Endothelial dysfunction and systemic inflammation in persons with echolucent carotid plaques

Abstract

Echolucent carotid plaques are associated with high risk for future ischemic cerebrovascular events independent of the degree of stenosis. Elevated levels of markers of systemic inflammation and endothelial dysfunction are predictors for future myocardial infarction and stroke. The present study was undertaken to investigate the relations between plaque morphology, endothelial dysfunction assessed by tissue-plasminogen activator antigen (t-PA ag) and vonWillebrand factor (vWF), and systemic inflammation in persons with carotid stenosis. We conducted a crosssectional study including 133 persons with carotid stenosis and 138 controls without stenosis recruited from the populationbased Tromsø Study. High-resolution B-mode and colour Doppler/pulsed-wave Doppler ultrasonography of both carotid arteries was performed, and plaque morphology in terms of echogenicity was assessed. Persons with carotid stenosis had significantly higher plasma t-PA and vWF concentrations than controls. There was a significant inverse relationship between t-PA ag and plaque echogenicity (p = 0.034). The increased plasma t-PA ag in persons with carotid stenosis was not associated with increased plasminogen activator inhibitor-I (PAI-1). Persons with echolucent carotid plaques had higher degree of systemic inflammation, and plasma t-PA and vWF concentration increased significantly across quartiles of WBC, fibrinogen, and hs-CRP. Our findings may suggest that plasma t-PA may be superior to vWF as a marker for endothelial dysfunction due to its ability to discriminate between various plaque echogenicity, and that the predictive role of t-PA ag in cardiovascular disease is independent of inhibited fibrinolysis.

Endothelial Dysfunction of the Peripheral Vascular Bed in the Acute Phase after Ischemic Stroke

“…In our study, patients with large-artery atherosclerotic infarcts did not exhibit peripheral ED to the same extent as other stroke subtypes compared with controls. This contradicts previous studies [35,36] and needs further investigations. All subgroup analyses should, however, be viewed with some caution due to small patient cohorts in each subgroup.…”

Von Willebrand Factor Regulation in Patients with Acute and Chronic Cerebrovascular Disease: A Pilot, Case–Control Study

“…On the one hand, a high VWF level at admission is indicated as a marker of severe IS; on the other hand, VWF level is influenced by a variety of other variables (e.g. ABO blood group [38]–[41], existence and composition of carotid plaques [15], [16]) which complicates its interpretation. Only recently, it has been shown that extracellular sodium levels within the high physiological range can raise VWF levels thereby increasing the risk of pathological thrombosis [42].…”

“…Also, the relationship of VWF levels to other parameters, such as genetic polymorphisms [13] and demographic features [14], is not well understood. Additionally, only limited data exist on the regulation of VWF in patients with chronic cerebrovascular disease (CCD) [15]–[17].…”

Endothelial Dysfunction, Vascular Disease and Stroke: The ARTICO Study

“…Decreased brachial FMD and decreased cerebrovascular reactivity to L-A are present in stroke patients [19,77,78,79] and in patients with carotid stenosis [57, 80, 81]. L-A reactivity is impaired in the stenotic side of patients with severe unilateral internal carotid stenosis and normalizes 3 months after endarterectomy [80].…”

“…L-A reactivity is impaired in the stenotic side of patients with severe unilateral internal carotid stenosis and normalizes 3 months after endarterectomy [80]. Moreover, the presence of carotid stenosis is related to higher plasma t-PA and vWF concentrations, and persons with echolucent carotid plaques have a higher degree of systemic inflammation [81]. Impaired FMD seems to be especially important in lacunar infarction and may be considered an independent predictor for this stroke subtype [19].…”