https://orcid.org/0000-0003-1009-9772
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Na Li, Liufu Cui, Panagiotis Korantzopoulos, Nan Zhang, Rong Shu, Haicheng Song, Jierui Wang, Shuohua Chen, Gregory Y H Lip, Gary Tse, Konstantinos P Letsas, George Bazoukis, Gan-Xin Yan, Xuemei Yang, Shouling Wu, Tong Liu, Association between cumulative uric acid exposure and the risk of incident cardiac conduction block, Cardiovascular Research, Volume 120, Issue 10, July 2024, Pages 1104–1106, https://doi.org/10.1093/cvr/cvae115
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Cardiac conduction block is a type of bradyarrhythmia that can occur at any level of the conduction system, therefore resulting in a higher risk of syncope, heart failure, and death, representing a substantial health burden.1,2 Given the potential impact of cardiac conduction block on patients’ outcomes, the clarification of underlying risk factors would be of special interest. In a previous cross-sectional study, Mantovani et al.3 observed a significant association between a higher level of single measurement of uric acid (UA) and increased risk of cardiac conduction defects in patients with type 2 diabetes. However, a single measurement cannot reflect the longitudinal variation and cumulative burden of UA. We therefore explored the associations between cumulative UA (cumUA) and time-weighted average UA (TWAUA) with the risk of cardiac conduction block based on data from the Kailuan study, a prospective population-based cohort.
This prospective study used data from the Kailuan cohort, where participants underwent health check-up surveys every 2 years. Details have been published previously.4 To calculate the cumUA, adult participants with four consecutive examinations from 2006 to 2012, without prior cardiac conduction block, were enrolled (Figure 1A). Participants were followed from the date of the 2012 survey (baseline) to the occurrence of cardiac conduction block, death, or the end of the follow-up (31 December 2019). CumUA was defined as the summed average UA for each pair of consecutive examinations multiplied by the time interval between two consecutive examinations in years.5 TWAUA was calculated as the cumulative exposure to UA divided by the duration of exposure. The study population was divided into three groups according to the tertiles of cumUA and TWAUA, respectively. For cumUA, the tertile cut-offs were 1558.3 and 1944.0 μmol/L × year; for TWAUA, they were 249.3 and 311.4 μmol/L. The diagnosis of cardiac conduction block was based on the 12-lead electrocardiogram (ECG) confirmed by experienced cardiologists. The specific ECG abnormalities were classified according to the Minnesota Code criteria. Cardiac conduction block was defined as any conduction disease, with definitions for cardiac conduction block, atrioventricular block (AVB), and bundle branch block (BBB) previously published.6 Multivariable Cox regression models were constructed to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). HRs were adjusted for age, sex, smoking, drinking, physical activity, body mass index, hypersensitive C-reactive protein (hs-CRP), triacylglycerol, estimated glomerular filtration rate, urea, K+, hypertension, diabetes, antihypertensive drugs, hypoglycaemic drugs, and lipid-lowering drugs. We also stratified the analyses by age (<60, ≥60 years), sex, and hs-CRP concentrations (<2 or ≥2 mg/L). Restricted cubic splines (RCS) were used to examine the shape of the association between cumUA and outcomes with three knots. A two-sided P < 0.05 was considered statistically significant.
