TL;DR
Prediabetes was associated with a modestly increased risk of new-onset AF, particularly persistent AF, and was associated with HF development among individuals without established arrhythmia.
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.
AIMS/HYPOTHESIS Heart failure (HF) is a common complication of diabetes, associated with a high mortality rate and a substantial healthcare burden. Residual HF risk persists despite achieving current treatment targets, suggesting a role for additional mechanisms beyond conventional risk factors. We sought to prospectively assess HF incidence and independent risk factors in individuals with new-onset diabetes. METHODS We used a prospective inception cohort (ANDIS, n=19,892) that included all individuals with newly diagnosed diabetes from southern Sweden between 2008 and 2021. Baseline clinical, biochemical and questionnaire data were linked to the Region Scania Care Database to obtain data on cardiovascular events and to the National Diabetes Registry to gather further data on cardiovascular risk factors that were not collected in the ANDIS study protocol. All-cause HF included all cases of HF regardless of underlying aetiology, whereas non-ischaemic HF was defined as HF occurring in individuals without prior acute myocardial infarction at baseline or during follow-up before the HF diagnosis. Cardiovascular disease incidence was estimated using the Kaplan-Meier method, and the associations with risk factors and incident HF were assessed using Cox proportional hazards regression. RESULTS The median age of the overall population was 62.5 years (IQR 52.6-70.3), while the median age among individuals who developed incident all-cause HF was 69.8 years (IQR 62.7-76.7). A total of 819 individuals (4.1%) with prevalent HF were excluded. During up to 14 years of follow-up (median 5.0), the cumulative incidence of HF was 4.8%, exceeding that of myocardial infarction (3.0%). No individuals with type 1 diabetes developed HF, but the incidence was similar across those with type 2 diabetes, latent autoimmune diabetes in adults, and secondary diabetes. A lower eGFR and higher HOMA2-IR, were associated with increased risk of all-cause and non-ischaemic HF, independently of the presence of conventional risk factors. Insulin resistance predicted all-cause HF independently of the established SCORE2-Diabetes risk score. The hazard ratio (HR) per 1 SD increase in HOMA2-IR was highest in the low-risk group (HR 1.89; 95% CI 1.02, 3.48; p=4.3 × 10-2), with concordant results observed for non-ischaemic HF. CONCLUSIONS/INTERPRETATION The HF incidence was high, with approximately 1 in 20 individuals developing HF within 5 years after diagnosis of diabetes other than type 1, highlighting a notably high risk of developing HF soon after diabetes diagnosis. Beyond conventional risk factors, higher HOMA2-IR and lower renal function, but not hyperglycaemia or autoantibodies, were independent risk factors for HF. Measuring HOMA2-IR also provided prognostic information in addition to that provided by the SCORE2-Diabetes risk score, supporting its value in HF risk stratification.
A supervised machine learning algorithm for AF in a Western Pacific population was derived and demonstrated that higher risk was associated with hospitalisation for other cardio-renal diseases and death.
The findings are best interpreted as evidence of cardiovascular and multimorbidity complexity, not as proof of a COVID-specific, temporal, or causal AF–HF effect.
It is suggested that AF remains a risk factor for OHCA, even after adjustments for ischemic heart disease and heart failure, even after adjustments for ischemic heart disease and heart failure.
Background: Black individuals have a lower incidence of atrial fibrillation (AF) than White individuals despite a higher burden of many traditional cardiovascular risk factors. Differences in left atrial (LA) structure and function by race could partly explain the observed pattern of AF risk. Methods: This analysis included 4,576 (978 Black and 3,598 White) participants from the Atherosclerosis Risk in Communities (ARIC) study, followed between 2011 and 2021. The association of selected echocardiographic measures of LA structure and function with AF incidence was evaluated with race-specific Cox proportional hazards models with adjustment for sociodemographic and clinical covariates. Additional analyses assessed whether LA measures attenuated the association between race and incident AF. Results: The analysis included 778 AF cases (113 in Black and 665 in White participants, mean age 75 years). Larger LA size and worse LA function were associated with higher AF risk in both Black and White individuals, with most associations of similar magnitude in both groups, except for a slightly stronger association of LA reservoir strain in Black than White participants (Black: hazard ratio (HR) 0.89, 95% CI 0.86-0.92 per 1% increase; White: HR 0.94, 95% CI 0.92-0.95, p for interaction = 0.01). In the overall sample, White participants showed higher AF risk compared to Black participants (HR 1.59, 95% CI 1.24-2.03). Adjustment for most individual LA measures did not attenuate the association between race and AF risk. Conclusion: Larger LA size and worse LA function were associated with incident AF in both Black and White ARIC participants. However, these measures did not explain the lower AF incidence observed among Black participants. LA remodeling appears to be an important predictor of AF risk, but it is not the primary explanation for the Black-White AF paradox.
