Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning?
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Obstructive 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.
This 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.
In 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.
Our 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.
KeywordsObstructive sleep apnea Myocardial infarction Intermittent hypoxemia Cardiac enzymes Ischemic preconditioning
Dr. Shah has funding support from the American Sleep Medicine Foundation. In addition, pilot funding for purchasing sleep monitors was provided by the Divisions of Pulmonary and Cardiology at Montefiore Medical Center.
The authors would like to express their deepest gratitude to the Department of Respiratory Therapy at Montefiore Medical Center for their assistance in the application of the portable sleep monitors for this study.
The authors have indicated no financial conflicts of interest. A research grant ($2,000) from Resmed was received for scoring and reviewing of sleep studies by independent reviewers with no relationship to Resmed.
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