Sleep disordered breathing as a risk of cardiac events in subjects with diabetes mellitus and normal exercise echocardiographic findings

Sleep disordered breathing (SDB) is associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease; however, the contribution of SDB to incident heart failure (HF), coronary artery disease (CAD), and atrial fibrillation (AF) in patients with T2DM is unknown. We followed up 834 consecutive asymptomatic patients with T2DM (age 56 ± 11 years, 369 women) with normal exercise echocardiographic findings for ≤8 years using electronic health records. The demographics, cardiac risk factors, symptoms, diagnoses, and medications were collected at the echocardiography and validated from the electronic health records. SDB was confirmed by a comprehensive sleep evaluation and/or polysomnography before echocardiography. SDB was diagnosed in 188 patients (21%) at baseline; 116 were untreated. During a median follow-up of 4.9 years (interquartile range 3.9 to 6.1), 22 congestive HF, 72 CAD, and 40 AF incident events were observed. In the Cox proportional hazards models, SDB was associated with incident CAD (hazard ratio 1.8, 95% confidence interval 1.1 to 3.0, p = 0.01; adjusted hazard ratio 1.9, 95% confidence interval 1.2 to 3.2, p <0.01) and AF (hazard ratio 2.6, 95% confidence interval 1.4 to 4.7, p = 0.01; adjusted hazard ratio 2.9, 95% confidence interval 1.5 to 5.9, p <0.01). Limiting SDB to only those patients diagnosed using polysomnography (n = 132), SDB was associated with incident CAD (hazard ratio 1.9, 95% confidence interval 1.1 to 3.3, p = 0.03; adjusted hazard ratio 2.2, 95% confidence interval 1.2 to 3.9, p = 0.01) and HF (hazard ratio 2.7, 95% confidence interval 1.1 to 7.0, p = 0.03; adjusted hazard ratio 3.5, 95% confidence interval 1.4 to 9.0, p <0.01). Female gender, age, elevated blood pressure, and left ventricular mass were additional correlates of CAD in those with asymptomatic T2DM. In conclusion, the association of SDB with incident CAD, AF, and HF in patients with T2DM justifies more liberal screening for SDB in patients with T2DM, realizing that SDB is a potentially modifiable risk factor.