Impact of Oral Anticoagulants on Platelets Function

Marcin Makowski 1 Ireneusz Smorag 2 Monika Szewczyk 1 Anna Lewandowska 3 Joanna Makowska 3 Andrzej Lubinski 1 Marzenna Zielinska 4 Zbigniew Baj 2
1Interventional Cardiology and Cardiac Arrhythmias, Medical University of Lodz, Poland
2Pathophysiology and Immunology Department, Medical University of Lodz, Poland
3Department of Rheumatology, Medical University of Lodz, Poland
4Intensive Cardiology Department, Medical University of Lodz, Poland

Atrial fibrillation is one of the risk factors of ischaemic stroke, which probably results from haemostatic abnormalities and platelet activation. Oral anticoagulants are routinely use drugs in AF patients with CHA2DS2Vasc score more than 1 point.

The aim of the study was to assess impact of oral anticoagulants (Acenocumarol) on platelet activation.

The study included 36 (mean age 48,3; range 21-60) male patients with lone atrial fibrillation one month after sinus rhythm restoration, with exclusion of concomitant diseases known to trigger hypercoagulable state. The AF patients were compare with 20 sex and age matched healthy volunteers.

Parameters of resting platelets collected from peripheral blood activation was measured using flow cytometry. Platelet activation was assessed by expression of p-selectin (CD62) on platelets (CD61 positive cells). The platelet aggregate number was presented as a percentage of CD61+ blood elements bigger then platelets . The platelet derived microparticles (PDMPs) were assessed based on FSC histogram profile as CD61+ particles smaller than platelets. The leukocyte-platelet aggregates were detected based on coexpression of CD11b and CD62 antigens. Also differances in mean platelet volume were assessed.

Mean fluorescence intensity (MFI) of CD62, CD42b, CD41 on platelets were significantly lower than in control group (CD62: 10.26 +/-2.6 vs. 4.71 +/-1.8; p<0,001; CD42b: 34.66+/-13.22 vs 13.52+/-8.08, p<0.0005; CD41: 444.2+/-77.64 vs 318.6+/-87.74, p<0.001).

The percentage of platelet-leukocyte aggregates and microparticles was not significantly different comparing to control group (platelet-leukocytes aggregates: 7.4+/-3.04 vs. 6.82+/-4.16; PMPs: 1.04+/-0.36 vs. 1.34 +/-1.15). There was significant decrease of platelet aggregates ( 4.94+/-1.56 vs. 3.67+/-1.61; p<0.01). There were no significant changes in MPV (9.4 +/- 1.09 vs 8.87+/- 0.97).

The changes of platelet activation prove that Acenocumarol has an impact on platelets.

Marcin Makowski
Dr. Marcin Makowski
USK im WAM








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