The result of this study indicates that NAC treatment decreases the incidence of postoperative AF.

No abstract

Electromagnetic radiation (EMR) or radiofrequency fields of cellular mobile phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation, and by changing the antioxidant defense systems of human tissues, thus leading to oxidative stress. Mobile phones are used in close proximity to the heart, therefore 900 MHz EMR emitting mobile phones may be absorbed by the heart. Caffeic acid phenethyl ester (CAPE), one of the major components of honeybee propolis, was recently found to be a potent free radical scavenger and antioxidant, and is used in folk medicine. The aim of this study was to examine 900 MHz mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and the role of CAPE on myocardial tissue against possible oxidative damage in rats. Thirty rats were used in the study. Animals were randomly grouped as follows: sham-operated control group (N: 10) and experimental groups: (a) group II: 900 MHz EMR exposed group (N: 10); and (b) group III: 900 MHz EMR exposed+CAPE-treated group (N: 10). A 900 MHz EMR radiation was applied to groups II and III 30 min/day, for 10 days using an experimental exposure device. Malondialdehyde (MDA, an index of lipid peroxidation), and nitric oxide (NO, a marker of oxidative stress) were used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status. In the EMR exposed group, while tissue MDA and NO levels increased, SOD, CAT and GSH-Px activities were reduced. CAPE treatment in group III reversed these effects. In this study, the increased levels of MDA and NO and the decreased levels of myocardial SOD, CAT and GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced heart tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative heart injury. These results show that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative heart impairment in rats.

Our results suggest that the increased level of MMP-3, MMP-9, and IL-6 may be responsible for ectasia formation in patients with CAE.

No abstract

Carvedilol plus NAC decreased POAF incidence and duration of hospitalization compared with metoprolol and decreased POAF incidence compared with carvedilol.

Backround: The aim of the present observational study is to search the incidence of postoperative atrial fibrillation (AF) in patients with or without preoperative statin treatment. Methods andResults: The population consisted of 362 consecutive patients (267 on and 95 not on statin). Diabetes mellitus was more frequent in statin group (p = 0.03). Other demographic and procedural variables were similar in the both groups (All p > 0.05). Postoperative AF was less frequent and its duration was shorter in statin group compared to non-statin group (p = 0.03 and 0.0001, respectively). The Kaplan-Meier analysis showed the protective effect of statins against the risk of developing AF (p = 0.01). Conclusion: Statin treatment before the by-pass surgery decreases the incidence and shortens the duration of postoperative AF.

We investigated whether the lymphocyte-to-monocyte ratio (LMR) 48 hours after admission is related to 30-day and long-term mortality in patients with ST-elevation myocardial infarction (STEMI) who were treated with primary percutaneous coronary intervention (PCI). We evaluated 318 consecutive patients with STEMI who were undergoing primary PCI. The relationship between the LMR and all-cause mortality (30-day and long-term) was analyzed by categorizing the patients into tertiles (T) according to LMR-T1 (>2.46), T2 (1.67-2.46), and T3 (<1.67). The T3 group exhibited the highest risk of 30-day all-cause mortality (hazard ratio [HR]: 8.093 [1.006-65.074]; P = .049). For long-term mortality, a significantly higher mortality risk was observed in both T2 (HR: 2.005 [1.021-3.939]; P = .043) and T3 groups (HR: 2.374 [1.160-4.857]; P < .001) compared to the T1 group (reference group). In multivariate analysis, these associations remained unaltered even after adjusting for confounders. A low LMR at 48 hours after admission may be independently associated with both 30-day and long-term mortality in patients with STEMI who were treated with primary PCI. This marker may be used for identifying patients with STEMI at high risk.