Pathophysiology and Medical Treatment of Carotid Artery Stenosis

Prasad, Kailash

doi:10.1055/s-0035-1554911

Cited by 46 publications

(47 citation statements)

References 225 publications

(191 reference statements)

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“…The mechanisms of atherosclerotic formation in CA are similar to those in other arteries. A hemodynamic shear stress triggers EC dysfunction and induces SMC accumulations in the subendothelial space, initiating atherosclerosis formation at arterial branch sites as intimal cell masses [20,21] . Physical or metabolic injuryinduced disturbance of EC integrity makes ECs transduce hemodynamic stress into biochemical signals, which change the expressions of cell adhesion molecules (CAMs) and other cell surface receptors to alter blood cell adhesion [20] .…”

Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

“…Physical or metabolic injuryinduced disturbance of EC integrity makes ECs transduce hemodynamic stress into biochemical signals, which change the expressions of cell adhesion molecules (CAMs) and other cell surface receptors to alter blood cell adhesion [20] . Several mediators including reactive oxygen species induce CAMs such as intercellular adhesion molecule (ICAM)-1, vascular CAM (VCAM)-1, and endothelial-leukocyte adhesion molecules on ECs [21] . The first step of atherogenesis is that low-density lipoprotein (LDL) cholesterol (Cho) (LDL-C) enters into the subendothelial spaces, and is trapped by a high affinity to the glycoprotein molecules at the lesion [22] .…”

Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

“…Moreover, ox-LDLs induce the differentiation of monocytes into macrophages. Macrophages develop receptors for ox-LDLs to become lipid-laden foam cells through the receptor-mediated incorporation of ox-LDLs [21] . Thus, Cho is trapped within the arterial walls, which is the hallmark of early-stage atherosclerotic lesion formation.…”

Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

“…Numerous epidemiology and clinical studies have demonstrated that dyslipidemia is a major risk factor for atherosclerosis formation [2,21] . Hypercholesterolemia increases levels of cellular free Cho about 2-to 4-fold in vascular ECs [31] .…”

Section: Total Chomentioning

confidence: 99%

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Dyslipidemia and atherosclerotic carotid artery stenosis

Miura¹,

Suzuki²

2019

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Carotid artery atherosclerosis or stenosis is frequently present at the carotid bifurcation or the internal carotid artery, accounting for at least 20% of all ischemic strokes. High levels of serum total cholesterol and low-density lipoprotein cholesterol are established risk factors for genesis and progression of atherosclerotic lesions through various mechanisms. In addition, accumulating evidence has shown that a high level of triglyceride is associated with increased atherosclerosis risks. The so-called "vulnerable plaque" with a large lipid core, thin fibrous cap and intra-plaque hemorrhage tends to cause subsequent thromboembolic ischemic events. Statins are known not only to lower serum cholesterol levels but also to promote plaque stabilization via pleiotropic effects such as reducing subclinical systemic inflammation, endothelial activation, leukocyte intra-plaque infiltration, and increasing intimal smooth muscle cell migration. This article discusses the mechanisms of atherosclerosis formation induced by dyslipidemia and the role of lipid-lowering agents including statins in patients with symptomatic and asymptomatic atherosclerotic carotid artery stenosis.

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Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

Section: The Formation Of Atherosclerotic Ca Plaque [Figure 1]mentioning

confidence: 99%

Section: Total Chomentioning

confidence: 99%

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Dyslipidemia and atherosclerotic carotid artery stenosis

Miura¹,

Suzuki²

2019

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“…1,2 The main modifiable factors accounting for the development of atherosclerosis in the carotid artery are hypertension, diabetes mellitus, dyslipidaemia, obesity and smoking. 3 Anti-thrombotic therapy reduces the risk of embolization of the carotid plaque and is also considered an important component of medical therapy in carotid stenosis. 4 In the past, there was a tendency for physicians to recommend life style changes and drug treatment for vascular risk factors without closely monitoring the patient's compliance or response to treatment.…”

Section: Introductionmentioning

confidence: 99%

Contemporary medical therapies of atherosclerotic carotid artery disease

Cheng

Brown

2017

Seminars in Vascular Surgery

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Contemporary medical therapy consists of identification and treatment of all patient-modifiable vascular risk factors. Specific atherosclerotic disease therapies are designed to reduce the risk of thrombosis, and the disease progression in order to reduce the risk of future cardiovascular events. Contemporary medical management emphasizes the need to support the patient in achieving lifestyle modifications and to adjust medication to achieve individualized target values for specific quantifiable risk factors. Antiplatelet therapy in the form of aspirin or clopidogrel is routinely used for the prevention of ischemic stroke in patients who have had a transient ischemic attack or stroke. There is evidence from a recent trial that the use of combination antiplatelet therapy with aspirin and clopidogrel started within 24 hours of minor stroke or transient ischemic attack reduces the risk of recurrent stroke compared to the use of aspirin alone, and therefore we use aspirin plus clopidogrel in recently symptomatic patients with carotid stenosis pending carotid revascularization. Anticoagulation with heparins or vitamin K antagonist is not recommended except in patients at risk for cardio-embolic events. Lowering blood pressure to target levels has been shown to slow down the progression of carotid artery stenosis and reduces the intima-media thickness of the carotid plaque, while lowering lipid levels with statins has become an essential element in the medical therapy of carotid artery stenosis. Diabetes management should be optimized. Lifestyle choices, including tobacco smoking, physical inactivity, unhealthy diet, obesity, and excessive alcohol intake, are all important modifiable vascular risk factors. The combination of dietary modification, physical exercise, and use of aspirin, a statin, and an antihypertensive agent can be expected to give a cumulative relative stroke risk reduction of 80%. The evidence suggests that intensive medical therapy is so effective that carotid revascularization may no longer be necessary in many of the patients in whom carotid surgery or stenting is currently performed. Two large ongoing trials are therefore comparing the risks and benefits of carotid revascularization versus intensive medical therapy alone.

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