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Jul 2026

Associations between prediabetes, type 2 diabetes, and incident arrhythmias: a population-based cohort study and Mendelian randomization analysis.

BACKGROUND Type 2 diabetes (T2D) is a known risk factor for arrhythmias, yet evidence for prediabetes is limited, and the two main diagnostic criteria (ADA, prioritizing sensitivity; WHO/IEC, prioritizing specificity) have not been directly compared across arrhythmia subtypes. METHODS In this prospective cohort study of 383,995 UK Biobank participants, glycemic status was defined by ADA and WHO/IEC criteria. Outcomes included atrial fibrillation, supraventricular tachycardia, bradyarrhythmia, and ventricular arrhythmia. Cox models were adjusted for clinical, lifestyle, and genetic confounders. Mendelian randomization (MR) was performed to infer causality. RESULTS Over a median 13.0 years, prediabetes and T2D were each associated with increased risks of all arrhythmias. Under ADA criteria, prediabetes hazard ratios ranged from 1.12 to 1.15; risks were higher for T2D and for progression from prediabetes to T2D. ECG changes included shortened RR and prolonged QTc intervals.MR analyses provided genetic evidence supporting a potential causal role of dysglycemia in arrhythmogenesis. CONCLUSIONS These findings highlight the differential prognostic utility of ADA and WHO/IEC criteria for arrhythmia risk stratification: the ADA criteria offer broader sensitivity for early detection, whereas the stricter WHO/IEC criteria identify a higher-risk subgroup warranting more intensive management.

Yanjun Song, Zhihao Zheng, K. Cui et al. · 0 citations
Jul 2026

Evidence from two large prospective cohorts: variations in remnant cholesterol inflammation index and the risk of cardiometabolic multimorbidity in middle-aged and elderly populations.

OBJECTIVE While residual cholesterol (RC) and high-sensitivity C-reactive protein (hs-CRP) are independent risk factors for cardiometabolic multimorbidity (CMM), their combined predictive value remains unclear. We investigated the predictive utility of the remnant cholesterol inflammation index (RCII) for CMM incidence. METHODS The RCII was derived from 5,870 participants in the China Health and Retirement Longitudinal Study (CHARLS) and 2,295 in the English Longitudinal Study of Ageing (ELSA), calculated as RC (mg/dL) × hs-CRP (mg/L) / 10. Longitudinal analyses in a subcohort (n = 5,966) further assessed the associations between cumulative RCII, changes in RCII and CMM incidence. RESULTS Each ln-unit increase in baseline RCII was associated with a 14% (CHARLS: HR 1.14, 95% CI 1.09-1.19) and 21% (ELSA: HR 1.21, 95% CI 1.10-1.34) higher CMM risk. Similarly, cumulative RCII increments raised CMM risk by 20% (CHARLS: HR 1.20, 95% CI 1.11-1.29) and 30% (ELSA: HR 1.30, 95% CI 1.11-1.51). Transition patterns analysis showed that stable high RCII levels conferred the highest CMM risk compared to stable low RCII levels. RCII demonstrated moderate independent predictive capability for CMM and outperformed RC or hs-CRP alone. CONCLUSION By integrating lipid and inflammatory pathways, the RCII was significantly associated with incident CMM and may enhance early risk stratification.

Song Wen, Zhonghua Sun, Yanjun Song et al. · 0 citations