Micro- and Macrovascular Risk and Complications In T2DM Males With Obstructive Sleep Apnea
Back to listIntroduction
Obstructive sleep apnea syndrome (OSAS) is a frequently overlooked comorbidity in the common form of type 2 diabetes mellitus (T2DM), which is associated with obesity, a metabolic syndrome (MetS) phenotype, and/or central fat accretion. We recently reported on the phenotype of OSAS from a large group of T2DM males and showed that it was associated with insulin resistance (IR) and its covariables, as well as with prevalent major adverse cardiovascular events (MACE), including stroke (1). The following cross-sectional study performed in a larger sample with an updated higher OSAS prevalence (11%), aimed at characterizing standard and emerging CV risk factors/markers in T2DM males with and without OSAS together with relevant metabolic biometrics.
Abstract
BACKGROUND
Obstructive sleep apnea syndrome (OSAS) is a comorbidity of obesity. OSAS is also an independent risk factor for type 2 diabetes (T2DM). OSAS promotes incident major adverse cardiovascular events (MACE). The prevalence of OSAS and its association with MACE are poorly documented in T2DM, a high-risk population.
METHODS
We analyzed 580 consecutive male T2DM outpatients in whom OSAS was diagnosed through combined evaluation, including (hetero)anamnesis, Epworth's Sleepiness Scale (ESS), overnight oximetry, and confirmed by polysomnography. OSAS (+) (n=66) were compared to OSAS (–) (n=514) regarding cardiovascular (CV) risk factors, microvascular complications, MACE, and UKPDS 10-year absolute CVD risk.
RESULTS
Mean (1 SD) age was 63 (11) years, diabetes duration 13 (9) years. Metabolic syndrome (MetS) prevalence was 77%, and HbA 7.5 (1.5)%. OSAS prevalence was 11.4%. There were no differences in age, diabetes duration, smoking, blood pressure (BP), and lipids (except for triglycerides) between OSAS (+) and (–). There were significant differences in the ESS score, BMI, waist, relative/absolute fat, skeletal muscle, conicity index, and visceral fat, all significantly higher in OSAS (+). Micro- and macrovascular complication prevalences were high, though not significantly different, in both groups, except for stroke prevalence, which was doubled in OSAS (+): 15 vs 7%; P=.05). Fasting triglycerides and cystatin-C levels were significantly higher in OSAS (+), the increase in the latter being unrelated to differences in eGFR between groups. UKPDS Risk Engine input variables and predicted risk were all similar in both groups, with a 10-year risk for CAD 20% and 22%, respectively in OSAS (–) and OSAS (+) patients (NS).
CONCLUSIONS
OSAS is frequent in male T2DM patients who exhibit a high-risk cardiometabolic phenotype characterized by severe MetS score and prevalence, central fat accretion, insulin resistance, hypertriglyceridemia, and raised cystatin-C. The data indicate an association between OSAS and stroke prevalence. Using the T2DM-specific UKPDS Risk Engine, absolute 10-year CVD risk estimates were elevated, though not significantly different, between OSAS subgroups in primary CV prevention.
Keywords
sleep apnea syndrome, metabolic syndrome, T2DM, UKPDS, cystatin-C, triglycerides
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