The Effect of Left Ventricular Diastolic Dysfunction on Sleep-Disordered Breathing Pathophysiology
Physician Scientist Training Grant
THOMAS TOLBERT, MD
ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
Key Project Outcomes
Obstructive sleep apnea (OSA) has a complex pathophysiology involving multiple mechanisms called “endotypes”, which differ across patients. The extent to which co-morbidities, like cardiopulmonary disease, influence OSA endotypes is unclear, in part because quantifying endotypes is challenging, historically requiring complex apparatus and maneuvers. Recently, however, an advanced signal analysis tool called Phenotyping Using Polysomnography (PUP) was developed to estimate OSA mechanisms from routine sleep study data. PUP potentially offers a method to examine the influence of cardiopulmonary comorbidities on OSA endotypes. Existing evidence suggests that impaired relaxation of the left ventricle, a cause of pulmonary vascular congestion, contributes to instability of breathing control. PUP can quantify breathing control instability by estimating loop gain. We therefore hypothesized that PUP-estimated loop gain would increase with increasing impairment of left ventricular relaxation. We conducted a prospective observational study in patients with obstructive sleep apnea who were at risk for or were known to have impaired left ventricular relaxation. Participants underwent in-lab attended overnight sleep studies and echocardiographic studies. Contrary to our primary hypothesis, we found no relationship between echocardiographic measures of impaired left ventricular relaxation and loop gain estimated by PUP from in-lab sleep studies. Further study is needed to determine whether the lack of any discernible relationship between impaired relaxation of the left ventricle and unstable ventilatory control is a true physiologic finding or an artifact of PUP methodology.