1033 Association of the Cardiopulmonary Coupling Sleep Spectrogram with Incident Parkinson’s Disease in Older Men

The cardiopulmonary coupling (CPC) sleep spectrogram is an increasingly recognized measure of sleep quality which integrates sleep, autonomic drive, and respiration. Specifically, CPC is an estimate of the sleep state modulated synchronization and coupling between heart rate variability and respiration. Those with Parkinson’s disease (PD) have been shown to exhibit alterations in CPC and have higher rates of sleep disturbances, respiratory abnormalities, and autonomic dysfunction. However, little is known about the longitudinal association of CPC with incident PD in community-dwelling older men.

We studied 2859 men (mean [SD] age = 76.2 [5.4] years) without PD who underwent polysomnography between 2003 and 2005 and were followed until 2016 for incident self-reported PD as part of the Osteoporotic Fractures in Men (MrOS) prospective study. CPC was calculated from the electrocardiogram (ECG) during rapid eye movement (REM) sleep, N2 and N3 (N2N3) stages of non-REM sleep, and across the whole night. CPC metrics included high, low, and very low frequency coupling (HFC, LFC, and VLFC, respectively). Ratios of the 3 power bands were computed to assess deviation from or concordance with typical stage specific CPC patterns. Associations between tertiles of CPC metrics and incident PD were assessed using multivariable logistic regression.

During 11 years of follow-up, 64 incident PD cases were identified. After adjustment for covariates including age, comorbidities, and apnea-hypopnea index (AHI), men in the lowest tertile of VLFC/(LFC+HFC) during REM sleep had approximately twice the risk of developing PD [OR (95% CI) = 2.22 (1.20,4.35)] relative to men in the highest tertile. Whole-night and N2N3 CPC metrics were not associated with incident PD.

Disruption of the typical CPC pattern during REM, representing potential altered interactions between brain (sleep electrocortical activity), cardiac (heart rate variability) and respiratory output mechanisms, was associated with an increased risk of incident PD. Our findings may reflect a prodromal alteration of interactions between sleep subsystems, though future studies are needed to understand potential mechanisms linking CPC to incident PD.

Support comes from the National Institute on Aging (R21AG085495) and the Institute for Personalized Sleep Health (Beth Israel Deaconess Medical Center).