Enhanced P-selectin expression on platelet-a marker of platelet activation, in young patients with angiographically proven coronary artery disease

Abstract

P-selectin (CD62p) exposure is an established marker for platelet activation. P-selectin exposure can trigger variety of thrombotic and inflammatory reactions. In patients with coronary artery disease (CAD), platelets are activated, and hence, there is increased P-selectin exposure. The role of P-selectin exposure in patients on treatment with statins and anti-platelets is conflicting. A case-control study was performed to determine P-selectin exposure in consecutively recruited 142 patients (age ≤ 55 years) with angiographically proven CAD on treatment and 92 asymptomatic controls. P-selectin exposure was determined by flow cytometry. Data on conventional risk factors were obtained along with estimation of levels of thrombotic [fibrinogen, lipoprotein (a), tissue plasminogen activator, plasminogen activator inhibitor-1, homocysteine and von Willebrand factor] and anti-thrombotic factors (antithrombin III). The P-selectin exposure was compared among patient groups who had different modes of presentation of CAD and categories of CAD disease severity. The patients were followed up for a period of 26 months. The results indicate that P-selectin exposure was significantly elevated in patients (mean ± SD 9.24 ± 11.81) compared to controls (mean ± SD 1.48 ± 2.85) with p < 0.0001. Similarly, conventional risk factors were significantly elevated in patients. P-selectin exposure showed significant negative correlation with antithrombin III levels. P-selectin exposure was higher in patients who presented with acute coronary syndromes than those who presented with effort angina. Cardiovascular event rate was 6 % on follow-up. The study establishes that thrombotic-inflammatory pathways enhancing P-selectin exposure unrelated to treatment might be activated in patients, while the event rate remained lowered, and hence, treatment strategies should be inclusive to control these factors.

Diagnostic value of platelet‑derived microparticles in pulmonary thromboembolism: A population‑based study

“…P-selectin, on the other hand, was another known marker of platelet procoagulant activity that exposed on the platelet membrane when the platelet was activated (39). Besides, P-selectin can mediate the adhesion of activated platelet with other cells, leading to the hypercoagulant state of the blood (40). More recently, Prakash et al found that P-selectin can even promote thrombus propagation independently of both von Willebrand factor and thrombospondin-1 in mice (41).…”

P-selectin (CD62P) and soluble TREM-like transcript-1 (sTLT-1) are associated with coronary artery disease: a case control study

“…Furthermore, CD62P exposure is known to be an established marker for platelet activation. Current research has found that the percentage expression of CD62P on platelets without any stimulation by platelet-activating factors, such as ADP, collagen, and thrombin, is higher in CAD patients compared to participants in a control group [3]. Tenaglia et al [4] also reported significantly greater CD62P staining on atherectomy specimens from patients with unstable angina than from patients with stable angina.…”

Si-Miao-Yong-An Decoction Protects Against Cardiac Hypertrophy and Dysfunction by Inhibiting Platelet Aggregation and Activation

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