Author + information
- Ines Abdesselam,
- Anne Dutour, MD, PhD,
- Frank Kober, PhD,
- Patricia Ancel, MS,
- Thierry Bege, MD, PhD,
- Patrice Darmon, PhD,
- Nathalie Lesavre, MD,
- Monique Bernard, PhD and
- Bénédicte Gaborit, MD, PhD∗ ()
- ↵∗Inserm U1062, Inra U1260, Aix Marseille Université, Faculté de Médecine, 27 Boulevard Jean Moulin, 13385 Marseille Cedex 05, France
More than body mass index (BMI), adiposity distribution in visceral area and in ectopic sites likely plays an important role in the obesity-related risk. Ectopic fat accumulation in the heart, the liver, and the pancreas, namely steatosis, could induce accumulation of toxic lipid intermediates leading ultimately to organ dysfunction. Whether ectopic fat stores are subjected to modification through intervention approaches is therefore crucial. The development of noninvasive imaging has made it possible to quantify ectopic fat stores with accuracy. Myocardial triglyceride content (MTGC), hepatic triglyceride content (HTGC), and pancreatic triglyceride content (PTGC) can be measured in humans by proton magnetic resonance spectroscopy (1). We previously demonstrated that after 6 months, bariatric surgery (BS) significantly decreased visceral fat (VAT), HTGC, PTGC, and to a lesser extent, epicardial adipose tissue (EAT) (1). However, we found no significant change in myocardial fat, although it was increased at baseline (1). Whether more sustained weight loss is able to modulate cardiac fat depots is the question we addressed here.
We obtained the ethics committee’s approval to re-evaluate ectopic fat deposits 2 or 3 years after surgery (mean 32 months) in a group of 23 severe obese patients who already underwent cardiac magnetic resonance imaging and proton magnetic resonance spectroscopy. EAT, MTGC, HTGC, and PTGC could be evaluated in 21 patients. The majority of patients were female (81%). Mean age was 42 ± 2 years, and mean BMI was 43.2 ± 1.1 kg/m2. Changes in ectopic fat levels were tested with the paired Student t test or Wilcoxon test. The associations between relative changes in each variable were tested with Spearman correlation. A p value <0.05 was considered statistically significant.
At 32 months, weight significantly decreased from 118 ± 15 kg to 84 ± 18 kg and BMI from 43.2 ± 4.3 kg/m2 to 30.7 ± 4.9 kg/m2 (both, p < 0.0001). The mean percentage of excess weight loss and fat mass loss at 32 months was 67 ± 27% and 21 ± 14%, respectively. All patients lost weight between 6 and 32 months, except for 5 patients who regained weight (+10 ± 9 kg) and 1 patient who remained stable. We observed complete remission of obstructive apnea syndrome for 8 of 8 patients and diabetes remission for 6 of 8 patients. After BS, we observed an important decrease in visceral fat (VAT −46 ± 27%; p < 0.0001), hepatic (HTGC −31 ± 36%; p = 0.0001) and pancreatic fat (PTGC −44 ± 20%; p = 0.0010) compared with baseline, but no more reduction was found at 32 months compared with 6 months (Figure 1B). EAT (−33 ± 16%) and subcutaneous abdominal fat (−33 ± 26%) continued to decrease to a significant extent compared with their 6-month values (p = 0.008 and p = 0.03, respectively). Importantly, MTGC significantly decreased at 32 months compared with baseline (−40 ± 7%; p = 0.001), and left ventricular mass decreased at 6 months and continued to decrease between 6 and 32 months (−9 ± 10%; p = 0.001). The high-density lipoprotein/triglycerides ratio significantly increased at 32 months (Figure 1A) and was significantly associated with VAT, but not with MTGC (r = 0.56, p = 0.02; r = 0.05, p = NS, respectively).
No association was observed between percentage of ectopic fat losses and body weight changes (p = NS). Neither EAT and VAT loss nor HTGC and MTGC loss were correlated, suggesting discrepancies in adiposity reduction.
Our findings suggest that cardiac fat has a more delayed response to BS than that seen in visceral fat, or other steatoses. Significance of triglyceride accumulation in the heart is still debated (2). The contracting heart has much higher metabolic demand than other organs. Whether the presence of lipid droplets in cardiomyocytes is detrimental or a beneficial compensatory response to altered systemic metabolic changes in obesity needs further evaluation. Our results also confirm those obtained for skeletal muscle, with reversal of systemic and muscle metabolic derangements only 9 months after BS (3). The improvement in life-style habits may have also contributed to the late reduction in cardiac steatosis. Compared with usual care, BS is the most effective treatment for severe obesity, and the long-term results regarding reduction of cardiovascular mortality have been well established. To the best of our knowledge, this study is the first to show a significant improvement in all types of ectopic fat depots, even cardiac steatosis, long-term after BS. Whether these improvements participate in the reduction of cardiovascular risk and mortality in obese patients needs to be confirmed.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
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