Abstract

Objective Obesity has been linked to a spectrum of cardiovascular abnormalities from subclinical changes in cardiac structure to overt heart failure. Uncomplicated obesity (i.e. obesity without any other co-morbidity or cardiovascular risk factors) has been shown to cause increased LV mass and LV dilatation. Our hypothesis was that these changes are, at least in part, reversible following significant weight loss over one year. Method Forty-one obese (BMI 37.7 ± 7.4 SD) and 12 age, sex matched controls (BMI 21.6 ± 1.8 SD) with no identifiable cardiac risk factors underwent cardiac MR imaging for the assessment of LV Mass (g), LV end-diastolic volume (EDV; ml), stroke volume (SV; ml) and LV EF (%). Fourteen obese subjects underwent repeat imaging after a one year period of weight loss, averaging 14.6 ± 11.5 % total body weight. Results Obesity per se was associated with elevated LV mass (125 ± 27 vs 89 ± 23g; p<0.001), LV mass indexed to height (74.4 ± 14.3 vs 52.3 ± 11.4g/m; p<0.001) and EDV (147 ± 28 vs 119 ± 24 ml; p<0.001). ESV and SV were also elevated in obesity (47 ± 12 vs 39 ± 12ml; p=0.05, and 100 ± 14 vs 80 ± 18 ml; p<0.001, respectively). LV EF was similar between groups (p=0.83). After weight loss, there was a significant reduction in LV mass (by 16 ± 11g; 135 ± 31 vs 119 ± 28g; p<0.001), LV mass indexed to height (76.4 ± 15.7 vs 68.9 ± 12 g/m; p<0.001). EDV and ESV were significantly smaller after weight loss (146 ± 25 vs 133 ± 23 ml; p<0.001, and 43 ± 12 vs 41 ± 10 ml; p<0.001 respectively). LV EF and SV did not change significantly. Conclusion In subjects with obesity in the absence of identifiable cardiac risk factors, LV hypertrophy and LV dilatation were partially reversible after a one year period of weight loss.

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