Pulmonary hypertension in patients with severe obstructive sleep apnea
address: Hiroki Yamakawa, Department of Medicine, Aichi Medical University School of Medicine, 21 Karimata, Yazako, Nagakute-cho, Aichi 480-1195, Japan. Email: firstname.lastname@example.org
Abstract Thirty-seven patients (35 men and two women) with obstructive sleep apnea–hypopnea syndrome (OSAHS) without any known cardiovascular and lung diseases were examined by Doppler echocardiography. Eight of the 37 (21.6%) patients experienced daytime pulmonary hypertension (PH), and all of them had severe OSAHS with an apnea–hypopnea index of > 30. The study suggested that one-third of patients with severe OSAHS had daytime PH.
Transient and repetitive elevations of pulmonary artery pressure (PAP) during nocturnal sleep have been reported in association with obstructive sleep apnea–hypopnea syndrome (OSAHS).1–3 These elevations may be prominent during rapid eye movement (REM) sleep.4 However, some authors have claimed that OSAHS does not induce permanent pulmonary hypertension (PH) in the daytime.1 This study was undertaken to clarify the prevalence of daytime PH as a complication of OSAHS using Doppler echocardiographic measurements.
SUBJECTS AND METHOD
Thirty-seven patients (35 men and two women; mean age 45.5 ± 2.8 years) were admitted to the Sleep Disorders Center of Aichi Medical University Hospital for heavy snoring and/or excessive daytime sleepiness. Patients with coronary artery disease, renal and liver failure, and known lung disease were excluded from the study. We investigated PAP in all subjects by Doppler echocardiography during the day after a full overnight polysomnography (PSG).4 The PAP was calculated using the modified Bernoulli equation.5
Eight of the 37 (21.6%) patients with OSAHS had daytime PH. All of the patients with daytime PH suffered from severe OSAHS, having an apnea– hypopnea index (AHI; /h) of > 30, whereas patients with mild or moderate OSAHS had no daytime PH (Table 1). Of the 13 patients with OSAHS who were judged as obese with a body mass index (BMI; kg/m2) of > 30 according to the World Health Organization classification, four (30.7%) had daytime PH. The average minimum arterial oxygen saturation (SpO2) value obtained from each PSG for those patients with daytime PH tended to be lower than that in patients without PH. In terms of age, AHI, BMI, and the Epworth sleepiness scale (ESS), patients with daytime PH did not differ from those patients without PH (Table 2).
Table 1. . The prevalence of pulmonary hypertension (PH) in patients with obstructive sleep apnea–hypopnea syndrome (OSAHS)
|n of PH||0||0||8||8|
Table 2. . Comparisons between pulmonary hypertension (PH)(+) and PH(–) groups in patients with obstructive sleep apnea–hypopnea syndrome (OSAHS)
|Age (years)||40.8 ± 13.0||46.8 ± 12.7||0.249|
|BMI (kg/m2)||30.2 ± 4.7||28.5 ± 5.0||0.413|
|AHI (/h)||61.2 ± 17.3||44.3 ± 29.5||0.126|
|MinSpO2 (%)||66.5 ± 8.4||76.3 ± 13.0||0.051|
|ESS (/24)||7.8 ± 4.0||10.6 ± 6.3||0.257|
Although earlier studies have reported a high prevalence of PH in patients with OSAHS, most recent studies agree on a prevalence of approximately 20%, which is similar to the value of 21.6% we obtained. The severity of OSAHS in patients participating in the present study was severe rather than mild-to-moderate, whereby one-third of these patients who suffered from severe OSAHS had daytime PH. It is known that the involvement of severe PH and/or right-sided heart failure influences the mortality in obesity hypoventilation syndrome. However, Kessler et al. have described recently that PH which is generally mild-to-moderate does not need specific treatment.6 Further studies are needed on the treatment therapies of PH and/or pulmonary circulation in patients with OSAHS, and we suggest that investigations of PH by Doppler echocardiography, which can be performed easily, are necessary in patients with severe OSAHS.