Akademik Veri Yönetim Sistemi
Kardiologia Polska, cilt.75, sa.1, ss.35-41, 2017 (SCI-Expanded)
Background: Platelets play a significant role in the pathogenesis of atherosclerosis. In atherosclerotic plaques, the risk of plaque rupture is more crucial than the severity of the stenosis they cause. Non-calcified carotid artery plaques are more unstable than calcified plaques, and they are associated with a higher risk of rupture, thromboembolism, and consequently, stroke. Aim: The purpose of the present study is to compare calcified and non-calcified plaques that cause intermediate carotid artery stenosis, with respect to mean platelet volume (MPV) and platelet distribution width (PDW). Methods: A total of 139 asymptomatic patients with 50-70% stenosis of the carotid artery were included in this study. Carotid Doppler ultrasound imaging and computed tomography angiography were performed to divide the carotid artery plaques into two groups as calcified and non-calcified. Patients included in the calcified (n - 73) and non-calcified (n - 66) plaque groups were compared with respect to MPV and PDW. Results: Mean platelet volume was statistically significantly higher in the non-calcified plaque group compared to the calcified plaque group (MPV in non-calcified/calcified plaque groups [fL]: 10.0/9.0, respectively) (p < 0.01). PDW was not significantly different between the two groups (p - 0.09). Platelet count was statistically significantly higher in the calcified plaque group compared to the non-calcified plaque group (platelet count in calcified/non-calcified plaque groups [103/mm3]: 250 ± 63/226 ± 56, respectively) (p - 0.019). Multivariate regression analysis showed that MPV was independently associated with non-calcified carotid artery plaque (odds ratio 5.95, 95% confidence interval 2.63-13.45, p < 0.001). Conclusions: Mean platelet volume is increased in the presence of non-calcified carotid artery plaques that cause asymptomatic intermediate stenosis. Increased MPV can be used as a marker to predict the risk of rupture of the non-calcified carotid artery plaques.