Obstructive Sleep Apnea and Myocardial Injury in Refractory Angina
Does severe obstructive sleep apnea (OSA) result in overnight myocardial injury?
This was a single-center cross-sectional study of patients with refractory angina, which was defined according to published guidelines: chronic angina >3 months which cannot be controlled with revascularization. Excluded patients included: stable angina, previous stroke with disability, or unstable clinical picture. Patients underwent overnight polysomnography and high-sensitivity cardiac troponin T (hs-cTnT) was obtained under resting conditions.
A total of 89 patients were evaluated and 80 (age: 62 ± 10 years; male: 66%; body mass index [BMI]: 29.5 ± 4 kg/m2) were included for final analysis after exclusions listed above. On average, patients had suffered a myocardial infarction 5 months to 33 years (121 ± 95 months) and 94% had undergone at least one revascularization (percutaneous coronary intervention or coronary artery bypass grafting) in the past. A total of 60 (75%) had moderate or severe OSA (apnea-hypopnea index [AHI] >15). Compared with patients with no OSA (≤15 events/hour), patients with OSA were more obese (BMI: 30.5 ± 4 vs. 27.5 ± 4 kg/m2, p = 0.01), and had a higher proportion of hypertension (98% vs. 80%, p = 0.01) and diabetes mellitus (68% vs. 40%, p = 0.02), respectively. Patients in the highest AHI quartile (≥51 events/hour) had significantly higher morning levels of hs-cTnT. This group of severe OSA patients was the only variable associated with the highest hs-cTnT after adjusting for age, male gender, or obesity.
The authors concluded that in a small cohort of refractory angina patients, OSA is common, and among the group with very severe OSA, myocardial injury is independently associated with refractory angina.
OSA is associated with atherosclerosis and predicts worse cardiovascular outcomes. OSA remains underdiagnosed in cardiology practice. Repetitive apnea leading to hypoxia is repeatedly reported in the literature to trigger sympathetic activation, oxidative stress, and endothelial dysfunction. Refractory angina is estimated to exist at between 5-10% in the catheterization laboratory population, and a search for unrecognized comorbidities that contribute to this condition is important (Mannheimer C, et al., Eur Heart J 2002;23:355-70). The findings here support the hypothesis that the imbalance between oxygen demand and supply could result in subtle nocturnal myocardial injury in a population with severe coronary artery disease. The next steps might include the impact that OSA treatment with positive airway pressure might have in this setting.
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