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Updated: Jun 24, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
Impact of diabetes on treatment-induced changes in left ventricular structure and function in hypertensive patients
Insights
Diabetes hinders left ventricular hypertrophy regression and systolic function improvement in hypertensive patients undergoing treatment. This suggests diabetes negatively impacts cardiac remodeling and function despite blood pressure control.
Area of Science:
- Cardiology
- Endocrinology
- Hypertension Research
Background:
- Diabetes mellitus is linked to left ventricular hypertrophy (LVH) and impaired systolic function in hypertensive individuals.
- Limited data exists on diabetes' effect on LVH regression and functional recovery during antihypertensive therapy.
Purpose of the Study:
- To investigate the impact of diabetes on left ventricular hypertrophy (LVH) regression and systolic function improvement in hypertensive patients receiving antihypertensive treatment.
Main Methods:
- Annual echocardiography was conducted over 4.8 years in hypertensive patients with electrocardiographic LVH from the LIFE study.
- Patients received losartan- or atenolol-based treatment; 730 were non-diabetic and 93 were diabetic.
- Multivariate analyses assessed independent predictors of LVH regression and functional improvement.
Main Results:
- Diabetic patients had higher baseline body mass index, pulse pressure, and albuminuria, with lower LV ejection fraction and midwall shortening.
- Despite similar blood pressure reduction, diabetic patients showed a higher prevalence of persistent LVH (47% vs. 39%).
- Diabetes independently predicted less LV mass reduction and reduced improvement in stress-corrected LV midwall shortening.
Conclusions:
- In hypertensive patients with LVH, diabetes is associated with more persistent LVH.
- Diabetes independently predicts poorer LVH regression and less improvement in systolic function during antihypertensive treatment.
Background And Aim:
Diabetes is associated with left ventricular hypertrophy (LVH) and impaired systolic function in hypertensive patients, but less is known about its impact on LVH regression and functional improvement during antihypertensive treatment.
Methods And Results:
We performed annual echocardiography in 730 non-diabetic and 93 diabetic patients (aged 55-80 years) with hypertension and electrocardiographic LVH during 4.8-year losartan- or atenolol-based treatment in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Baseline mean blood pressure (BP) and LV mass did not differ between groups. Diabetic patients had higher body mass index and pulse pressure, and lower LV ejection fraction, midwall shortening, stress-corrected midwall shortening, and estimated glomerular filtration rate (all p<0.05), and were more likely to have albuminuria. Despite comparable BP reduction in diabetic and non-diabetic groups during treatment (33/18 vs. 28/16mmHg (ns)), diabetes was associated with higher prevalence of persistent LVH (47 vs. 39%, p<0.05). In multivariate analyses, diabetes independently predicted less LV mass reduction and less improvement in stress-corrected LV midwall shortening (both p<0.01).
Conclusion:
Among hypertensive patients with LVH, diabetes is associated with more residual LVH and less improvement in systolic LV function by echocardiography over 4.8 years of antihypertensive treatment.
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