Carotid atherosclerotic disease: A systematic review of pathogenesis and management

Abstract

Carotid stenosis is an important contributor to ischemic stroke risk with resultant significant impact on neurological disability and death in adults and with worldwide implications. Management of carotid stenosis is impacted by whether there are associated symptoms along with the degree of stenosis. Understanding of the pathogenesis of carotid atherosclerosis or stenosis is important in management of carotid stenosis. Atherosclerotic plaque formation is a chronic insidious process with a number of potential contributors to the formation of such a plaque. The definition of atherosclerosis is not simply limited to abnormal deposition of lipid but also includes a chronic, complex, inflammatory process. Molecularly, in atherosclerosis, there is decreasing nitric oxide (NO) bioavailability, activity and/or expression of endothelial NO synthase, or increasing degradation of NO secondary to enhanced superoxide production. These above changes cause endothelial dysfunction leading to formation of foam cell followed by formation on lipid plaque. After lipid plaque formation, stable or unstable atherosclerotic plaque is formed depending on the calcium deposition over the lipid plaque. It continues to be clearly established that carotid intervention for symptomatic high-grade carotid stenosis is best managed with intervention either by carotid endarterectomy or carotid stenting. However, asymptomatic carotid stenosis is the subject of considerable controversy in terms of optimal management. This review of carotid atherosclerosis is an attempt to incorporate the information provided by more recent studies on pathogenesis and management which may help in the decision-making process for optimal management for protection against stroke.

Induced Inflammatory and Oxidative Markers in Cerebral Microvasculature by Mentally Depressive Stress

“…Animal experiments have proved excess inflammatory responses and oxidative injuries in cardiovascular systems from mental stress. Endothelial inflammation is noted to be the initial step in atherosclerosis [ 40 , 41 ], and cerebrovascular inflammation has been found to play an important role in intracranial atherosclerosis [ 29 , 42 , 43 ] and CVD [ 44 , 45 ]. Studies have confirmed the involvement of inflammatory mediators in the early proatherogenic processes, such as upregulation of adhesion molecules and highly activated inflammatory responses on endothelial cells [ 46 ].…”

Night shift work was associated with functional outcomes in acute ischemic stroke patients treated with endovascular thrombectomy

“…This phenomenon was also found in AIS who underwent EVT in the current study. Large-artery atherosclerosis was seen at a greater frequency in night shift work patients compared to non-night shift work patients in our study, which may explain the relationship between night shift work and poor functional outcomes [ 15 ]. Large-artery atherosclerosis was found to be associated with early neurological deterioration and an increased risk of reocclusion in the AIS population receiving EVT [ [16] , [17] , [18] ].…”

Remote ischemic conditioning improves cerebral hemodynamics in symptomatic intracranial atherosclerosis: A PET/CT‐guided randomized controlled study

“…The resistance capacity under ischemic challenge is impaired in patients with ICAS (Lee & Lee, 2011). Therefore, patients with ICAS usually suffer more severe stroke at admission and stay longer in hospitals, with a high risk of recurrent stroke (Chimowitz et al., 2011; Wang et al., 2014; Bir & Kelley, 2022). By now, there is no powerful evidence supporting a clear choice of optimal therapy for patients with symptomatic ICAS (sICAS) (Benesch & Chimowitz, 2000).…”