Those who presented glucose >= 140 mg/dl selleck inhibitor showed higher rates of malignant ventricular tachyarrhythmias (28% vs. 18%, P = .001), complicative bundle branch block (5% vs. 2%, P = .005), new atrioventricular block (9% vs. 5%, P
= .05) and in-hospital mortality (15% vs. 5%, P < .001). Multivariate analysis showed that those with glycemia >= 140 mg/dl exhibited a 2-fold increase of in-hospital mortality risk (95% CI: 1.2-3.5, P = .008) irrespective of diabetes mellitus status (P-value for interaction = 0.487 and 0.653, respectively).
Conclusions: Stress hyperglycemia on admission is a predictor of mortality and arrhythmias in patients with STEMI and could be used in the stratification of risk in these patients. Full English text available from: www.revespcardiol.org (C) 2010 Sociedad Espanola de Cardiologia. Published by Elsevier Espana, S.L. All rights reserved.”
“Background: Preclinical evidence of the preventive benefits of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) in breast cancer continues to fuel interest in selleckchem the potential role of dietary fat content in reducing breast cancer risk. The dose of fish-oil/omega-3
PUFAs needed to achieve maximal target tissue effects for breast cancer prevention remains undefined.
Objective: To determine the dose effects of omega-3 fatty acids on breast adipose tissue fatty acid profiles, we conducted a study of 4 doses of omega-3 PUFAs in women at high risk of breast cancer.
Design: Bafilomycin A1 manufacturer In this 6-mo randomized open-label study,
48 women with increased breast cancer risk received 1, 3, 6, or 9 capsules/d of an omega-3 PUFA supplement that provided 0.84, 2.52, 5.04, and 7.56 g docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) daily, respectively. Subjects made monthly visits, at which time pill counts were made and fasting blood samples were collected to determine fatty acid profiles; anthropometric measurements were made, breast adipose tissue samples were collected, and laboratory tests of toxicity (alanine aminotransferase, LDL cholesterol, and platelet function) were made at baseline and at 3 and 6 mo.
Results: All doses led to increased serum and breast adipose tissue EPA and DHA concentrations, but the response to 0.84 g DHA+EPA/d was less than the maximum possible response with >= 2.52 g/d. Body mass index attenuated the dose response for serum tissue DHA and EPA (P = 0.015 and 0.027, respectively) and breast adipose tissue DHA (P = 0.0022) in all of the treatment groups. The incremental increase in DHA and EPA correlated inversely with baseline fat and serum values. Compliance over 6 mo was 92.9 +/- 9.2% and was unaffected by treatment arm. No severe or serious toxicities were reported.
Conclusions: Daily doses up to 7.56 g DHA+EPA were well tolerated with excellent compliance in this cohort at high risk of breast cancer.