Background-Atrial fibrillation (AF) promotes atrial remodeling and can develop secondary to heart failure or mitral valve disease. Cardiac endothelin-1 (ET-1) expression responds to wall stress and can promote myocyte hypertrophy and interstitial fibrosis. We tested the hypothesis that atrial ET-1 is elevated in AF and is associated with AF persistence. Methods and Results-Left atrial appendage tissue was studied from coronary artery bypass graft, valve repair, and/or Maze procedure in patients in sinus rhythm with no history of AF (SR, nϭ21), with history of AF but in SR at surgery (AF/SR, nϭ23), and in AF at surgery (AF/AF, nϭ32). The correlation of LA size with atrial protein and mRNA expression of ET-1 and ET-1 receptors (ETAR and ETBR)was evaluated. LA appendage ET-1 content was higher in AF/AF than in SR, but receptor levels were similar. Immunostaining revealed that ET-1 and its receptors were present both in atrial myocytes and in fibroblasts. ET-1 content was positively correlated with LA size, heart failure, AF persistence, and severity of mitral regurgitation. Multivariate analysis confirmed associations of ET-1 with AF, hypertension, and LA size. LA size was associated with ET-1 and MR severity. ET-1 mRNA levels were correlated with genes involved in cardiac dilatation, hypertrophy, and fibrosis. Conclusions-Elevated atrial ET-1 content is associated with increased LA size, AF rhythm, hypertension, and heart failure. ET-1 is associated with atrial dilatation, fibrosis, and hypertrophy and probably contributes to AF persistence.Interventions that reduce atrial ET-1 expression and/or block its receptors may slow AF progression. (Circ Arrhythm Electrophysiol. 2010;3:369-379.)

Atrial fibrillation (AF), the most common cardiac arrhythmia, is an electrocardiographic description of a condition with multiple and complex underlying mechanisms. Oxidative stress is an important driver of structural remodeling that creates a substrate for AF. Oxidant radicals may promote increase of atrial oxidative damage, electrical and structural remodeling, and atrial inflammation. AF and other cardiovascular morbidities activate angiotensin (Ang-II)-dependent and independent cascades. A key component of the renin–angiotensin-aldosterone system (RAAS) is the mineralocorticoid aldosterone. Recent studies provide evidence of myocardial aldosterone synthesis. Aldosterone promotes cardiac oxidative stress, inflammation and structural/electrical remodeling via multiple mechanisms. In HF patients, aldosterone production is enhanced. In patients and in experimental HF and AF models, aldosterone receptor antagonists have favorable influences on cardiac remodeling and oxidative stress. Therapeutic approaches that seek to reduce AF burden by modulating the aldosterone system are likely beneficial but underutilized.

Low serum vitamin D is associated with MSP along with low calcium intake, depression, and anxiety. Supplementation with vitamin D improved MSP and associated disorders.
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Dietary FO attenuated AF inducibility following cardiac surgery by modulating autonomic tone and heart rate. FO also reduced atrial inflammation, iNOS, and ET-1 expression.

Inflammation plays a pivotal role in the etiology of coronary artery disease (CAD). Myeloperoxidase (MPO) is a potent inflammatory factor and a critical modulator of coronary inflammation and oxidative stress. The goal of this study was to determine the impact of the plasma MPO (pMPO) level and neutrophil/lymphocyte ratio on the clinical characteristics and outcomes of patients with CAD. Blood samples were collected from 210 patients with underlying chest pain or recent myocardial infarction (MI) prior to coronary angiography in order to measure pMPO levels. The pMPO levels and neutrophil/lymphocyte ratio were correlated with clinical characteristics and outcomes following catheterization. The pMPO level and neutrophil/lymphocyte ratio were higher in patients with recent MI than in patients with CAD (coronary occlusion ≥50%) or without CAD (coronary occlusion <50%). Patients with ST segment elevated MI (STEMI) had a higher neutrophil/lymphocyte ratio relative to patients with non-STEMI. The pMPO level was identified to correlate with the neutrophil/lymphocyte ratio and the need for coronary artery reperfusion by coronary artery bypass surgery or percutaneous coronary intervention. Patients who were taking aspirin had lower pMPO levels and neutrophil/lymphocyte ratio compared with those who were not taking aspirin. The plasma neutrophil/lymphocyte ratio was negatively associated with the left ventricular ejection fraction at baseline and the 30-day follow-up, whereas pMPO showed no correlation. Multivariate analysis indicated that the pMPO level was positively associated with MI, the neutrophil/lymphocyte ratio and coronary intervention. The preoperative use of aspirin was associated with a lower pMPO level and neutrophil/lymphocyte ratio. In conclusion, pMPO is positively associated with MI, the neutrophil/lymphocyte ratio and coronary intervention. The preoperative use of aspirin is associated with a lower pMPO level and neutrophil/lymphocyte ratio. pMPO may serve as a predictor of coronary intervention and as a potential therapeutic target for the reduction of inflammation in patients with CAD.

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Sleep deprivation (SD) has been associated with memory impairment through induction of oxidative stress. Melatonin, which promotes the metabolism of many reactive oxygen species (ROS), has antioxidant and neuroprotective properties. In this study, the effect of melatonin on memory impairment induced by 4 weeks of SD was investigated using rat animal model. Animals were sleep deprived using modified multiple platform model. Melatonin was administered via oral gavage (100 mg/kg/day). Spatial learning and memory were assessed using the radial arm water maze (RAWM). Changes in oxidative stress biomarkers in the hippocampus following treatments were measured using ELISA procedure. The result revealed that SD impaired both short- and long-term memory (P < 0.05). Use of melatonin prevented memory impairment induced by SD. Furthermore, melatonin normalized SD-induced reduction in the hippocampus activity of catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD). In addition, melatonin enhanced the ratio of reduced to oxidized glutathione GSH/GSSG in sleep-deprived rats (P < 0.05) without affecting thiobarbituric acid reactive substance (TBARS) levels (P > 0.05). In conclusion, SD induced memory impairment, which was prevented by melatonin. This was correlated with normalizing hippocampus antioxidant mechanisms during chronic SD.

Background/Objectives Coronary artery disease (CAD) is responsible for significant morbidity and mortality. Inflammatory, pro-thrombotic and structural factors contribute to the etiology of CAD. This study sought to determine the relationship of plasma endothelin-1 (pET-1), a potent vasoconstrictor, mitogen and modulator of cardiac inflammation, to clinical characteristics and outcomes of CAD patients. Methods Blood samples were collected from 336 patients with underlying chest pain or recent myocardial infarction (MI), prior to coronary catheterization. pET-1 was correlated with clinical characteristics and outcomes following catheterization and at 30-day follow-up. Results pET-1 was higher in recent MI patients than in patients with CAD (coronary occlusion≥50%) or without CAD (<50%) (Mean±sem (pg/ml): 2.12±0.13, 1.51±0.10, 1.21±0.06; 95% confidence interval (1.85–2.38, 1.31–1.72, 1.07–1.32; respectively, P<.0001). Patients with ST elevation MI (STEMI) had higher pET-1 than non-STEMI (P=.008). pET-1 was associated with heart failure (HF) and low left ventricular ejection fraction (LVEF) and was highest in MI patients presented with acute HF. At 30-day follow up, pET-1 was not associated with the change in LVEF. In multivariate analysis, pET-1 was positively associated with age, smoking, HF, CAD status, and need for revascularization by coronary artery bypass surgery (CABG). pET-1 was negatively correlated with LVEF and preoperative statin use. Conclusions pET-1 is associated with recent MI, HF, age, smoking, CABG, and low LVEF. Preoperative statin use was associated with lower pET-1. pET-1 may serve as a risk marker and a potential therapeutic target in CAD patients.