ADVERTISEMENT

SLEEP STRATEGIES: Group 3 pulmonary hypertension linked to sleep-disordered breathing

AHI and PH

Various studies have looked at different polysomnographic variables to understand the relationship between PH and OSA. Initial studies showed that the apnea hypopnea index (AHI) does not predict development of PH among patients with OSA. Decrements in nocturnal oxygen saturation, however, is predictive of the development of PH; the only predictor of developing PH among patients with OSA in one study was time spent with oxygen saturation below 70% during sleep (Wong et al. Eur Arch Otorhinolaryngol. 2017;74:2601). In addition, recent data suggest there is no statistically significant association between age, gender, body mass index, or AHI and chance for development of PH (Wong et al. 2017). It was found that the percentage of time during sleep with oxygen saturation below 90% was significant and independently associated with higher PAP. Furthermore, a recent study demonstrated that patients with moderate to severe OSA (AHI over 15/h) who develop PH tend to have worse hemodynamics (higher PVR and mPAP) and subclinical myocardial damage (evaluated by troponin T), as well as increased ventricular wall stress (assessed by proBNP) when compared with patients with mild OSA (AHI less than 15/h).

Treatment

The mainstay treatment for OSA and OHS is positive airway pressure (PAP). This therapy has been shown to improve sleep and respiratory parameters, including sleep quality, overall quality of life, as well as promote reduction in mean pulmonary arterial pressure. The regular use of noninvasive positive-pressure ventilation has also been shown to reverse daytime hypoxia and hypercapnia, as well as influence inflammatory markers: decrease circulating levels of endothelin-1, interleukin-6, and C-reactive protein, thereby improving vascular endothelial function and reducing platelet activation and aggregation (Yokoe et al. Circulation. 2003;107[8]:1129). Indeed, there is a decrease in mean pulmonary arterial pressure in some patients with long-term daily use of PAP, but, in some patients, both pulmonary and right ventricular dysfunction persists, suggesting vascular remodeling and/or endothelial dysfunction. These findings indicate the need for early recognition of OSA and early treatment for patients, thus preventing remodeling and further development of PH and right ventricular dysfunction. Adequate control of OSA/OHS has important long-term effects on overall health, because it significantly reduces the risk of systemic hypertension, congestive heart failure, arrhythmias, and stroke. It is imperative to control underlying SDB before considering PAH-specific medications to treat PH associated with OSA or OHS unless the patient is demonstrating signs of right-sided heart failure; in such cases, concomitant therapy may be considered upfront. It is recommended that

Dr. Ravish Singhal
patients with SDB should have an assessment for PH before starting therapy for their SDB and then again after 3 to 4 months of effective PAP confirmed by device data monitoring. For patients who have persistent PH despite achieving adequate control of their SDB, pulmonary vasodilator therapy may be indicated following standard treatment guidelines for WHO group 1 PAH (Galie et al. J Am Coll Cardiol. 2013;62[suppl 25]:D60–72). Medications that are currently approved for the treatment of PAH have not been well studied in PH associated with SDB and, at present time, the available data do not demonstrate sustained benefit.

Dr. Singhal is a second-year fellow in Pulmonary/Critical Care and Dr. Minkin is Director, Pulmonary Hypertension Program, New York Presbyterian-Brooklyn Methodist Hospital. Dr. Minkin is also Assistant Professor of Clinical Medicine, Weill Cornell Medical College, New York.