PDF(Pubmed)
Abstract：
UNASSIGNED: This study aimed to explore the impact of a combination of hyperuricemia (HUA) and excessive high-sensitivity C-reactive protein (hs-CRP) levels on the likelihood of developing cardiac conduction block (CCB). Additionally, it sought to assess whether the influence of uric acid (UA) on CCB is mediated by hs-CRP.
UNASSIGNED: A prospective study was executed utilizing data from the Kailuan cohort, including 81,896 individuals initially free from CCB. The participants were categorized into four groups depending on the existence of HUA and low-grade inflammation (hs-CRP>3 mg/L). Cox regression analysis was employed to ascertain hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of incident CCB. A mediation analysis was performed to determine if hs-CRP functioned as a mediator in the connection between UA levels and the incidence of CCB.
UNASSIGNED: During a median observation period of 11.8 years, we identified 3160 cases of newly occurring CCB. Compared with the low UA/low CRP group, the combination of HUA and low-grade inflammation elevated the CCB risks (HR:1.56, 95% CI:1.22-1.99), atrioventricular block (AVB) (HR:1.88, 95% CI:1.27-2.77), and right bundle branch block (HR:1.47, 95% CI:1.02-2.12), respectively. Mediation analysis revealed that in the HUA group, compared with the non-HUA group, the risk of CCB elevated by 14.0%, with 10.3% of the increase mediated through hs-CRP.
UNASSIGNED: HUA combined with elevated hs-CRP increased the risk of CCB, especially AVB. The connection between UA and the CCB risk was partly mediated by hs-CRP.
UNASSIGNED: A prospective study was executed utilizing data from the Kailuan cohort, including 81,896 individuals initially free from CCB. The participants were categorized into four groups depending on the existence of HUA and low-grade inflammation (hs-CRP>3 mg/L). Cox regression analysis was employed to ascertain hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of incident CCB. A mediation analysis was performed to determine if hs-CRP functioned as a mediator in the connection between UA levels and the incidence of CCB.
UNASSIGNED: During a median observation period of 11.8 years, we identified 3160 cases of newly occurring CCB. Compared with the low UA/low CRP group, the combination of HUA and low-grade inflammation elevated the CCB risks (HR:1.56, 95% CI:1.22-1.99), atrioventricular block (AVB) (HR:1.88, 95% CI:1.27-2.77), and right bundle branch block (HR:1.47, 95% CI:1.02-2.12), respectively. Mediation analysis revealed that in the HUA group, compared with the non-HUA group, the risk of CCB elevated by 14.0%, with 10.3% of the increase mediated through hs-CRP.
UNASSIGNED: HUA combined with elevated hs-CRP increased the risk of CCB, especially AVB. The connection between UA and the CCB risk was partly mediated by hs-CRP.
摘要：
■本研究旨在探讨高尿酸血症（HUA）和超敏C反应蛋白（hs-CRP）水平对发生心脏传导阻滞（CCB）的可能性的影响。此外,它试图评估尿酸（UA）对CCB的影响是否由hs-CRP介导。
■一项前瞻性研究是利用开联队列的数据进行的，包括81,896名最初没有建行的人。根据HUA和低度炎症（hs-CRP>3mg/L）的存在，将参与者分为四组。Cox回归分析用于确定事件CCB风险的风险比（HR）和95％置信区间（CI）。进行了中介分析，以确定hs-CRP是否在UA水平与CCB发生率之间起中介作用。
■在11.8年的中位观察期内，我们确定了3160例新发生的CCB。与低UA/低CRP组比拟，HUA和低度炎症的组合升高了CCB风险(HR:1.56,95%CI:1.22-1.99),房室传导阻滞（AVB）（HR：1.88，95%CI：1.27-2.77），和右束支传导阻滞（HR：1.47，95%CI：1.02-2.12），分别。中介分析显示，在HUA组中，与非HUA组相比，建行风险上升14.0%，其中10.3％的增加是通过hs-CRP介导的。
■HUA合并hs-CRP升高会增加CCB的风险，尤其是AVB。UA与CCB风险之间的联系部分由hs-CRP介导。
■一项前瞻性研究是利用开联队列的数据进行的，包括81,896名最初没有建行的人。根据HUA和低度炎症（hs-CRP>3mg/L）的存在，将参与者分为四组。Cox回归分析用于确定事件CCB风险的风险比（HR）和95％置信区间（CI）。进行了中介分析，以确定hs-CRP是否在UA水平与CCB发生率之间起中介作用。
■在11.8年的中位观察期内，我们确定了3160例新发生的CCB。与低UA/低CRP组比拟，HUA和低度炎症的组合升高了CCB风险(HR:1.56,95%CI:1.22-1.99),房室传导阻滞（AVB）（HR：1.88，95%CI：1.27-2.77），和右束支传导阻滞（HR：1.47，95%CI：1.02-2.12），分别。中介分析显示，在HUA组中，与非HUA组相比，建行风险上升14.0%，其中10.3％的增加是通过hs-CRP介导的。
■HUA合并hs-CRP升高会增加CCB的风险，尤其是AVB。UA与CCB风险之间的联系部分由hs-CRP介导。
