TY - JOUR
T1 - Patients with obstructive sleep apnea exhibit impaired endothelial function after myocardial infarction
AU - Sert Kuniyoshi, Fatima H.
AU - Singh, Prachi
AU - Gami, Apoor S.
AU - Garcia-Touchard, Arturo
AU - Van Der Walt, Christelle
AU - Pusalavidyasagar, Snigdha
AU - Wright, R. Scott
AU - Vasquez, Elisardo Corral
AU - Lopez-Jimenez, Francisco
AU - Somers, Virend K.
N1 - Funding Information:
Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Somers has served as a consultant for ResMed, Cardiac Concepts, Sova Pharmaceuticals, Apnex Medical, Merck, and Johnson and Johnson and has been a principal investigator or coinvestigator on research grants funded by the Respironics Foundation, the ResMed Foundation, Select Research, and the Sorin Corporation. Dr Somers is working with Mayo Health Solutions and their industry partners on intellectual property related to sleep and cardiovascular disease. Dr Sert Kuniyoshi became a full-time employee for Philips Respironics after the collection of the data provided in this article. Drs Singh, Gami, Garcia-Touchard, Pusalavidyasagar, Wright, Vasquez, and Lopez-Jimenez; and Ms van der Walt have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
PY - 2011/7/1
Y1 - 2011/7/1
N2 - Background: Impaired brachial flow-mediated dilation (FMD) is associated with risk for subsequent cardiovascular events in patients after myocardial infarction (MI). These patients often have obstructive sleep apnea (OSA). We tested the hypothesis that patients with OSA post MI will exhibit more severe impairment in FMD. Methods: We studied 64 patients with MI admitted to our hospital. OSA was determined using polysomnography. FMD was measured using high-resolution ultrasonography, with researchers blind to the OSA diagnosis. Results: The mean age was 60 ± 11 years, and the mean BMI was 29 (26, 32 kg/m2), 84% of patients were men, 39% had moderate to severe OSA (apnea-hypopnea index [AHI]> 15), and 31% of the patients had mild OSA (5 ≤ AHI< 15). FMD was severely impaired in patients with moderate to severe OSA (0.8% ± 0.7%) as compared with patients without OSA (4.7% ± 0.8%, P =.001) and with mild OSA (3.9% ± 0.8%, P =.015). Linear regression showed that FMD was associated with log nocturnal nadir oxygen saturation (minSaO2) (β = 31.17, P =.0001), age (β = - 0.11, P =.006). MinSaO2 was an independent predictor of FMD after adjustment for possible confounders (β = 26.15, P =.001). Conclusions: FMD is severely impaired in patients with moderate to severe OSA post MI, which may be partially related to nocturnal hypoxemia. Patients with OSA may, therefore, be at higher risk for subsequent cardiovascular events after an MI. Identifying and treating OSA may have important implications in the long-term prognosis of patients post MI. Further studies are necessary to determine if the presence of OSA would affect the long-term occurrence of cardiovascular events after an MI.
AB - Background: Impaired brachial flow-mediated dilation (FMD) is associated with risk for subsequent cardiovascular events in patients after myocardial infarction (MI). These patients often have obstructive sleep apnea (OSA). We tested the hypothesis that patients with OSA post MI will exhibit more severe impairment in FMD. Methods: We studied 64 patients with MI admitted to our hospital. OSA was determined using polysomnography. FMD was measured using high-resolution ultrasonography, with researchers blind to the OSA diagnosis. Results: The mean age was 60 ± 11 years, and the mean BMI was 29 (26, 32 kg/m2), 84% of patients were men, 39% had moderate to severe OSA (apnea-hypopnea index [AHI]> 15), and 31% of the patients had mild OSA (5 ≤ AHI< 15). FMD was severely impaired in patients with moderate to severe OSA (0.8% ± 0.7%) as compared with patients without OSA (4.7% ± 0.8%, P =.001) and with mild OSA (3.9% ± 0.8%, P =.015). Linear regression showed that FMD was associated with log nocturnal nadir oxygen saturation (minSaO2) (β = 31.17, P =.0001), age (β = - 0.11, P =.006). MinSaO2 was an independent predictor of FMD after adjustment for possible confounders (β = 26.15, P =.001). Conclusions: FMD is severely impaired in patients with moderate to severe OSA post MI, which may be partially related to nocturnal hypoxemia. Patients with OSA may, therefore, be at higher risk for subsequent cardiovascular events after an MI. Identifying and treating OSA may have important implications in the long-term prognosis of patients post MI. Further studies are necessary to determine if the presence of OSA would affect the long-term occurrence of cardiovascular events after an MI.
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U2 - 10.1378/chest.10-1722
DO - 10.1378/chest.10-1722
M3 - Article
C2 - 21349927
AN - SCOPUS:79960391943
SN - 0012-3692
VL - 140
SP - 62
EP - 67
JO - Chest
JF - Chest
IS - 1
ER -