Neuroadrenergic activation noted in obstructive sleep apnea via MSNA, heart rate

Obstructive sleep apnoea syndrome (OSAS) exhibits an evident sympathetic activation even when uncomplicated by other cardiometabolic diseases, as manifested by the muscle sympathetic nerve activity (MSNA) and heart rate (HR) behaviour, a study has shown.

Such activity can be a target of therapeutic interventions aimed at exerting sympathomoderating effects, such as continuous positive airway pressure, according to the investigators.

A total of 850 participants recruited in 26 microneurographic studies, based on MSNA quantification in uncomplicated OSAS of different clinical severity, were assessed in this meta-analysis. The investigators then extended the evaluation to the relationships of MSNA with HR, anthropometric and blood pressure (BP) values, metabolic variables, apnoea–hypopnoea index (AHI), and oxygen saturation.

MSNA was evidently activated and almost homogeneously between studies, which indicated a progressive increase from the healthy state to mild, moderate, and severe OSAS (41.6, 48.3, 65.5, and 70.7 bursts/100 heart beats, respectively; p<0.01).

Of note, MSNA significantly correlated with AHI, a marker of OSAS severity (r, 0.55; p<0.02) and O₂ saturation but not with body weight and body mass index, since it occurred in obesity-related OSAS. In addition, HR was significantly and directly associated with MSNA and AHI (r, 0.56 and 0.46, respectively; p<0.03 for both), representing a surrogate marker of the sympathetic overdrive.

“Neuroadrenergic overdrive occurs in OSAS,” the investigators said. “However, the small sample size of the microneurographic studies, heterogeneity of the patients examined, presence of comorbidities, represented major weaknesses not allowing to precisely define the main features of the phenomenon, particularly in nonobese patients.”