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

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dc.contributor.authorGeorge, R
dc.contributor.authorBhatt, A
dc.contributor.authorNarayani, J
dc.contributor.authorThulaseedharan, JV
dc.contributor.authorSivadasanpillai, H
dc.contributor.authorTharakan, JA
dc.date.accessioned2017-03-10T03:26:33Z
dc.date.available2017-03-10T03:26:33Z
dc.date.issued2016
dc.description.abstractP-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 aecurrency sign 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.
dc.identifier.citation419 ,42767;125-133en_US
dc.identifier.uri10.1007/s11010-016-2756-4
dc.identifier.urihttps://dspace.sctimst.ac.in/handle/123456789/9696
dc.publisherMOLECULAR AND CELLULAR BIOCHEMISTRY
dc.subjectCell Biology
dc.titleEnhanced P-selectin expression on platelet-a marker of platelet activation, in young patients with angiographically proven coronary artery disease
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