No abstract

The initial steps in the pathogenesis of atherosclerosis involve changes to the vascular endothelium, which produces numerous substances involved in the regulation and maintenance of vascular integrity and the homeostasis of the coagulation/fibrinolysis system. A further change in endothelial physiology is an increase in the surface expression of cell adhesion molecules, such as E-selectin, which regulate adhesive interactions between certain blood cells and endothelium. As E-selectin is only expressed on activated endothelium, it therefore provides an opportunity to study pathophysiological aspects of this cell in cardiovascular and other disease. However, a soluble form of E selectin (i.e. sE-selectin) can be found in the plasma. This review will focus on sE-selectin, and its potential role in the pathogenesis of cardiovascular disease as raised levels have been found in hypertension, diabetes and hyperlipidemia, although its association in established atherosclerosis disease and its value as a prognostic factor is more controversial.

In a "real world" cohort of consecutive patients with nonvalvular atrial fibrillation, a high SAMe-TT2R2 score (reflecting poor anticoagulation control with poor time in therapeutic range) was associated with more bleeding, adverse cardiovascular events, and mortality during follow-up.

No abstract

In anticoagulated AF patients, a validated specific bleeding risk score, HAS-BLED, should be used for assessing major bleeding. The practice of using CHADS2 and CHA2DS2-VASc as a measure of high bleeding risk should be discouraged, given its inferior predictive performance compared with the HAS-BLED score.

No abstract

High plasma vWF levels (≥221 IU/dl) are an independent risk factor for adverse events in anticoagulated permanent AF patients. This biomarker may potentially be used to refine stroke and bleeding clinical risk stratification in AF.

High levels of IL-6 in AF suggest an inflammatory state, which appears to be more related to clinical variables of the patients, rather than to the presence of AF per se. There was no association of inflammation with endothelial activation (sEsel) or the presence of abnormal thrombogenesis (high F1+2 levels) in AF. Moreover, no changes in IL-6 levels were found despite the reduction of the other markers by oral anticoagulant therapy.