Oliver J Rider, Steffen E Petersen, Jane M Francis, Mohammed K Ali, Lucy E Hudsmith, Monique R Robinson, Kieran Clarke, and Stefan Neubauer (2011)
Ventricular hypertrophy and cavity dilatation in relation to body mass index in women with uncomplicated obesity.
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/m(2)) to severely obese (45.0 +/- 4.6 kg/m(2)), 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.