Underdiagnosis of Obstructive Sleep Apnoea in Peripheral Arterial Disease.

Background: Obstructive sleep apnoea (OSA) has interdependently been related to the onset and progression of a large portion of atherosclerotic cardiovascular disorders. In due consideration of OSA-mediated endothelial dysfunction, its impact on peripheral artery disease is conceivable, but undefined. Objectives: The aim of this study was to identify the prevalence of OSA in a lower extremity artery disease (LEAD) study population. Methods: A total of 91 patients receiving in- and outpatient treatment for LEAD were included in this prospectively conducted trial. In addition to an angiological examination, all patients underwent nocturnal screening for sleep-disordered breathing by use of SOMNOcheck micro® (SC micro) and - depending on the results obtained - polysomnography. Results: Patients were principally late middle-aged (69.3 ± 10.8 years), male (71.4%) and slightly overweight (BMI 26.8 ± 3.9). Overnight screening determined a sleep apnoea prevalence of 78.0%, of which 90.1% exhibited a predominantly obstructive genesis. The mean apnoea-hypopnoea index (AHI; events/h) and oxygen desaturation index (events/h) averaged 11.8 ± 13.4 and 8.9 ± 14.2, respectively. The individual AHI categories of non-pathological (<5), mild (5 to <15), moderate (15 to <30) and severe sleep apnoea (≥30) accounted for 22.0, 59.3, 13.2 and 5.5%, respectively. A distributive examination of AHI within LEAD severity groups evinced a significant association (p = 0.047). In cases of at least moderate sleep apnoea (AHI ≥15) polysomnography was performed (n = 17, 18.7% of the whole collective). Correlative analysis revealed a significant correlation between values obtained by SC micro recording and polysomnography, establishing the diagnostic accuracy of the screening results. Conclusions: OSA exhibits an important prevalence of 70.3% in LEAD patients with prior undiagnosed sleep-disordered breathing, indicating major OSA unawareness in this cardiovascular cohort. However, the impact of OSA treatment on LEAD propagation remains to be determined. © 2015 S. Karger AG, Basel.