# Left Atrial Strain as a Marker of Supraventricular Arrhythmia Risk in Type 2 Diabetes Mellitus

## TL;DR

This study shows that left atrial strain measured by echocardiography can predict supraventricular arrhythmia risk in type 2 diabetes patients without heart disease.

## Contribution

The study introduces left atrial conduit strain as a novel, non-invasive marker for arrhythmia risk in type 2 diabetes.

## Key findings

- Type 2 diabetes patients showed impaired left atrial mechanics compared to controls.
- Left atrial conduit strain (LAScd) best predicted supraventricular arrhythmias with a cut-off of -8%.
- Combining LAScd with left ventricular ejection fraction improved risk prediction accuracy.

## Abstract

Background/Objectives: To determine whether left atrial (LA) strain by speckle-tracking echocardiography can identify supraventricular arrhythmia risk in patients with type 2 diabetes mellitus (T2DM) without overt structural heart disease. Methods: Prospective, single-center observational cohort study including 107 adults: 57 with T2DM and 50 age-matched controls. Participants underwent clinical assessment and echocardiography at baseline and 12 months. LA reservoir, conduit, and contractile strain (LASr, LAScd, LASct) were measured; left atrial volume indexed (LAVI) and LA stiffness index (LASI) were calculated. The primary endpoint was clinically significant supraventricular arrhythmia at 12 months on 24 h Holter (atrial fibrillation (AF)/atrial flutter (AFL) ≥ 30 s and/or excessive supraventricular ectopy). Predictors were assessed using penalized logistic regression and discrimination by ROC analysis. Results: At baseline and 12 months, T2DM showed impaired LA mechanics versus controls (baseline: LASr 20.1 ± 5.7 vs. 25.8 ± 6.3%, LAScd −11.6 ± 4.2 vs. −15.6 ± 4.9%, LASct −9.9 ± 3.2 vs. −13.1 ± 3.7%; all p < 0.001) and higher LASI (0.4 ± 0.2 vs. 0.3 ± 0.1, p < 0.001). LAVI was higher in T2DM at 12 months (34.0 ± 7.0 vs. 29.9 ± 6.5 mL/m2, p = 0.003). Supraventricular arrhythmias occurred in 20/57 patients (35.1%) of the T2DM vs. 1/50 patients (2.0%) of the control group (p < 0.001). Arrhythmias were assessed by 24 h Holter monitoring at the 12-month follow-up. In T2DM, LAScd provided the best single-parameter discrimination (AUC 0.692), with an optimal cut-off around −8% (sensitivity 55.6%, specificity 81.8%); a LAScd+left ventricular ejection fraction (LVEF) model improved AUC to 0.772. Conclusions: In this prospective observational cohort, T2DM was associated with subclinical LA dysfunction and a higher burden of supraventricular arrhythmias. LAScd emerged as the most clinically informative LA deformation marker for arrhythmic risk stratification and may support targeted rhythm surveillance in diabetic patients. These findings require external validation in larger, independent multicenter cohorts.