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Short-term fat feeding could exert adverse cardiac effects by altering myocardial glutathione-related antioxidant defenses. We have here assessed total glutathione (TG), the activities of glutathione reductase (GSSG-Red), γ-glutamylcysteine synthetase (γ-GCS), γ-glutamyl transpeptidase (γ-GT) and glutathione peroxidase (GSH-Px), fluorescent damage products of lipid peroxidation (FDPL), thiobarbituric acid-reactive substances (TBARS), HO, and ATP in the aerobically perfused hearts of control rabbits and of rabbits fed a fat-enriched diet for 18 days. Such biochemical parameters, myocardial hemodynamics and infarct size were assessed in the perfused hearts of other control and fat-fed rabbits subjected to 60 min global ischemia plus 30 min reperfusion. Compared to controls, a reduced activity of GSSG-Red and γ-GT associated with decreased TG content was detected in the aerobically perfused hearts of fat-fed rabbits, which also showed insignificant γ-GCS activation, GSH-Px depressed activity, FDPL, TBARS and HO burden, and unaltered ATP content. Ischemia-reperfusion decreased the myocardial levels of TG, ATP, and γ-GCS activity and augmented those of FDPL, TBARS, and HO especially in the fat-fed rabbits, without significant changes in myocardial GSSG-Red, γ-GT, and GSH-Px activities. Ischemia-reperfusion induced greater hemodynamic dysfunction and infarct size in the hearts of fat-fed rabbits than in those of controls. Thus, short-term fat feeding and hyperlipidemia alter glutathione metabolic status of the rabbit myocardium, inducing a GSSG-Red- and γ-GT-related decrement of myocardial glutathione content, which, together with GSH-Px dysfunction, may favor tissue oxidative stress and render the myocardium more susceptible to ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

Hypertension and other risk factors (RFs) predispose to carotid plaques (CPs). An association between left ventricular hypertrophy (LVH) or epicardial adipose tissue (EAT) and CPs has also been reported. The aim of the study was to evaluate whether the assessment of LVH and EAT thickness, beyond RFs, would be of additive value in predicting CPs in hypertensive subjects. We studied 548 hypertensive patients aged ≥50 years without carotid bruit. LVH and CPs were evaluated and defined according to standard criteria. EAT was measured by echocardiography above the free wall of the right ventricle at end diastole. The presence of LVH and EAT thickness above the median value (3.9 mm) together significantly increased prevalence of CPs in subjects with 0-1 risk factor, but not in those with ≥2 RFs who showed high prevalence of CPs independently of LVH and/or EAT. Receiver operating characteristic curve analysis showed that the addition of LVH and higher EAT thickness together significantly improved prediction of CPs in patients with 0-1 risk factor. Indeed, the area under the curve improved from 0.63 (0.56-0.69) to 0.73 (0.67-0.79), which was significantly higher ( p < 0.05). In patients with ≥2 RFs, the addition of LVH and EAT did not significantly improve prediction of CPs. This study shows that the presence of LVH and higher EAT thickness together improves prediction of CPs in hypertensive patients with 0-1 risk factor and that those with ≥2 RFs show high prevalence of CPs independently of LVH and/or EAT. [ABSTRACT FROM AUTHOR]

Soft drinks and sugar-sweetened beverages have been targeted as one of the primary culprits in the escalating rates of obesity and diabetes and reduction of added sugars is considered between the goals to achieve in order to promote cardiovascular health and to reduce deaths from cardiovascular causes. Many reliable mechanisms, such as dislypidemia, inflammation and enhanced oxidative stress, have been proposed to support a causal link between sugar sweetened beverages intake and cardiovascular risk, but the ultimate underlying pathways remain to be determined in adequately designed studies. Furthermore, while epidemiological evidence strongly supports an association between sugar sweetened beverages consumption and obesity, type 2 diabetes mellitus or cardiovascular risk, incongruous findings yielded by clinical trials, or formal meta-analyses make difficult to draw firm conclusions in this regard. Further and rigorous studies are needed to better understand the role of sugar sweetened beverages in the etiology of cardiovascular diseases and to better address the warnings and decisions of regulatory authorities on public health worldwide. [ABSTRACT FROM AUTHOR]

The receptor for advanced glycation end-products (RAGE) and its ligands are intimately involved in the pathobiology of a wide range of diseases that share common features, such as enhanced oxidative stress, immune/inflammatory responses, and altered cell functions. Soluble forms of RAGE (sRAGE), including the splice variant endogenous secretory (es)RAGE, have been found circulating in plasma and tissues. Experimental data suggest that these isoforms may neutralize the ligand-mediated damage by acting as a decoy. Moreover, evidence is mounting to support a role for both sRAGE and esRAGE as biomarkers or endogenous protection factors against RAGE-mediated pathogenesis. In this review, we will focus on clinical and therapeutical implications arising from studies investigating the significance of soluble RAGE isoforms in several clinical settings, including cardiovascular disease, diabetes mellitus, hypercholesterolemia, chronic renal failure, immune/inflammatory diseases, pulmonary diseases, neurodegeneration, and cancer. [ABSTRACT FROM AUTHOR]

Cyclooxygenase-2 (COX-2) may modulate atherosclerotic plaque stability or instability according to the prostaglandin synthase coupled with it. Whereas upregulation of COX-2 and prostaglandin (PG) E synthase is associated with plaque instability, overexpression of COX-2 and lipocalin-type PGD synthase leads to plaque stability. Thus, the role of COX-2 in atherothrombosis appears to be quite complex. In this article we summarize our recent papers investigating mechanisms regulating the expression and pharmacologic modulation of COX-2 in atherosclerotic plaques. [ABSTRACT FROM AUTHOR]