Neck and total body fat deposition in nonobese and obese patients with sleep apnea compared with that in control subjects.

Abstract

Around 50% of patients with the sleep apnea/hypopnea syndrome (SAHS) are not obese: body mass index (BMI) < 30 kg/m2. We hypothesized that local fat deposition around the upper airway may be different in nonobese patients with SAHS from that in normal subjects with the same body mass. We therefore examined the relationship between indices of general obesity; BMI, neck circumference (NC), and percentage total body fat with neck fat deposition measured by magnetic resonance imaging in three matched subject groups. Nine nonobese, nonsnoring control subjects (BMI, 25 SE 0.7 kg/m2; NC, 38.1 SE 0.5 cm; age, 37.5 SE 2.5 yr), nine nonobese patients with SAHS (BMI, 25.7 SE 0.4 kg/m2; NC, 39.8 SE 0.8 cm; age, 40 SE 4.2 yr), and nine obese patients with SAHS matched to the other groups for age (BMI, 34 SE 1.1 kg/m2; NC, 43.9 SE 0.6 cm; age, 40 SE 2.7 yr). Neck volume and fat content were assessed from the hard palate to the vocal cords using T1-weighted images. Percentage total body fat was 30 and 44% greater in nonobese and obese patients with SAHS, respectively, than in control subjects. Neck tissue volume was 10% greater in nonobese and 28% greater in obese patients with SAHS than in control subjects. The percentage of neck tissue volume attributed to fat was 27% greater in nonobese and 67% greater in obese patients with SAHS than in control subjects. The excess fat in both the nonobese and obese patients with SAHS compared with that in control subjects was localized to areas anterolateral to the upper airway, the differences were 52 and 88%, respectively. There were no significant differences between nonobese patients with SAHS and control subjects with respect to fat located in other areas of the neck; obese patients with SAHS had 42% more fat than control subjects (p < 0.05). We conclude that even relatively nonobese patients with SAHS have excess fat deposition, especially anterolateral to the upper airway when compared with control subjects with the same level of obesity assessed using BMI and NC. This may contribute to their predisposition to SAHS.