Key result
In T2DM with preserved LVEF, cDTI-derived |E2A| increased with diabetes duration and independently predicted diastolic dysfunction (OR 2.549, 95% CI 1.538-4.224; p<0.001; AUC 0.904).
Why the study?
The ability of second-order motion-compensated cardiac diffusion tensor imaging to characterize diabetes-duration-related myocardial microstructural abnormalities and their associations with myocardial mechanics in patients with T2DM and preserved LVEF required evaluation.
Does second-order motion-compensated cardiac diffusion tensor imaging (cDTI) characterize diabetes-duration-related myocardial microstructural abnormalities and their associations with diastolic dysfunction in patients with type 2 diabetes mellitus and preserved ejection fraction?
Observational (n=115)
No
Does second-order motion-compensated cardiac diffusion tensor imaging (cDTI) characterize diabetes-duration-related myocardial microstructural abnormalities and their associations with diastolic dysfunction in patients with type 2 diabetes mellitus and preserved ejection fraction?
Second-order motion-compensated cardiac diffusion tensor imaging detects progressive, diabetes-duration-related myocardial microstructural remodeling that strongly correlates with and discriminates early diastolic dysfunction in patients with type 2 diabetes and preserved ejection fraction.
Answers are grounded in this paper and cite their sources.
cDTI may detect diabetes-duration-related microstructural changes in T2DM with preserved LVEF; leaves open clinical utility pending prospective validation.
To evaluate the ability of second-order motion-compensated cardiac diffusion tensor imaging (cDTI) to characterize diabetes-duration-related myocardial microstructural abnormalities and their associations with myocardial mechanics in patients with type 2 diabetes mellitus (T2DM) and preserved left ventricular ejection fraction (LVEF). In this prospective single-centre study, 70 patients with T2DM and preserved LVEF (30 with ≤5 years and 40 with >5 years of diabetes duration) and 45 age-matched controls underwent cDTI. Short-duration T2DM already showed higher mean diffusivity (MD), higher absolute secondary eigenvector angle (|E2A|), and lower helix angle transmurality (HAT), whereas fractional anisotropy (FA) was reduced only with longer duration (all p < 0.05). In covariate-adjusted analyses, longer diabetes duration was independently associated with lower FA and HAT and higher MD and |E2A| (all p ≤ 0.001). FA and HAT correlated positively and MD and |E2A| inversely with peak longitudinal diastolic strain rate (PDSR-L; all Holm-adjusted p < 0.004). In adjusted logistic regression, |E2A| was independently associated with diastolic dysfunction (OR 2.549, 95% CI 1.538–4.224; p < 0.001) and discriminated diastolic dysfunction (AUC 0.904). Second-order motion-compensated cDTI identifies diabetes-duration-related myocardial microstructural remodelling that is associated with early diastolic mechanical impairment in patients with T2DM and preserved LVEF.
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Zhong et al. (2026) conducted an observational in Type 2 diabetes mellitus with preserved ejection fraction (n=115). Type 2 diabetes mellitus duration and myocardial microstructural remodeling (absolute secondary eigenvector angle |E2A|) vs. Age-matched healthy controls and short-duration (<=5 years) T2DM was evaluated on Left ventricular diastolic dysfunction (defined as longitudinal peak diastolic strain rate <=1.029 s-1) (OR 2.549, 95% CI 1.538-4.224, p=<0.001). In T2DM with preserved LVEF, cDTI-derived |E2A| increased with diabetes duration and independently predicted diastolic dysfunction (OR 2.549, 95% CI 1.538-4.224; p<0.001; AUC 0.904).
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