunity in late restenosis is further stressed.…”

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confidence: 99%

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Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

et al. 2003

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Background-Innate immunity is of major importance in vascular repair. The present study evaluated whether systemic and transient depletion of monocytes and macrophages with liposome-encapsulated bisphosphonates inhibits experimental in-stent neointimal formation. Methods and Results-Rabbits fed on a hypercholesterolemic diet underwent bilateral iliac artery balloon denudation and stent deployment. Liposomal alendronate (3 or 6 mg/kg) was given concurrently with stenting. Monocyte counts were reduced by Ͼ90% 24 to 48 hours after a single injection of liposomal alendronate, returning to basal levels at 6 days. This treatment significantly reduced intimal area at 28 days, from 3.88Ϯ0.93 to 2.08Ϯ0.58 and 2.16Ϯ0.62 mm 2 . Lumen area was increased from 2.87Ϯ0.44 to 3.57Ϯ0.65 and 3.45Ϯ0.58 mm 2 , and arterial stenosis was reduced from 58Ϯ11% to 37Ϯ8% and 38Ϯ7% in controls, rabbits treated with 3 mg/kg, and rabbits treated with 6 mg/kg, respectively (meanϮSD, nϭ8 rabbits/group, PϽ0.01 for all 3 parameters). No drug-related adverse effects were observed. Reduction in neointimal formation was associated with reduced arterial macrophage infiltration and proliferation at 6 days and with an equal reduction in intimal macrophage and smooth muscle cell content at 28 days after injury. Conversely, drug regimens ineffective in reducing monocyte levels did not inhibit neointimal formation. Conclusions-Systemic

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Section: Danenberg Et Al Liposomal Alendronate Inhibits In-stent Restmentioning

confidence: 99%

mentioning

confidence: 99%

Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

et al. 2003

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“…Several studies have supported the critical role of inflammation in this process. There are some animal and human studies implicating pre-exiting inflammation in the development of restenosis (10)(11)(12). Current study excluded patients with infectious and active inflammatory diseases (rheumatoid arthritis, inflammatory bowel disease, etc).…”

Section: Discussionmentioning

confidence: 99%

An important role for VCAM-1, but not for ICAM-1 in restenosis following coronary stent implantation

Bayata¹,

Arıkan²,

Yeşìl³

et al. 2010

Anadolu Kardiyol Derg

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Amaç: Bu çalışmada stabil koroner arter hastalığı nedeni ile stent implante edilen olgularda, adezyon moleküllerinin seviyesi ile restenoz arasındaki ilişki araştırılmıştır. Yöntemler: Stabil angina pectoris nedeni ile proksimal sol ön inen artere stent implante edilen 15 olguda işlem öncesi ve sonrasında dolaşım-daki hücreler arası adezyon molekül-1 (ICAM-1) ve vasküler hücre adezyon molekül -1 (VCAM-1) seviyeleri prospektif gözlemsel olarak araştı-rılmıştır. Hastalarda çıplak metal stent kullanılmıştır. Tüm hastalara restenoz değerlendirmesi amacı ile tespiti için implantasyonun 6. ayında tekrar koroner anjiyografi yapıldı. Çalışma sonunda restenoz saptanan ve saptanmayan hastalara ait sürekli değişkenler Mann-Whitney U testi ile karşılaştırıldı. Tekrarlanan ölçümlere ait sürekli değişkenlerin karşılaştırılmasında Wilcoxon T testi kullanıldı. Kategorik veriler ise Ki-kare testi ile karşılaştırıldı. Bulgular: Perkütan koroner girişim (PKG) öncesi bazal ICAM-1 ve VCAM-1 konsantrasyonları sırası ile 4.89±2.28 ve 46.35±22.96 ng/ml bulunmuş-tur. Ölçülen ICAM-1 ve VCAM-1 seviyeleri PKG' den 24 saat sonra istatistik olarak anlamsız derecede artış göstermiştir (5.01±2.35ng/ml ve 52.57±19.40 ng/ml). Altı olguda (%40) 6. ayda restenoz tespit edilmiştir. Restenoz gelişen ve gelişmeyen hasta grupları arasında ortalama stent uzunluğu, çapı ve balon şişme basıncı bakımından fark bulunmamıştır. Stent implantasyonundan önce ve sonra ölçülen VCAM değerleri restenoz olmayan grupta anlamlı değişiklik göstermemiş, bununla birlikte restenoz grubunda anlamlı artış göstermiştir (45.1±21.0' den 57.2±14.3 ng/ml'ye, p<0.05). Bazal ve post PKG ICAM-1 değerleri restenoz olan ve olmayan gruplarda anlamlı değişiklik göstermemiştir. Sonuç: Bu sonuçlar koroner stent implantasyonunu takip eden restenozda adezyon moleküllerinden ICAM-1'e göre VCAM-1'in daha önemli rolü olduğunu düşündürmektedir. (Anadolu Kardiyol Derg 2010; 10: 405-9) Anahtar kelimeler: Restenoz, stent, inflamasyon, vasküler hücre adezyon molekül -1, hücreler arası adezyon molekül-1 ÖZET Objective: In this study, we evaluated the possibility that, levels of circulating adhesion molecules following direct stent implantation may be a marker of restenosis. Methods: This prospective, observational study investigated levels of circulating intercellular (ICAM-1), and vascular cell (VCAM-1) adhesion molecules in 15 patients with stable angina pectoris before and after coronary stent implantation for single vessel-single lesion disease in proximal left anterior descending artery. All patients received bare-metal stents. Patients underwent repeat coronary angiography for detection of restenosis at 6 month. Continuous data between patients with and without restenosis were compared using Mann-Whitney U test. Repeated measurements were compared using Wilcoxon T test. Categorical data were compared using Chi-square statistics. Results: Baseline ICAM-1 and VCAM-1 concentrations before percutaneous coronary intervention (PCI) were 4.89±2.28 and 46.35±22.96 ng/ml respectively. Levels of ICAM ...

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“…[6][7][8] Percutaneous transluminal coronary angioplasty (PTCA) with or without stent implantation is an established revascularization procedure; however, restenosis rates still range between 30-60% 6 and 15-30%, 7 respectively Preprocedural identification of low-and high-risk patients who might benefit from additional procedures 6,8 would be desirable. However, the predictors of early [7][8][9][10] and late complications [11][12][13][14][15] have a low predictive value, [15][16][17][18] are available only after procedures, 9,14 or are not easily applicable in clinical practice. 10,12,13 Inconsistent and weak correlation with early complications following PTCA was reported for female gender, extreme age, diabetes, multivessel disease, lesion characteristics, and hemostatic variables.…”

Section: Introductionmentioning

confidence: 99%

The relation between preprocedural C‐reactive protein levels and early and late complications in patients with acute myocardial infarction undergoing interventional coronary angioplasty

Magadle

Hertz²,

Merlon³

et al. 2004

Clinical Cardiology

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SummaryBackground: Inflammation is an important feature of arteriosclerotic disease, and the vulnerability of coronary plaques in acute myocardial infarction (AMI) may be related to the levels of serum C-reactive proteins (CRP). While some risk factors for early and late complications have been suggested, an accurate and definitive preprocedural risk stratification of patients undergoing percutaneous transluminal coronary angioplasty (PTCA) is still lacking.Hypothesis: The study was undertaken to investigate whether early and late complications after PTCA could be predicted by evaluation of baseline serum CRP levels in patients with AMI.Methods: Levels of serum CRP were measured in a total of 230 patients with AMI undergoing PTCA and provisional stent. They were divided into two groups: Group 1 (n = 48) with elevated CRP levels (≥ 5 mg/l) and Group 2 (n = 182) with normal CRP levels (< 5 mg/l).Results: There were no significant differences in baseline clinical, angiographic, and procedural characteristics between the two groups. However, the incidence of in-hospital adverse coronary events (reinfarction, coronary reocclusion, target vessel revascularization, and death) and severe left ventricular dysfunction was significantly higher in Group 1 (18.3 vs. 6.1%,

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Late Lumen Loss After Coronary Angioplasty Is Associated With the Activation Status of Circulating Phagocytes Before Treatment

Abstract: Background The purpose of this pilot study was to identify biological risk factors for restenosis after percutaneous transluminal coronary angioplasty (PTCA) to predict the long-term outcome of PTCA before treatment.

Cited by 131 publications

References 25 publications

Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

An important role for VCAM-1, but not for ICAM-1 in restenosis following coronary stent implantation

The relation between preprocedural C‐reactive protein levels and early and late complications in patients with acute myocardial infarction undergoing interventional coronary angioplasty

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