Key result
Baseline obesity in patients with Type 2 diabetes mellitus predicted a greater longitudinal increase in left ventricular mass (β=0.29, P<0.01) and decrease in ejection fraction (β=-0.15, P<0.05).
Why the study?
Few prospective studies have evaluated the natural progression of left ventricular remodelling in patients with Type 2 diabetes mellitus.
Does obesity accelerate longitudinal adverse cardiac remodeling and dysfunction in patients with Type 2 diabetes mellitus?
Cohort (n=274)
Does obesity accelerate longitudinal adverse cardiac remodeling and dysfunction in patients with Type 2 diabetes mellitus?
Effect estimate: β = 0.29 (LVM), β = -0.15 (LVEF)
p-value: p=<0.01 (LVM), <0.05 (LVEF)
In patients with Type 2 diabetes, baseline obesity is associated with a greater longitudinal increase in left ventricular mass and deterioration in systolic function.
Obesity may accelerate adverse LV remodeling in T2DM; hypothesis-generating for weight-loss intervention trials.
AIMS: Few prospective studies have evaluated the natural progression of left ventricular (LV) remodelling in patients with Type 2 diabetes mellitus (T2DM). The aim of this study was to evaluate the impact of obesity on longitudinal cardiac structural and functional changes in patients with T2DM. METHODS AND RESULTS: This study comprised of 274 patients with T2DM (mean age, 62.2 ± 11.4 years; male, 51.5%). Echocardiographic parameters including LV geometry, systolic, and diastolic functions were measured at baseline and follow-up. The median follow-up was 24 months (from 12 months to 48 months). The entire cohort showed a significant increase in LV wall thickness, LV mass (LVM), and prevalence of concentric hypertrophy (19.6-27.3%). Further, systolic function and diastolic function had deteriorated at follow-up assessment. Multivariable adjusted linear regression demonstrated that baseline body mass index (BMI) predicted longitudinal change to LVM (β = 0.29, P < 0.01) and LV ejection fraction (β = -0.15, P < 0.05). Patients were divided into three groups according to their BMI: normal weight (BMI <23 kg/m2), overweight (BMI between 23 kg/m2 and 27.5 kg/m2), or obese (BMI ≥27.5 kg/m2). Importantly, obesity at baseline predicted a greater longitudinal increase in LVM and decrease in LV ejection fraction compared with overweight and normal weight patients. CONCLUSION: Being obese at baseline was associated with greater longitudinal increase in LV mass and greater deterioration in LV systolic function.
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Wu et al. (2018) conducted a cohort in Type 2 diabetes mellitus (n=274). Obesity (BMI ≥27.5 kg/m2) vs. Normal weight (BMI <23 kg/m2) or overweight (BMI 23-27.5 kg/m2) was evaluated on Longitudinal change to left ventricular mass and ejection fraction (β = 0.29 (LVM), β = -0.15 (LVEF), p=<0.01 (LVM), <0.05 (LVEF)). Baseline obesity in patients with Type 2 diabetes mellitus predicted a greater longitudinal increase in left ventricular mass (β=0.29, P<0.01) and decrease in ejection fraction (β=-0.15, P<0.05).
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