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.
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Acknowledgments
Authors wish to thank Dr. Lissy K. Krishnan and all staff of Thrombosis Research Unit (SCTIMST) for providing facilities to conduct experiments related to thrombotic risk factors and flow cytometry for P-selectin analysis. Help rendered by all staff of Central Clinical Lab—Department of Biochemistry and Department of Cardiology (SCTIMST)—is also acknowledged. The grant provided by Kerala State Council for Science, Technology and Environment, Pattom P.O. Thiruvananthapuram, Kerala, India (File No.: 041/SRSLS/07/CSTE), for the work is greatly acknowledged. Ms. Reema George received the Junior Research Fellowship and now receiving Senior Research Fellowship from Council of Scientific and Industrial Research (CSIR), Pusa, New Delhi, India, Pin: 110001 (File No.: 09/523(0075)/2011-EMR-I).
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George, R., Bhatt, A., Narayani, J. et al. Enhanced P-selectin expression on platelet-a marker of platelet activation, in young patients with angiographically proven coronary artery disease. Mol Cell Biochem 419, 125–133 (2016). https://doi.org/10.1007/s11010-016-2756-4
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DOI: https://doi.org/10.1007/s11010-016-2756-4