Key result
Class I obesity is linked to ~3-point worse LV GLS and increased visceral fat thickness.
Why the study?
It remained unclear whether early-stage obesity in young patients without other chronic noncommunicable diseases leads to metabolic disturbances and alterations in intracardiac hemodynamics that increase cardiovascular risk.
Does class I obesity (BMI 30-34.9 kg/m²) impair myocardial structural and functional remodeling and metabolic profiles compared to BMI <30 kg/m² in young individuals without diagnosed noncommunicable diseases?
Cross-Sectional (n=131)
Does class I obesity (BMI 30-34.9 kg/m²) impair myocardial structural and functional remodeling and metabolic profiles compared to BMI <30 kg/m² in young individuals without diagnosed noncommunicable diseases?
In young individuals with stage 1 obesity and no other chronic diseases, increased visceral and epicardial adipose tissue thickness and metabolic disturbances are already associated with subclinical left ventricular and left atrial longitudinal strain impairment.
Background Obesity is one of the most important independent risk factors for cardiovascular (CV) disease. The presence of comorbid conditions such as hypertension, diabetes, and dyslipidemia significantly increases the risk of complications. However, it remains unclear whether early-stage obesity in young patients without other chronic noncommunicable diseases (NCDs) leads to metabolic disturbances and alterations in intracardiac hemodynamics, thereby increasing CV risk. Aim To assess differences in adipose tissue (AT) distribution, myocardial structural and functional remodeling and metabolic profile in individuals with different body mass index (BMI). Methods The study included data from 131 individuals aged 21-59 years who underwent preventive examination, had no diagnosed NCDs, and were not receiving drug therapy. Participants were divided into two groups according to BMI and were comparable in terms of age and sex. The first group included 70 individuals (77.1% women) with BMI <30 kg/m², median age 41.0 [37.0; 50.0] years. The second group included 61 individuals (75.4% women) with BMI of 30-34.9 kg/m², median age 46.0 [39.0; 54.0] years. All participants underwent anthropometric assessment, echocardiography, ultrasound-assisted assessment of AT distribution using the Philips EPIQ CVx 2D system. Metabolic parameters were assessed, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) using the Architect C8000 automatic analyzer (Abbott, USA). The insulin resistance (IR) index (HOMA-IR) was calculated as fasting glucose×fasting insulin/22.5 (IR defined as >2.77). Visceral Adiposity Index (VAI) was calculated using sex-specific formulas. Statistical analysis was performed using StatTech v. 4.8.0. Results Patients with stage 1 obesity had significantly higher median glycemia (5.7 vs 5.3 mmol/l, p<0.001), TG (1.33 vs 0.88 mmol/l, p<0.001), TG/HDL-C ratio (1.06 vs 0.54, p<0.001), VAI (2.15 vs 0.87, p<0.001), HOMA-IR (3.62 vs 1.55, p<0.001). Obesity was associated with significantly greater visceral AT (VAT) and epicardial AT (EAT) thickness (both p<0.001). EAT showed a moderate inverse correlation with left atrial reservoir strain (LASr) (r = –0.4; p<0.001); each 1 mm increase in EAT was associated with a 1.21% decrease in LASr. Left ventricular global longitudinal strain (LV GLS) was significantly reduced in the obesity group (–19.0% vs –21.8%; p<0.001) and correlated with VAT thickness (r = 0.6; p<0.001). Each 1 mm increase in VAT corresponded to a 0.043% worsening in LV GLS. Conclusions Metabolic disturbances and increased VAT and EAT thickness in young individuals are associated with impaired longitudinal deformation of the left heart chambers. These findings indicate early myocardial dysfunction in patients with stage 1 obesity, even in the absence of other chronic diseases.
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Alieva et al. (2026) conducted a cross-sectional in Class I obesity (n=131). Class I obesity (BMI 30-34.9 kg/m²) and epicardial/visceral adiposity vs. BMI <30 kg/m² was evaluated on Left ventricular global longitudinal strain (LV GLS) (r = 0.6 (correlation with VAT thickness), p=<0.001). Class I obesity was associated with reduced left ventricular global longitudinal strain (-19.0% vs -21.8%; p<0.001) and greater visceral and epicardial adipose tissue thickness (both p<0.001).
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