Title: Vascular Inflammation in Obesity and Sleep Apnea
Topic: Prevention/Vascular
Date Posted: 2/24/2010
Author(s): Jelic S, Lederer DJ, Adams T.
Citation: Circulation 2010;121:1014-1021.
Clinical Trial: No
Study Question: Both obesity and obstructive sleep apnea (OSA) are associated with vascular endothelial inflammation and increased risk for cardiovascular diseases. Are the endothelial alterations that are attributed commonly to obesity in fact related to OSA?
Methods: Seventy-one subjects with a body mass index ranging from normal to obese underwent attended polysomnography. To assess vascular inflammation and oxidative stress directly, the expression of nuclear factor-ĸB and nitrotyrosine were quantified by immunofluorescence in freshly harvested venous endothelial cells. Basal endothelial nitric oxide (NO) production and activity were quantified by the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS. Vascular reactivity was measured by brachial artery flow-mediated dilation.
Results: Expression of eNOS and phosphorylated eNOS and flow-mediated dilation were significantly lower, whereas expression of nitrotyrosine was significantly greater in OSA patients (n = 38) than in OSA-free subjects (n = 33) regardless of central adiposity. Expression of nuclear factor-ĸB was greater in obese OSA patients than in obese OSA-free subjects (p = 0.004). Protein expression and flow-mediated dilation were not significantly affected by increasing body mass index or central obesity in OSA patients and in OSA-free subjects. After 4 weeks of continuous positive airway pressure therapy, flow-mediated dilation and expression of eNOS and phosphorylated eNOS significantly increased, whereas expression of nitrotyrosine and nuclear factor-ĸB significantly decreased in OSA patients who adhered to continuous positive airway pressure ≥4 hours daily.
Conclusions: Untreated OSA rather than obesity is a major determinant of vascular endothelial dysfunction, inflammation, and elevated oxidative stress in obese patients.
Perspective: This study adds to the body of evidence that OSA may contribute to coronary risk and cardiovascular events. A few of the cardiometabolic effects of OSA include hypertension, increase in high-sensitivity C-reactive protein, heightened sympathetic tone, reactive platelets, dysglycemia, insulin resistance, and increase in cortisol, leptin, and growth hormone. Melvyn Rubenfire, M.D., F.A.C.C.
Title: Early and Late Outcome of Treated Patients Referred for Syncope to Emergency Department: the EGSYS 2 Follow-Up Study
Topic: Arrhythmias
Date Posted: 2/24/2010
Author(s): Andrea U, Attilio DR, Franco G, et al., on behalf of the Evaluation of Guidelines in Syncope Study 2 (EGSYS 2) Group.
Citation: Eur Heart J 2010;Feb 18:[Epub ahead of print].
Clinical Trial: yes
Study Question: What is the prognosis of patients with syncope?
Methods: This was a multicenter, prospective study of 380 patients (mean age 66 years) with syncope initially evaluated in an emergency department (ED). Therapy was at the discretion of the treating physician. The mean duration of follow-up was 20 months. The 1° endpoint was death from any cause or syncope recurrence.
Results: The most common causes of syncope were neurocardiogenic syncope in 64% of patients, orthostatic hypotension in 17%, cardiac syncope in 15%, and an arrhythmia in 11%. All-cause mortality was 9.2%. The strongest predictors of mortality were structural heart disease or an abnormal electrocardiogram (hazard ratio [HR], 5.6), hypertension (HR, 3.0), and trauma from syncope (HR, 2.24). Mortality in patients with cardiac syncope was significantly higher than in patients with other causes of syncope (37% vs. 7-11%). Syncope recurred in 16% of patients and the recurrence rate was unrelated to the etiology of syncope. The strongest predictors of recurrent syncope were palpitations before syncope (HR, 3.4), male gender (HR, 1.8), and absence of prodrome (HR, 0.4).
Conclusions: The risk of death during follow-up in patients with syncope is related to associated cardiac disease. Syncope recurrence is unrelated to the cause of syncope.
Perspective: A limitation of this study is that left ventricular ejection fraction was not included in the analysis and probably would have been a stronger predictor of mortality than simply the presence of structural heart disease. Fred Morady, M.D., F.A.C.C.
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