While the relationship between sleep-disordered breathing and pulmonary hypertension (PH) is not new, it can be unclear. During the CHEST 2024 session, Pulmonary Hypertension in Sleep Disorders, on Monday in Boston, four experts used evidence-based medicine to try to answer some of the everlasting questions about this relationship.

Echocardiographic changes in patients with sleep-disordered breathing

Paul Forfia, MD, Professor of Medicine and Co-Director of the Pulmonary Hypertension, Right Heart Failure, and CTEPH Program at Temple University Hospital, discussed the many different pathophysiologic presentations of sleep-disordered breathing.

“If you’re wondering what the unifying echocardiographic changes are in sleep-disordered breathing, it depends on the pathophysiology of the person’s background, medical conditions, and sleep disorder,” Dr. Forfia said.

Understanding that the cardiac, structural, and functional changes will mirror the pathophysiology is important. However, the echo pattern most commonly reflects non-systolic left heart dysfunction with signs of left atrial enlargement, left ventricular hypertrophy, and heart failure with preserved ejection fraction. In a smaller percentage of patients, it is possible to have an overlapping pattern where they have some left heart disease and a modest amount of PR elevation.

“If you see a heart where you have a severely enlarged right ventricle, severe right ventricular (RV) dysfunction, systolic notching—all clearly indicating this person has a very strong precapillary PH phenotype—please be careful to not just ascribe this to the patient’s sleep apnea. It’s probably not related, strictly speaking, to sleep-disordered breathing. It may be a Group 1 or Group 4 disease,” Dr. Forfia said.

Sleep-disordered breathing and PH

Rama El-Yafawi, MD, Clinical Instructor in Medicine at Harvard Medical School, addressed the question, “Should clinicians be worried about sleep-disordered breathing and PH?” The short answer is yes.

“The reason why is because they have this bidirectional relationship. Not only does sleep disordered-breathing cause PH, but PH also predisposes to sleep-disordered breathing,” Dr. El-Yafawi said.

The mechanisms linking sleep disorders and PH are multifaceted, involving intermittent hypoxia, oxidative stress, increased sympathetic activity during sleep disturbance, and hypercapnia. All of those ultimately lead to pulmonary vasculature vasoconstriction.

Studies have shown that the coexistence of sleep-disordered breathing and PH causes a vicious cycle that increases the risk of worsening PH, RV dysfunction, cardiovascular events, and mortality.

“Early screening of PH and obstructive sleep apnea (OSA) patients and vice versa, OSA and PH patients, is imperative, and treating hypoxemia is crucial with these patients,” Dr. El-Yafawi said.

Effect of therapy on sleep-disordered breathing and PH

Session Chair, M. Safwan Badr, MD, FCCP, Professor of Internal Medicine, Physiology, and Biomedical Engineering at Wayne State University School of Medicine, explored the role of positive airway pressure (PAP) therapy on PH in patients with sleep-disordered breathing.

PH occurs in a fifth of patients with sleep-disordered breathing, and several pathways may lead to this.

“Our job in a given patient is to identify which one of these pathways is potentially relevant,” Dr. Badr said.

It is critical to consider what is happening beyond the severity of sleep apnea. Host factors, including obstructive airway disease and gas exchange variables, are stronger determinants of PH than the apnea-hypopnea index (AHI). For example, the presence of daytime or nocturnal hypoxia is predictive of a worse prognosis.

“PAP therapy will result in decreased pulmonary artery pressure. As of now, we don’t have data yet to say that it would have an impact on long-term patient-reported outcomes,” Dr. Badr said.

Obesity hypoventilation syndrome and PH

Session Co-Chair, Bhavin Dalal, MBBS, MD, FCCP, Professor of Pulmonary, Critical Care, and Sleep Medicine at the Oakland University William Beaumont School of Medicine, used a series of case vignettes to examine obesity hypoventilation syndrome (OHS) and PH, from diagnosis to treatment.

Approximately 8% to 10% of patients with obesity will develop OHS, and the prevalence increases as BMI goes up, he said. There are two different OHS phenotypes. One is an obstructive phenotype, meaning patients have OSA along with OHS. With the other phenotype, patients do not have OSA but they do have hypoventilation during the night.

When clinicians have a low suspicion of OHS, a serum bicarbonate level of <27 mmol/L can rule out most cases.

“We do an echo in almost every patient and start the PAP treatment as soon as available, either in a clinic or when the patients are admitted,” Dr. Dalal said.

If the apnea-hypopnea index (AHI) is more than 30, patients should be started on CPAP, he said. If AHI is less than 30 or CPAP fails, they should be started on noninvasive ventilation treatment. While PAP can improve PH, these patients should also consider adjusting their diets.