Objective The traditionally accepted mechanism for ventricular adaptation to obesity suggests that cavity dilatation in response to increased blood volume and elevated filling pressure results in ventricular hypertrophy as a compensatory mechanism. Our hypothesis was that, instead, initiation of ventricular hypertrophy in obesity may be explained by changes in hormonal milieu and not by cavity dilatation.

Research design and methods 88 female subjects without identifiable cardiovascular risk factors, covering a wide range of body mass indices (BMI), from normal (21.2±1.6 kg/m²) to severely obese (45.0±4.6 kg/m²), underwent cardiovascular MRI to determine left ventricular (LV) and right ventricular (RV) mass and volumes.

Results BMI correlated positively with LV and RV mass and end-diastolic volumes (EDV). However overweight is associated with a significant LV and RV hypertrophy (LV: 78±11 g vs 103±16 g, p<0.01; RV: 26±7 g vs 40±11 g, p<0.01) was observed in the absence of differences in LV and RV volumes (LV: EDV 119±15 vs 121±21 ml, p>0.99, RV: 131±17 vs 130±24 ml; p>0.99). Furthermore, significant increases of serum leptin occurred at this pre-obese stage (15.6±19 vs 36.5±22 ng/ml; p=0.013).

Conclusion In a cohort of healthy female subjects with a wide range of BMIs, ventricular hypertrophy occurs without associated cavity dilatation in overweight individuals, while in manifest obesity, both cavity dilatation and ventricular hypertrophy occur. Elevated leptin levels may have a role in this effect on ventricular mass.