What does this research mean for the field?

Clinical obesity increases the risk of any arrhythmias by 28% and atrial fibrillation by 34% compared to non-obesity. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

What question did this study set out to answer?

This research aims to compare arrhythmia risk and ECG characteristics among different obesity statuses.

February 8, 2026

How excess fat affects cardiac electrophysiology: preclinical obesity, clinical obesity with cardiac arrhythmias and ECG features

Key Result

Clinical obesity increased risk of any arrhythmias by 28% (aHR 1.28) and atrial fibrillation by 34% (aHR 1.34) versus non-obesity over 14.6 years.

Key Points

This research aims to compare arrhythmia risk and ECG characteristics among different obesity statuses.
Analyzed data from UK Biobank participants with defined obesity statuses and no previous arrhythmias.
Stratified participants into non-obesity, preclinical obesity, and clinical obesity groups.
Utilized multivariable Cox models to assess links between obesity status and arrhythmias.
Preclinical obesity linked to an increased risk of any arrhythmias, SVA, and atrial fibrillation.
Clinical obesity associated with significantly higher risks of various arrhythmias and cardiac events compared to non-obesity.
ECG changes observed in clinical obesity, showing prolonged intervals and altered ventricular rates.

Structured PICO

Does preclinical and clinical obesity increase the risk of new-onset arrhythmias in individuals without prior arrhythmias?

Population

n=428,562 UK Biobank participants without prior arrhythmias

Intervention

Preclinical obesity and clinical obesity (classified using The Lancet Diabetes & Endocrinology Commission definitions)

Comparator

Non-obesity

Outcome

New-onset any arrhythmias, supraventricular arrhythmias (SVA), bradyarrhythmias, and ventricular arrhythmias (VA)hard clinical

Both preclinical and clinical obesity, as defined by the novel Lancet framework, are associated with a significantly increased risk of various arrhythmias and proarrhythmic ECG changes over a 14.6-year follow-up.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Abstract Background Obesity has been associated with increased risk of arrhythmias. However, current BMI-based diagnostic paradigm is unable to capture the complexity of obesity. The Lancet Diabetes 0.001), SVA (aHR 1.09, P0.001), atrial fibrillation (aHR 1.10, P0.001), and cardiac block (aHR 1.08, P0.001) (Figure 1). Compared to non-obesity, clinical obesity significantly increased the risk of any arrhythmias (aHR 1.28, P0.001), SVA (aHR 1.31, P0.001), bradyarrhythmias (aHR 1.24, P0.001), VA (aHR 1.16, P0.001), AF (aHR 1.34, P0.001), cardiac block (aHR 1.28, P0.001), pacemaker insertion (aHR 1.18, P0.001), ventricular tachycardia (aHR 1.22, P0.001), implantable cardioverter defibrillator insertion (aHR 1.44, P0.001), and cardiac arrest (aHR 1.16, P=0.009) (Figure 1). When compared to preclinical obesity, clinical obesity was associated with significantly higher risk of any arrhythmias, SVA, bradyarrhythmias, VA, AF, supraventricular tachycardia, cardiac block, sinus node dysfunction, pacemaker insertion, premature ventricular beats, VT, and cardiac arrest (all p0.05) (Figure 2). Additionally, clinical obesity exhibited significant correlations with ECG alterations, including prolonged P-wave duration, PR interval, QTc interval, and QRS duration, accompanied by shortened RR interval, elevated ventricular rate, significant altered P-wave axis and R-wave axis (all P0.05), compared to preclinical obesity (Figure 2). Conclusions Both preclinical and clinical obesity confer elevated arrhythmia risks, with clinical obesity demonstrating particularly pronounced associations across atrial, ventricular, and conduction system arrhythmias and presenting with significant proarrhythmic electrophysiological shifts.Figure 1 Figure 2

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