Related Experiment Video
Updated: Jul 19, 2026

Murine Echocardiography of Left Atrium, Aorta, and Pulmonary Artery
Published on: February 20, 2017
Predictors of left ventricular dilatation in young adults (from the Bogalusa Heart Study)
Showkat A Haji1, Rifat Eralp Ulusoy, Dharmendrakumar A Patel
1Department of Cardiology, Medical Center, Tulane University, New Orleans, Louisiana, USA.
Insights
Childhood obesity and adult obesity with hypertension predict left ventricular dilatation in young adults. Early detection of these risk factors is crucial for preventing cardiac issues.
Area of Science:
- Cardiology
- Public Health
Background:
- Left ventricular (LV) dilatation can signal early cardiac decompensation and dysfunction.
- Determinants of LV dilatation in young, asymptomatic adults are not well understood.
Purpose of the Study:
- To investigate the predictors of left ventricular dilatation in a young, asymptomatic population.
- To identify associations between obesity, hypertension, and LV dilatation.
Main Methods:
- Echocardiography was used to measure LV end-diastolic diameter in 506 asymptomatic subjects (mean age 32 years).
- Statistical analyses, including regression, were performed to identify predictors of LV dilatation.
- Subjects were categorized based on body mass index (BMI) and hypertension status.
Main Results:
- LV dilatation was observed in 6% of subjects.
- Higher BMI, systolic, and diastolic blood pressures were associated with LV dilatation.
- Adulthood obesity (BMI >30 kg/m2) and hypertension were independently associated with a threefold increased odds of LV dilatation.
- Childhood BMI was the only significant predictor of adult LV dilatation in multiple regression analysis (OR 1.47).
Conclusions:
- Obesity starting in childhood is a significant predictor of LV dilatation in young adulthood.
- Obesity and hypertension in young adulthood are also key predictors of LV dilatation.
- These findings highlight the importance of early lifestyle interventions to prevent cardiac remodeling.
Abstract:
Left ventricular (LV) dilatation may be an early sign of cardiac decompensation progressing to LV dysfunction. Determinants of LV dilatation in young asymptomatic adults are unknown. Five hundred six asymptomatic subjects (mean age 32 +/- 3 years) enrolled in the Bogalusa Heart Study underwent echocardiographic examination. LV dilatation (LV end-diastolic diameter >5.5 cm) as measured by M-mode echocardiography was found in 31 subjects (6%). Subjects with LV dilatation had greater body mass indexes (32 +/- 9 vs 27 +/- 6 kg/m2, p <0.0001), systolic (119 +/- 15 vs 112 +/- 12 mm Hg, p = 0.007) and diastolic (79 +/- 12 vs 75 +/- 9 mm Hg, p = 0.04) blood pressures, and LV mass (230 +/- 50 vs 123 +/- 39 g, p <0.0001). Age, gender, race, and metabolic parameters (glucose, insulin, and lipoprotein levels) did not differ significantly between the subjects with and without LV dilatation. After correction for age, gender, and race differences, adulthood obesity (body mass index >30 kg/m2) was associated with a threefold odds ratio (2.9, 95% confidence interval 1.4 to 6.1), and hypertension (defined as per the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) was also associated with a threefold odds ratio (3.0, 95% confidence interval 1.2 to 7.1) for an increased incidence of LV dilatation. There was an incremental increase in LV end-diastolic dimension depending on the presence of hypertension or obesity, and subjects with obesity and hypertension in adulthood had the greatest degree of LV end-diastolic dimensions. In multiple regression analyses, body mass index in childhood was the only significant predictor of LV dilatation in adulthood (odds ratio 1.47, 95% confidence interval 1.03 to 2.09). In conclusion, obesity beginning in childhood and obesity and hypertension in young adulthood are predictors of LV dilatation in an otherwise healthy young adult population.
Related Concept Videos
Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Heart Failure II: Pathophysiology