國家衛生研究院 NHRI:Item 3990099045/15954
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/15954


    Title: Carotid atherosclerosis as a mediator of the relationship between lipoprotein(a) and ischemic stroke
    Authors: Chien, KL;Hsu, HY;Fan, HY;Hwang, LC;Lin, HJ;Su, TC;Hsu, HC
    Contributors: Center for Neuropsychiatric Research
    Abstract: Objective: Lipoprotein(a) is a known risk factor for ischemic stroke, driven by its hereditary nature. Understanding potential mediators in the association between lipoprotein(a) and ischemic stroke is crucial for improved monitoring and prevention, yet mediation analysis in this context is limited. This study aims to explore the cardiovascular pathophysiological changes that mediate the link between lipoprotein(a) and ischemic stroke risk. Design and method: This study utilizes data from the Chin-Shan Community Cardiovascular Cohort in Taiwan, a community-based cohort initiated in 1990-1991, which enrolled participants aged 35 years and older and followed them until 2005. Participants with established ischemic stroke and those lacking lipoprotein(a) or carotid sonography data were excluded. Lipoprotein(a) levels greater than the 90th percentile were categorized as higher lipoprotein(a), while levels below this threshold were classified as normal lipoprotein(a). The study employed inverse propensity score-weighted Cox regression to investigate the association between lipoprotein(a) and ischemic stroke, considering carotid atherosclerosis (defined by the presence of carotid artery plaque or intima thickness >= 1mm) and left ventricular hypertrophy (defined by an increased left ventricular mass index) as potential mediators. Causal mediation analysis divided the total effects into direct and indirect components. Results: A total of 2572 participants (average age, 53.8 years; women, 54.6%) were enrolled. In the higher lipoprotein(a) group, participants were more likely to be women and had elevated levels of low-density lipoprotein and hypertension when compared to the normal lipoprotein(a) group. After a 49,958 person-year follow-up, 167 events of ischemic stroke were documented. Compared with the normal lipoprotein(a) group, the higher lipoprotein(a) group had a higher risk of ischemic stroke (adjusted hazard ratio: 1.60, 95% confidence interval: 1.30-1.95). Carotid atherosclerosis was a significant mediator, accounting for 6.8% (p=0.049) of the relationship between lipoprotein(a) and ischemic stroke. Conclusions: Carotid atherosclerosis was a significant mediator, accounting for 6.8% of the relationship between lipoprotein(a) and ischemic stroke. Monitoring carotid atherosclerosis is a potential preventive strategy to disrupt the association between high lipoprotein(a) and ischemic stroke. Further, a two-step Mendelian randomization analysis is warranted for confirming a causal relationship in this mediation model.
    Date: 2024-05
    Relation: Journal of Hypertension. 2024 May;42(Suppl. 1):Meeting Abstract e168.
    Link to: http://dx.doi.org/10.1097/01.hjh.0001021072.65179.c6
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0263-6352&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:001256619700435
    Appears in Collections:[Others] Conference Papers/Meeting Abstract

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