Relation between Carotid Intima-Media Thickness, Platelet Surface Activation and Endothelial Cell Markers

Abstract

Background: The role of platelet activation and endothelial cell damage in the pathogenesis of atherosclerosis was investigated. Methods: Flow-cytometric detection of platelet activity was accomplished by measuring the surface expression of activated platelet glycoprotein IIb/IIIa (activated CD41) and the lysosomal integral membrane protein (CD63). Levels of thrombomodulin (TM) and von Willebrand factor (vWF) were estimated by the ELISA technique as markers of endothelial cell damage. These procedures were performed in healthy male subjects without obvious signs of atherosclerosis. Also, the intima-media thickness of the carotid artery was measured with high-resolution B- mode ultrasound to quantitate the presence and/or the extent of carotid atherosclerosis. Results: According to ultrasound findings patients were divided into those with apparent evidence of atherosclerosis (AS+) with intima-media thickness >1.1 mm (n = 19) and those without such evidence (AS–) with intima-media thickness <1.1 mm (n = 17). The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS– subjects. TM levels were elevated in the former group compared to the latter, while vWF levels were not different in the two groups. Multivariate analysis indicated the independent association of carotid atherosclerosis with each of the expression of activated CD41, CD63 as well as TM levels after adjustment of other risk factors. Conclusion: This study demonstrates that platelets circulate in an enhanced activation state in asymptomatic atherosclerosis, which is closely related to the degree of endothelial cell damage as expressed by increased plasma levels of TM. The detection of platelet activation can be used as a potential marker for oncoming atherosclerosis.

Association between Snoring and Leukocyte Telomere Length

“…One study showed that habitual snoring is associated with carotid atherosclerosis, 10 which is associated with systemic inflammation 11 as well as endothelial cell damage. 23 The strengths of our study include that the data were derived from a general population, LTL measurements were taken of a large sample size, and both subjective and objective snoring assessments were used. However, our study also has some limitations.…”

Serial Measurement of Surface Expressions of CD63, P-Selectin and CD40 Ligand on Platelets in Atherosclerotic Ischemic Stroke

“…However, this platelet hyperactivation had already been in existence during the process of carotid atherosclerosis before any acute vascular events [9, 10]and still remained in patients with chronic atherosclerotic ischemic stroke [11, 12]. Therefore, it is possible that the increased expression of CD63 and P-selectin on platelets may simply reflect the ongoing inflammatory processes of atherogenesis of the carotid or vertebrobasilary arteries rather than the effect of acute vascular events.…”

Compilation and Analysis of Atherosclerosis Gene Expression Data

“…However, in symptomatic plaque, increased expression of both CD163 and heme oxygenase-1 has been found, which suggests that these may have been upregulated in response to plaque hemorrhages [34]. CD63 was increased in a rabbit model of atherosclerosis as well as plaque isolated from human vessels [35]. The role of CSF2RB is largely unstudied in atherosclerosis.…”