Image_1_Association Between Low-Density Lipoprotein Cholesterol and Platelet Distribution Width in Acute Ischemic Stroke.tif
Objective: Elevated low-density lipoprotein cholesterol (LDL-C) is an established risk factor for ischemic stroke; however, whether LDL-C affects the platelet deformation function in the peripheral blood circulation in patients with acute ischemic stroke (AIS) is unknown. The present study aimed to investigate the relationship between LDL-C and platelet distribution width (PDW) in AIS patients.
Methods: We conducted a cross-sectional hospitalized-based study of consecutive 438 patients with AIS within 24 h. Blood samples were collected upon admission and prior to drug administration, and LDL-C and PDW (a parameter that reflects the heterogeneity of platelet volume) were assessed. The relationship between LDL-C and PDW were analyzed by linear curve fitting analyses. Crude and adjusted beta coefficients of LDL-C for PDW with 95% confidence intervals were analyzed using multivariate-adjusted linear regression models.
Results: The PDW was significantly higher in the high LDL-C group compared with those in the normal LDL-C group (16.28 ± 0.37 fl vs. 16.08 ± 0.37 fl, p < 0.001). Adjusted smoothed plots suggested that there are linear relationships between LDL-C and PDW, and the Pearson's correlation coefficient (95%) was 0.387 (0.304–0.464, p < 0.001). The beta coefficients (95% CI) between LDL-C and PDW were 0.15 (0.12–0.18, p < 0.001) and 0.14 (0.11–0.18, p < 0.001), respectively, in AIS patients before and after adjusting for potential confounders.
Conclusion: Our study suggested that the elevated LDL-C level was related to increased PDW among AIS patients.
History
References
- https://doi.org//10.1161/STROKEAHA.118.021109
- https://doi.org//10.1016/j.jacl.2016.09.017
- https://doi.org//10.1016/j.jns.2017.04.024
- https://doi.org//10.1016/j.atherosclerosis.2018.04.021
- https://doi.org//10.1007/s11883-019-0815-5
- https://doi.org//10.1161/01.STR.31.3.782
- https://doi.org//10.1001/archinte.1985.00360070150025
- https://doi.org//10.3389/fmed.2017.00146
- https://doi.org//10.1016/j.amjcard.2019.07.044
- https://doi.org//10.2147/NDT.S170823
- https://doi.org//10.3174/ajnr.A5853
- https://doi.org//10.1016/j.amjcard.2009.04.027
- https://doi.org//10.1152/physiolgenomics.00090.2010
- https://doi.org//10.1042/CS20180639
- https://doi.org//10.1016/j.atherosclerosis.2019.09.019
- https://doi.org//10.1016/j.freeradbiomed.2006.11.017
- https://doi.org//10.1016/j.amjcard.2003.12.059
- https://doi.org//10.1515/CCLM.2010.035
- https://doi.org//10.5603/KP.a2017.0135
- https://doi.org//10.1007/s10067-017-3647-0
- https://doi.org//10.1155/2013/181324
- https://doi.org//10.1155/2013/762759
- https://doi.org//10.1016/j.redox.2017.11.017
- https://doi.org//10.1093/cvr/cvz230
- https://doi.org//10.1016/S0143-4160(96)90118-9
- https://doi.org//10.1055/s-2007-995850
- https://doi.org//10.1089/met.2008.0045
- https://doi.org//10.1016/j.ijcard.2018.03.077
- https://doi.org//10.1155/2019/8563845
- https://doi.org//10.1160/TH12-03-0206
- https://doi.org//10.1177/0003319714548682
- https://doi.org//10.1042/CS20160234
- https://doi.org//10.1097/AAP.0000000000000520
- https://doi.org//10.3389/fmed.2019.00280
- https://doi.org//10.1080/09537104.2018.1475630
- https://doi.org//10.1021/acs.biochem.9b00430
CC BY 4.0