Alicia Sánchez-de-la-Torre1, Xavier Soler2, Ferran Barbé1, Marina Florés3, Alan Maisel4, Atul Malhotra2, Montserrat Rue5, Sandra Bertran5, Albina Aldomá6, Fernando Worner6, Joan Valls5, Chi-Hang Lee7, Cecilia Turino1, Estefanía Galera3, Jordi de Batlle1, Manuel Sánchez-de-la-Torre8. 1. Respiratory Department, Hospital Universitari Arnau de Vilanova and Santa Maria, IRBLleida. Lleida, Catalonia, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain. 2. Pulmonary Division, Department of Critical Care and Sleep Medicine, UC San Diego, San Diego, CA. 3. Respiratory Department, Hospital Universitari Arnau de Vilanova and Santa Maria, IRBLleida. Lleida, Catalonia, Spain. 4. Cardiology Division, Veterans Affairs Medical Center, San Diego, CA. 5. Department of Basic Medical Sciences, IRBLleida - University of Lleida. Lleida, Catalonia, Spain. 6. Cardiology Department, Hospital Universitari Arnau de Vilanova, IRBLleida. Lleida, Catalonia, Spain. 7. Department of Cardiology, National University Heart Centre, Singapore. 8. Respiratory Department, Hospital Universitari Arnau de Vilanova and Santa Maria, IRBLleida. Lleida, Catalonia, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain. Electronic address: sanchezdelatorre@gmail.com.
Abstract
BACKGROUND: An analysis of cardiac injury markers in patients with OSA who sustain an episode of acute coronary syndrome (ACS) may contribute to a better understanding of the interactions and impact of OSA in subjects with ACS. We compared peak cardiac troponin I (cTnI) levels in patients with OSA and patients without OSA who were admitted for ACS. METHODS: Blood samples were collected every 6 hours from the time of admission until two consecutive assays showed a downward trend in the cTnI assay. The highest value obtained defined the peak cTnI value, which provides an estimate of infarct size. RESULTS: We included 89 patients with OSA and 38 patients without OSA with an apnea-hypopnea index of a median of 32 (interquartile range [IQR], 20.8-46.6/h and 4.8 [IQR, 1.6-9.6]/h, respectively. The peak cTnI value was significantly higher in patients without OSA than in patients with OSA (median, 10.7 ng/mL [IQR, 1.78-40.1 ng/mL] vs 3.79 ng/mL [IQR, 0.37-24.3 ng/mL]; P = .04). The multivariable linear regression analysis of the relationship between peak cTnI value and patient group, age, sex, and type of ACS showed that the presence or absence of OSA significantly contributed to the peak cTnI level, which was 54% lower in patients with OSA than in those without OSA. CONCLUSIONS: The results of this study suggest that OSA has a protective effect in the context of myocardial infarction and that patients with OSA may experience less severe myocardial injury. The possible role of OSA in cardioprotection should be explored in future studies.
BACKGROUND: An analysis of cardiac injury markers in patients with OSA who sustain an episode of acute coronary syndrome (ACS) may contribute to a better understanding of the interactions and impact of OSA in subjects with ACS. We compared peak cardiac troponin I (cTnI) levels in patients with OSA and patients without OSA who were admitted for ACS. METHODS: Blood samples were collected every 6 hours from the time of admission until two consecutive assays showed a downward trend in the cTnI assay. The highest value obtained defined the peak cTnI value, which provides an estimate of infarct size. RESULTS: We included 89 patients with OSA and 38 patients without OSA with an apnea-hypopnea index of a median of 32 (interquartile range [IQR], 20.8-46.6/h and 4.8 [IQR, 1.6-9.6]/h, respectively. The peak cTnI value was significantly higher in patients without OSA than in patients with OSA (median, 10.7 ng/mL [IQR, 1.78-40.1 ng/mL] vs 3.79 ng/mL [IQR, 0.37-24.3 ng/mL]; P = .04). The multivariable linear regression analysis of the relationship between peak cTnI value and patient group, age, sex, and type of ACS showed that the presence or absence of OSA significantly contributed to the peak cTnI level, which was 54% lower in patients with OSA than in those without OSA. CONCLUSIONS: The results of this study suggest that OSA has a protective effect in the context of myocardial infarction and that patients with OSA may experience less severe myocardial injury. The possible role of OSA in cardioprotection should be explored in future studies.
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