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Bariatric Surgery-Induced Resolution of Hypertension and Obstructive Sleep Apnea: Impact of Modulation of Body Fat, Ectopic Fat, Autonomic Nervous Activity, Inflammatory and Adipokine Profiles

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Abstract

Background

Obesity-associated systemic hypertension (HTN) and obstructive sleep apnea (OSA) have multiple pathophysiological pathways including ectopic fat deposition, inflammation, altered adipokine profile, and increased sympathetic nervous activity. We characterized these potential mechanisms in severely obese patients with or without HTN and OSA. We also compared changes of these mechanisms at 12 months following biliopancreatic diversion with duodenal switch (BPD-DS) surgery according to HTN and OSA resolution.

Methods

Sixty-two severely obese patients were evaluated at baseline and 12 months; 40 patients underwent BPD-DS. Blood samples, bioelectrical impedance analysis, computed tomography scan, and 24-h heart rate monitoring were performed. OSA have been determined with polysomnography and HTN with blood pressure measurement and medical file.

Results

Patients with HTN (n = 35) and OSA (n = 32) were older men with higher ectopic fat deposition and lower parasympathetic nervous activity without difference in adipokines and inflammatory markers. Lower reduction in weight was observed in patients with unresolved HTN (−40.9 ± 3.3 kg vs. −55.6 ± 3.8 kg; p = 0.001) and OSA (−41.4 ± 10.7 kg vs. −51.0 ± 15.2 kg; p = 0.006). Visceral adipose tissue reduction was lower in patients with unresolved HTN (−171.0 ± 25.7 cm2 vs. −274.5 ± 29.0 cm2; p = 0.001) in contrast to a trend for lower abdominal subcutaneous adipose tissue reduction in patients with unresolved OSA (−247.7 ± 91.5 cm2 vs. −390.5 ± 109.1 cm2; p = 0.08). At 12 months, parasympathetic activity was lowest in unresolved HTN and OSA patients, without difference in adipokines and inflammatory biomarkers.

Conclusion

Lower ectopic fat mobilization, lower level of parasympathetic nervous activity, and lower subcutaneous adiposity mobilization may play a role in the pathophysiology of unresolved HTN and OSA following BPD-DS surgery.

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Correspondence to Paul Poirier.

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Funding

This study was funded by the Fondation Institut universitaire de cardiologie et de pneumologie de Québec. Funding support granted to P.P.

Conflict of Interest

S.M. has a financial relationship from Medtronic and Johnson & Johnson. The other authors (A.A., L.B., F.-S.H., S.B., S.L., F.J., O.L., Y.L., M.-E.P., K.C., S.D.P., K.G., J.M., M.B., D.H.S.-P., and P.P.) declare that they have no conflict of interest.

Ethical Approval Statement

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed Consent Statement

Informed consent was obtained from all individual participant included in the study.

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Auclair, A., Biertho, L., Marceau, S. et al. Bariatric Surgery-Induced Resolution of Hypertension and Obstructive Sleep Apnea: Impact of Modulation of Body Fat, Ectopic Fat, Autonomic Nervous Activity, Inflammatory and Adipokine Profiles. OBES SURG 27, 3156–3164 (2017). https://doi.org/10.1007/s11695-017-2737-z

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