Can obstructive sleep apnea (OSA) and obesity contribute to the development of pulmonary hypertension?

Can OSA and Obesity Cause Pulmonary Hypertension?

Yes, both OSA and obesity can contribute to pulmonary hypertension, but the prevalence is relatively low in isolated OSA (approximately 20%), while the risk increases substantially when obesity and other comorbidities coexist. 1

Prevalence and Risk Profile

Pulmonary hypertension occurs in OSA, but it is most strongly associated with concurrent risk factors rather than OSA alone. 1 The key contributing factors include:

• Left-sided heart disease 1
• Parenchymal lung disease 1
• Nocturnal desaturation 1
• Obesity 1

In pure OSA without comorbidities, approximately 20.7% of patients develop mild pulmonary hypertension, particularly those who are older, more obese, and have lower daytime oxygenation. 2 However, when obesity is severe (BMI >40 kg/m²), the risk increases dramatically. 3

Mechanisms of Pulmonary Hypertension Development

In OSA Patients:

• Repetitive hypoxemia during apneic episodes reduces oxygen delivery to the myocardium and triggers pulmonary vasoconstriction 4
• Pulmonary hypertension develops in 27-34% of OSA patients overall 4
• The lowest SpO2 <70% is a statistically significant predictor of pulmonary hypertension (p = 0.016), while AHI alone is not a reliable predictor 5

In Obesity:

• Obesity alone causes reduced functional residual capacity and decreased respiratory system compliance 1
• Obesity hypoventilation syndrome (OHS) leads to diurnal hypercapnia and hypoxia, which induce pulmonary hypertension, right ventricular hypertrophy, and cor pulmonale 6
• Approximately 90% of OHS patients have coexisting OSA, with nearly 70% having severe OSA (AHI >30 events/h) 6

Clinical Presentation and Diagnosis

Pretibial edema is a highly specific sign of pulmonary hypertension in OSA patients. 3 In one study, 93% of OSA patients with lower extremity edema had right heart failure, and 86% had pulmonary hypertension. 3

Key predictive factors for pulmonary hypertension in OSA patients include:

• Age >60 years 2
• BMI >40 kg/m² 2, 3
• Daytime PaO2 <85 mmHg 2
• Minimum oxygen saturation in NREM sleep 3

Polysomnography is the gold standard for OSA diagnosis, and echocardiography should be performed routinely in OSA patients to assess for pulmonary hypertension. 4, 5

Treatment Effects

CPAP therapy effectively reduces pulmonary artery pressures when pulmonary hypertension is mild. 1 Specific outcomes include:

• In pulmonary hypertensive OSA patients, CPAP reduced mean PAP from 25.6 ± 4.0 to 19.5 ± 1.5 mm Hg (p < 0.001) after 6 months 2
• In normotensive OSA patients, CPAP reduced mean PAP from 14.9 ± 2.2 to 11.5 ± 2.0 mm Hg (p < 0.001) 2
• CPAP addresses the underlying pathophysiology by improving oxygen delivery, reducing sympathetic activity, and normalizing intrathoracic pressures 4
• Even severe pulmonary hypertension (approximately 70 mmHg) has been successfully treated with nocturnal CPAP, resulting in near-normalization of pulmonary artery pressure 7

Critical Clinical Pitfalls

Do not rely on AHI alone to predict pulmonary hypertension risk – the real value of using AHI to predict health risk is doubtful. 5 Instead, focus on:

• Minimum oxygen saturation levels, particularly <70% 5, 3
• BMI and degree of obesity 2, 3
• Daytime oxygenation status 2

In overlap syndrome (COPD + OSA) or obesity hypoventilation syndrome, pulmonary hypertension is often severe and treatment of sleep-disordered breathing is essential to improve pulmonary hemodynamics. 8

Perform polysomnography in all patients with pulmonary hypertension, irrespective of severity, as OSA should be considered as a contributing factor. 7