Mandibular advancement device treatment and reverse left ventricular hypertrophic remodeling in patients with obstructive sleep apnea

Abstract

Study objectives: Obstructive sleep apnea (OSA) is associated with cardiovascular comorbidities such as left ventricular (LV) hypertrophy. Whether OSA is an independent etiological factor for this hypertrophic remodeling is yet unknown. Continuous positive airway pressure partially reverses this hypertrophy, but data regarding the effect of mandibular advancement devices on LV remodeling are scarce. The aim of this prospective trial is to evaluate the effect of mandibular advancement device therapy on LV geometry and function in patients with OSA.

Methods: At baseline and 6-month follow-up, participants underwent a home sleep apnea test, 24-hour ambulatory blood pressure monitoring and a 2-dimensional Doppler and tissue Doppler echocardiography.

Results: Sixty-three patients (age: 49 ± 11 years; body mass index: 27.0 ± 3.4 kg/m2; baseline apnea-hypopnea index home sleep apnea test: 11.7 [8.2; 24.9] events/h) completed the 6-month follow-up visit. Overall, blood pressure values and parameters of LV function were within normal ranges at baseline and did not change under mandibular advancement device therapy. In contrast, the interventricular septum thickness was at the upper limits of normal at baseline and showed a significant decrease at 6-month follow-up (11.1 ± 2.1 mm vs 10.6 ± 2.0 mm, P = .03). This significant improvement is only found in responders but not in nonresponders. There was no correlation between the decrease of interventricular septum thickness and the change in blood pressure.

Conclusions: In mildly obese, normotensive patients with OSA we observed significant reverse hypertrophic remodeling after 6 months of successful mandibular advancement device therapy, with maintained normotensive systemic blood pressure. This suggests that OSA is an independent factor in the pathophysiology of LV hypertrophy in these patients.

Clinical trial registration: Registry: ClinicalTrials.gov; Name: Evaluation of the Cardiovascular Effects of the MAS in the Treatment of Obstructive Sleep Apnea; URL: https://ichgcp.net/clinical-trials-registry/NCT02320877; Identifier: NCT02320877.

Citation: Dieltjens M, Vanderveken OM, Shivalkar B, et al. Mandibular advancement device treatment and reverse left ventricular hypertrophic remodeling in patients with obstructive sleep apnea. J Clin Sleep Med. 2022;18(3):903-909.

Keywords: cardiovascular aspects; hypertrophic remodeling; mandibular advancement treatment.

Conflict of interest statement

All authors have seen and approved this manuscript. This research project was partly supported by a grant at Antwerp University Hospital from SomnoMed, Sydney, New South Wales, Australia. M.D. holds a Postdoctoral Fellowship at the Research Foundation Flanders (FWO: 12H4520N). O.M.V. and M.C.B. report grants from SomnoMed at the Antwerp University Hospital. OMV and MJB report grants from SomnoMed at the Antwerp University Hospital and both authors are member of the advisory board of ResMed and SomnoMed. O.M.V. reports research support outside the submitted work from Philips and Inspire Medical Systems at the Antwerp University Hospital and consultancy for Zephyr Sleep Technologies and GSK. O.M.V. holds a Senior Clinical Investigator Fellowship from the Research Foundation Flanders (FWO: 1833517N). The other authors report no conflicts of interest.

© 2022 American Academy of Sleep Medicine.

Figures

Figure 1. Echocardiographic parasternal long-axis view with measurement of the IVS thickness in a 49-year-old male patient with severe obstructive sleep apnea (AHI = 45.3 events/h).

The patient had a normal body weight (body mass index 25 kg/m2) and was normotensive on 24-hour blood pressure measurement. At baseline (A), IVS thickness was at the upper limits of normal (11.5 mm). Six months after regular mandibular advancement device treatment (B), there was a clear reduction of obstructive sleep apnea severity (AHI = 3.7 events/h) and a 0.7-mm decrease of IVS thickness. AHI = apnea-hypopnea index, IVS = interventricular septum.

Figure 2. Evolution of the interventricular septum thickness after 6 months of MAD therapy in responders vs nonresponders.

The IVS thickness improved significantly after 6 months of MAD therapy in the responders (n = 40) (11.1 ± 2.0 mm vs 10.5 ± 1.8 mm, P = .022) but not in the nonresponders (n = 19) (10.8 ± 2.2 mm vs 10.8 ± 2.3 mm, P = .872). IVS = interventricular septum, MAD = mandibular advancement device.