INTRODUCTION: Obstructive sleep apnoea (OSA) merits increasing attention as cardiovascular risk factor. Whereas carotid and coronary artery disease have been associated with OSA, occurrence of peripheral arterial disease (PAD) in OSA remains undefined. METHODS: We screened 100 patients with suspected OSA for PAD. After polysomnography, each patient underwent standardized angiological testing including ankle-brachial index (ABI), central pulse wave velocity, pulse wave index and duplex sonography. RESULTS: Among total study population, PAD prevalence accounted for 88%, of those 68% had asymptomatic plaques and 20% were symptomatic Fontaine ≥ IIa. In confirmed OSA, prevalence raised up to 98%. Except for smoking habits, distribution of established risk factors did not differ between OSA groups (patients without, mild, intermediate and severe OSA). Presence of plaque, Fontaine PAD stages and intermittent claudication exhibited significant gain with increasing AHI. A logistic regression model revealed that age (OR = 1.199, 95% CI [1.066; 1.348]) and the logarithmically transformed AHI (OR = 5.426, 95% CI [1.068; 27.567]) had the strongest influence on plaque presence. Central pulse wave velocity as marker of arterial stiffness was positively correlated with AHI. CONCLUSION: OSA is associated with a high prevalence of PAD. This implies substantial diseasés under-recognition and a presumable atherogenic role of OSA in the pathogenesis of PAD. However, vasoprotective impact of OSA treatment remains to be determined.
INTRODUCTION:Obstructive sleep apnoea (OSA) merits increasing attention as cardiovascular risk factor. Whereas carotid and coronary artery disease have been associated with OSA, occurrence of peripheral arterial disease (PAD) in OSA remains undefined. METHODS: We screened 100 patients with suspected OSA for PAD. After polysomnography, each patient underwent standardized angiological testing including ankle-brachial index (ABI), central pulse wave velocity, pulse wave index and duplex sonography. RESULTS: Among total study population, PAD prevalence accounted for 88%, of those 68% had asymptomatic plaques and 20% were symptomatic Fontaine ≥ IIa. In confirmed OSA, prevalence raised up to 98%. Except for smoking habits, distribution of established risk factors did not differ between OSA groups (patients without, mild, intermediate and severe OSA). Presence of plaque, Fontaine PAD stages and intermittent claudication exhibited significant gain with increasing AHI. A logistic regression model revealed that age (OR = 1.199, 95% CI [1.066; 1.348]) and the logarithmically transformed AHI (OR = 5.426, 95% CI [1.068; 27.567]) had the strongest influence on plaque presence. Central pulse wave velocity as marker of arterial stiffness was positively correlated with AHI. CONCLUSION: OSA is associated with a high prevalence of PAD. This implies substantial diseasés under-recognition and a presumable atherogenic role of OSA in the pathogenesis of PAD. However, vasoprotective impact of OSA treatment remains to be determined.
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