Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning?

backgroundObstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH). In animal models, IH has been shown to protect the myocardium during periods of ischemia by reducing infarct size. However, this phenomenon of "ischemic preconditioning" has not been investigated among OSA patients with acute myocardial infarction (MI). This study investigates the role of OSA on MI severity as measured by cardiac enzymes, specifically troponin-T, among patients with an acute MI.

methodsThis is an observational cohort study of patients ≥18 years of age who were hospitalized with an acute MI. Each participant underwent portable sleep monitoring (Apnea Link Plus); OSA was defined as an apnea-hypopnea index ≥5/h. Multivariable regression analysis was conducted to assess the relationship between OSA and highly sensitive troponin-T levels.

resultsIn our entire cohort of acute MI patients (n = 136), 77 % of the sample had evidence of sleep disordered breathing, with 35 % of the sample having OSA (i.e., an AHI >5). Higher AHI was associated with lower peak troponin-T levels in partially adjusted models (β = -0.0320, p = 0.0074, adjusted for age, gender, and race) and fully adjusted models (β = -0.0322, p = 0.0085) (additionally adjusted for smoking, hypertension, hyperlipidemia, body mass index, history of prior cardiovascular or cerebrovascular disease, diabetes and baseline admission creatinine levels). The mean value of the log-transformed peak troponin-T variable was used to dichotomize the outcome variable. In both partially (OR 0.949, CI 0.905-0.995, p = 0.03) and fully adjusted (OR 0.918, CI 0.856-0.984, p = 0.0151) logistic regression models, the OR for AHI suggests a protective effect on high troponin-T level.

conclusionsOur study demonstrates that patients with OSA have less severe cardiac injury during an acute non-fatal MI when compared to patients without OSA. This may suggest a cardioprotective role of sleep apnea during acute MI via ischemic preconditioning.