Restenosis

Lerman, Amir

doi:10.1161/01.cir.0000152694.27996.3e

Cited by 22 publications

(8 citation statements)

References 25 publications

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“…Attempts to regenerate endothelial lining by seeding cells was found functionally ineffective and still permissive of neointima formation [34]. Though not demonstrated, it is likely that the newly seeded endothelium is “dysfunctional” in the sense of being unable to release nitric oxide and other anti-proliferative vasodilators [35]. Notably, such dysfunction also appears to occur in humans at sites of stenting [36].…”

Section: Regeneration Of the Endothelial Lining Prevents Thrombosimentioning

confidence: 99%

Healing arterial ulcers: Endothelial lining regeneration upon vascular denudation injury

McDonald

Iruela‐Arispe

2015

Vascular Pharmacology

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Thrombosis and restenosis are the most prevalent late complications of coronary artery stenting. Current standards of clinical care focus on prevention of smooth muscle proliferation by the use of drug-eluting stents able to release anti-proliferative drugs. Unfortunately, these drugs also block endothelial cell proliferation and, in this manner, prevent recovery of endothelial cell coverage. Continued lack of endothelial repair leaves the root cause of thrombosis and restenosis unchanged, creating a vicious cycle where drug-mediated prevention of restenosis simultaneously implies promotion of thrombosis. In this issue of Vascular Pharmacology, Hussner and colleagues provide in vitro evidence and a mechanistic basis for the use of atorvastatin in stents as a way to bypass this roadblock. Here we review the pathological mechanisms and therapeutic approaches to restore flow in occluded arteries. We argue that rational design of drug eluting stents should focus on specific inhibition of smooth muscle proliferation with concurrent stimulation of endothelial regeneration. We comment on our poor understanding of the cellular and molecular regulation of endothelial cell proliferation in the context of a functional artery, and on the pitfalls of extrapolating from the well-studied process of neovascularization by sprouting vessel formation.

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Section: Regeneration Of the Endothelial Lining Prevents Thrombosimentioning

confidence: 99%

Healing arterial ulcers: Endothelial lining regeneration upon vascular denudation injury

McDonald

Iruela‐Arispe

2015

Vascular Pharmacology

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“…The sex of patients may also have some influence on tested ED mediators. For example, the baseline value of P-selectin may be elevated in men, but no clinical predictive value for CVD has been found; whereas in women it is considered as a predictor of future cardiovascular events [27,28]. However, E-selectin is a marker of cigarette smoking and is also a serum marker of myocardial infarction in both sexes [27,28].…”

Section: Discussionmentioning

confidence: 99%

The association of ventricular tachycardia and endothelial dysfunction in the setting of acute myocardial infarction with ST elevation

et al. 2013

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BackgroundVentricular tachycardia (VT) is frequently seen in ischemic settings like acute myocardial infarction with ST segment elevation (STEMI). Endothelial dysfunction (ED) represents inflammation and the loss of all protective features of the endothelium. We aimed to examine the association between VT and ED in patients with STEMI.Material/MethodsThe study included 90 subjects (30 with VT and acute STEMI, 30 with STEMI without VT, and 30 controls). Sera of all subjects were tested on ED markers by enzyme immunoassay: sICAM-1 (intracellular adhesive molecule-1), sVCAM-1 (vascular adhesive molecule-1), P- and E-selectins, and VEGF (vascular endothelial growth factor). In addition, CRP (C-reactive protein) was detected.ResultsSignificantly increased values of low-density lipoprotein, triglycerides, leukocytes, creatinine, and the number of cigarettes smoked were observed among patients with VT+STEMI in comparison to controls. The levels of E-selectin were significantly lower in the VT+STEMI group than in the other groups, while the levels of VCAM-1 were significantly higher in the groups with STEMI and VT+STEMI compared to the controls. Lower levels of VEGF were recorded in STEMI and VT+STEMI groups compared to the control group. A significant correlation between CRP and VCAM-1 in patients with VT +STEMI was demonstrated.ConclusionsWe showed that ED may have a role in the immunopathogenesis of VT in patients with STEMI. The role of sE-selectin and correlation of sVCAM-1 with CRP as possible ED predictive markers in patients with VT+STEMI should be further investigated in a large cohort of patients.

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“…Interestingly, the group with vascular events was prescribed antiplatelet agents, statins, blood sugar-lowering medications, B-blocking agents, calcium antagonists and ACE inhibitors more frequently, which could be related with a higher risk of a new-onset vascular event in spite of this treatment. Although brachial endothelial dysfunction has been shown to predict restenosis after a percutaneus coronary intervention [41] and complications after vascular surgery [18], the predictive value of a recurrent major adverse vascular event after a first-ever stroke has not been previously analyzed. We consider that detection of endothelial dysfunction in patients with acute ischemic stroke is very important because this group of patients will be at higher risk of a poor outcome and of developing a new-onset vascular event after first-ever stroke, and may thus require more aggressive secondary prevention therapy.…”

Section: Discussionmentioning

confidence: 99%

Impaired Brachial Flow-Mediated Dilation Is a Predictor of a New-Onset Vascular Event after Stroke

Santos‐García¹,

Blanco²,

Serena³

et al. 2011

Cerebrovasc Dis

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Background and Objective: Brachial arterial flow-mediated dilation (FMD) is associated with an increased risk of vascular events. Our aim was to investigate the relationship between FMD measured in the acute phase of ischemic stroke and a new major adverse vascular event in a consecutive cohort of patients followed up for 48 months after an acute first-ever stroke. Methods: We measured FMD in 120 consecutive patients with acute ischemic stroke using high-resolution ultrasonography. FMD was calculated as the relationship between the basal diameter of the brachial artery before and after transient vascular occlusion. Intima-media thickness, extracranial carotid atherosclerosis, stroke severity National Institute of Health Stroke Scale, and modified Rankin Scale at 3 months were also evaluated. A vascular event was defined as any of the following: vascular disease (VD) death, nonfatal myocardial infarction (MI), nonfatal recurrent stroke (RS), claudication or peripheral arterial thrombosis (PVD), angioplasty or cardiac bypass graft surgery. Results: There were 34 new major adverse vascular events in 32 of 120 patients (26.7%): 21 (61.8%) RS, 5 (14.7%) VD death, 5 (14.7%) MI, and 3 (8.8%) PVD. The presence of carotid artery plaque (81.3 vs. 46%; p < 0.0001), atrial fibrillation (37.5 vs. 14.8%; p = 0.007) and FMD (5.30 ± 7.48 vs. 10.54 ± 7.02; p = 0.001) were associated with new-onset vascular events. FMD ≤4.5% was an independent predictor of new-onset vascular events (hazards ratio 3.48; 95% confidence interval 1.26–9.63; p = 0.01). Conclusions: FMD is an independent predictor for a new-onset vascular event after first-ever ischemic stroke.

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Restenosis

Cited by 22 publications

References 25 publications

Healing arterial ulcers: Endothelial lining regeneration upon vascular denudation injury

Healing arterial ulcers: Endothelial lining regeneration upon vascular denudation injury

The association of ventricular tachycardia and endothelial dysfunction in the setting of acute myocardial infarction with ST elevation

Impaired Brachial Flow-Mediated Dilation Is a Predictor of a New-Onset Vascular Event after Stroke

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