Comparison of sirolimus-eluting and bare metal stents in coronary bifurcation lesions: Subgroup analysis of the Stenting Coronary Arteries in Non-Stress/Benestent Disease Trial (SCANDSTENT)

Thuesen, Leif; Kelbæk, Henning; Kløvgaard, Lene; Helqvist, Steffen; Jørgensen, Erik; Aljabbari, Samir; Krusell, Lars Romer; Jensen, Gunnar V.H.; Bøtker, Hans Erik; Saunamäki, Kari; Lassen, Jens Flensted; Weert, Anton van

doi:10.1016/j.ahj.2006.06.035

Cited by 78 publications

(45 citation statements)

References 23 publications

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“…Inflammatory cells and SMC within lesions are important local sources of proangiogenic factors (21). Not surprisingly, antifibrotic/antiangiogenic agents like rapamycin decrease neointimal hyperplasia in coronary artery stents (31,40,41). The pathological processes involved in vascular disease parallel many of the cellular/molecular events that mediate normal WH/AG.…”

Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Secretome Contains Factors That Induce Angiogenesis and Wound Healing

Dumortier

Streblow

Moses

et al. 2008

J Virol

102

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Human cytomegalovirus (HCMV) is implicated in the acceleration of a number of vascular diseases including transplant vascular sclerosis (TVS), the lesion associated with chronic rejection (CR) of solid organ transplants. Although the virus persists in the allograft throughout the course of disease, few cells are directly infected by CMV. This observation is in contrast to the global effects that CMV has on the acceleration of TVS/CR, suggesting that CMV infection indirectly promotes the vascular disease process. Recent transcriptome analysis of CMV-infected heart allografts indicates that the virus induces cytokines and growth factors associated with angiogenesis (AG) and wound healing (WH), suggesting that CMV may accelerate TVS/CR through the induction and secretion of AG/WH factors from infected cells. We analyzed virus-free supernatants from HCMV-infected cells (HCMV secretomes) for growth factors, by mass spectrometry and immunoassays, and found that the HCMV secretome contains over 1,000 cellular proteins, many of which are involved in AG/WH. Importantly, functional assays demonstrated that CMV but not herpes simplex virus secretomes not only induce AG/WH but also promote neovessel stabilization and endothelial cell survival for 2 weeks. These findings suggest that CMV acceleration of TVS occurs through virus-induced growth factors and cytokines in the CMV secretome.Numerous epidemiological and animal studies link human cytomegalovirus (HCMV) to the acceleration of vascular diseases including arterial restenosis, atherosclerosis, and transplant vascular sclerosis (TVS) (23,24,37). Recent advances in transplantation have significantly impacted short-term allograft and patient survival; however, long-term graft survival has not improved, due largely to chronic rejection (CR). The prevalence of CR is a concern, since retransplantation is the sole effective therapy. TVS represents the hallmark of CR in vascularized solid organ transplants, and HCMV infection nearly doubles the 5-year rate of cardiac graft failure due to accelerated TVS (11). In heart transplant recipients, ganciclovir, a potent inhibitor of CMV replication, delays the time to allograft rejection (25, 44). A higher incidence of viral DNA in the explant vascular intima from patients with cardiac allograft TVS than in explants without vasculopathy further underscores the influence of HCMV on CR development (47). In kidney transplant patients, the presence of HCMV infection, whether asymptomatic or displaying overt symptoms, negatively impacts allograft survival (9). The role of HCMV in TVS/CR development is clear; however, the mechanisms involved in this process remain illusive for the following reasons: HCMV disease etiology is multifactorial; HCMV is ubiquitous throughout the human population; HCMV infection is lifelong and infects all of the cell types involved in TVS, including smooth muscle cells (SMC), endothelial cells (EC), and macrophages; and HCMV evades the immune system by remaining latent, and clinically silent reactivation is diffic...

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Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Secretome Contains Factors That Induce Angiogenesis and Wound Healing

Dumortier

Streblow

Moses

et al. 2008

J Virol

102

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“…82 These stents were superior to any bare metal stent available. 83 Stents releasing January 30, 2015…”

Section: Stent-based Delivery Of Rapamycin and Rapalogsmentioning

confidence: 99%

Autophagy in Vascular Disease

Meyer

Grootaert

Michiels

et al. 2015

Circulation Research

245

179

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A utophagy is a complex intracellular process that delivers cytoplasmic constituents for degradation into lysosomes.1,2 Three main types of autophagy have been described: (1) microautophagy, comprising direct engulfment of cytoplasmic material by lysosomes via inward invaginations of the lysosomal membrane, (2) macroautophagy, characterized by formation of double-membrane sequestering compartments termed autophagosomes that fuse with lysosomes for delivery of cytoplasmic cargo, and (3) chaperone-mediated autophagy, mediated by a chaperone complex and lysosomal-associated membrane protein type 2A to degrade cytosolic proteins with a specific targeting motif. The term autophagy usually refers to macroautophagy, which is the most prevalent and beststudied form of autophagy. Also in this review, we will focus exclusively on macroautophagy, further cited as autophagy.Autophagy occurs at basal levels in most tissues to allow constitutive turnover of cytosolic components but is stimulated by environmental stress-related signals (eg, nutrient deprivation and oxidative injury) to recycle nutrients and to generate energy for maintenance of cell viability in unfavorable conditions.1 In addition to cellular stress, basal autophagy can be intensified by specific drugs, 3 indicating that the autophagic machinery is a potential therapeutic target for diverse diseases. Indeed, given that autophagy is involved in the prevention

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“…2 The rate of PCI-associated restenosis in the bare metal stent era was reported to be up to 40%, and even worse in the side branch (SB). 3 The introduction of drug-eluting stents improved outcomes and resulted in low rates of main vessel (MV) restenosis. However, SB ostial residual stenosis and restenosis remained a problem.…”

mentioning

confidence: 99%

Randomized Comparison of Final Kissing Balloon Dilatation Versus No Final Kissing Balloon Dilatation in Patients With Coronary Bifurcation Lesions Treated With Main Vessel Stenting

et al. 2011

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MD; for the Nordic-Baltic PCI Study GroupBackground-It is unknown whether the preferred 1-stent bifurcation stenting approach with stenting of the main vessel (MV) and optional side branch stenting using drug-eluting stents should be finalized by a kissing balloon dilatation (FKBD). Therefore, we compared strategies of MV stenting with and without FKBD. Methods and Results-We randomized 477 patients with a bifurcation lesion to FKBD (nϭ238) or no FKBD (nϭ239) after MV stenting. The primary end point was major adverse cardiac events: cardiac death, non-procedure-related index lesion myocardial infarction, target lesion revascularization, or stent thrombosis within 6 months. The 6-month major adverse cardiac event rates were 2.1% and 2.5% (Pϭ1.00) in the FKBD and no-FKBD groups, respectively. Procedure and fluoroscopy times were longer and more contrast media was needed in the FKBD group than in the no-FKBD group. Three hundred twenty-six patients had a quantitative coronary assessment. At 8 months, the rate of binary (re)stenosis in the entire bifurcation lesion (MV and side branch) was 11.0% versus 17.3% (Pϭ0.11), in the MV was 3.1% versus 2.5% (Pϭ0.68), and in the side branch was 7.9% versus 15.4% (Pϭ0.039) in the FKBD versus no-FKBD groups, respectively. In patients with true bifurcation lesions, the side branch restenosis rate was 7.6% versus 20.0% (Pϭ0.024) in the FKBD and no-FKBD groups, respectively. Conclusions-MV

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Comparison of sirolimus-eluting and bare metal stents in coronary bifurcation lesions: Subgroup analysis of the Stenting Coronary Arteries in Non-Stress/Benestent Disease Trial (SCANDSTENT)

Cited by 78 publications

References 23 publications

Human Cytomegalovirus Secretome Contains Factors That Induce Angiogenesis and Wound Healing

Human Cytomegalovirus Secretome Contains Factors That Induce Angiogenesis and Wound Healing

Autophagy in Vascular Disease

Randomized Comparison of Final Kissing Balloon Dilatation Versus No Final Kissing Balloon Dilatation in Patients With Coronary Bifurcation Lesions Treated With Main Vessel Stenting

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