Background-Oxidative stress plays important role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). We aimed to determine the sources and selected molecular mechanisms of oxidative stress in CAD. Methods and Results-We examined basal and NAD(P)H oxidase-mediated superoxide (O 2 · Ϫ ) production using lucigenin chemiluminescence, ferricytochrome c and dihydroethidium fluorescence in human coronary arteries from 19 CAD and 17 non-CAD patients undergoing heart transplantation. NAD(P)H oxidase subunits and xanthine oxidase expression were measured. Superoxide production was greater in coronary arteries from patients with CAD, even in vessels without overt atherosclerotic plaques, and was doubled within branching points of coronary arteries. Studies using pharmacological inhibitors and specific substrates showed that NAD(P)H oxidases (60%) and xanthine oxidase (25%) are primary sources of O 2 · Ϫ in CAD. Losartan significantly inhibited superoxide production in coronary arteries. NAD(P)H oxidase activity and protein levels of the NADPH oxidase subunits p22phox, p67phox, and p47phox were significantly increased in CAD, as were mRNA levels for p22phox and nox2, and no NAD(P)H oxidase subunit mRNA levels correlated with NAD(P)H oxidase activity in vessels from individual patients. Activity and protein expression of xanthine oxidase were increased in CAD, whereas xanthine dehydrogenase levels were not changed. Key Words: endothelium Ⅲ NAD(P)H oxidase Ⅲ nitric oxide Ⅲ oxidant stress Ⅲ reactive oxygen species I ncreased vascular production of reactive oxygen species is a characteristic feature of vascular disease states, including coronary artery disease (CAD). In particular, superoxide (O 2 · Ϫ ) and products of O 2 · Ϫ promote atherosclerosis by quenching nitric oxide (NO) and activating redox-sensitive signaling pathways 1 that modulate vessel remodeling and plaque stability. 2 Accordingly, endothelial dysfunction associated with overproduction of O 2 · Ϫ has been shown to provide prognostic information in patients with coronary artery disease. 3,4 Potential sources of vascular O 2 · Ϫ include the NAD(P)H oxidases, xanthine oxidase, cyclooxygenases, nitric oxide synthases, or mitochondrial oxidases. 5 Recent studies have shown that the NAD(P)H oxidases and xanthine oxidase have important roles in human vessels. 6 Azumi et al first showed that NAD(P)H oxidase is present in human coronary arteries. 7 Several molecular homologues of the NAD(P)H oxidase large membrane subunit, (gp91phox; nox2) are present in vascular cells, 5 and could contribute to ROS production during development of CAD. More recent studies have shown that NAD(P)H oxidase subunit expression is correlated with both severity of atherosclerosis 5 and with features of plaque stability in human coronary arteries. 8 Despite these important findings, a systematic analysis of the sources of O 2 · Ϫ production in human coronary arteries is lacking. Furthermore, it is not clear how coronary O 2 · Ϫ production is regulated in the presence of ...

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Background According to the medical literature, both on-pump and off-pump coronary artery surgery is safe and effective in octogenarians. Objectives The aim of our study was to examine the epidemiology, in-hospital outcomes and long-term follow-up results in octogenarians undergoing off-pump and on-pump coronary artery surgery utilizing nationwide registry data. Methods All octogenarians (� 80 years) enrolled in the Polish National Registry of Cardiac Surgical Procedures (KROK Registry), who underwent isolated coronary surgery between January 2006 and September 2017 were identified. Preoperative data, perioperative complications, hospital mortality and long-term mortality were analyzed. Unadjusted and propensitymatched comparisons were performed between octogenarians undergoing off-pump and on-pump coronary artery bypass surgery.

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Iron is the most abundant transition metal in the human body and an essential element required for growth and survival. Our understanding of the molecular control of iron metabolism has increased dramatically over the past 10 years due to the discovery of hepcidin, which regulates the uptake of dietary iron and its mobilization from macrophages and hepatic stores. Although general practitioners and internists encounter iron deficiency and anemia in their everyday practice, little is known about iron metabolism in patients after solid-organ transplantation. The aim of this review was to summarize the current knowledge on iron metabolism in kidney, heart, and liver transplant recipients. Iron deficiency and/or anemia, as well as iron overload, are frequently observed but the precise mechanism of these disturbances have not been fully elucidated. Iron deficiency is more prevalent in kidney and heart transplant patients, while iron overload in liver transplant recipients. Secondary and potentially reversible causes of these disturbances should be considered such as inflammation, graft failure, and type of immunosuppression. Iron status check-up should be a part of long term follow-up because disturbances in iron metabolism are a possible risk factor of infections and mortality in solid transplant recipients. Internists and general practitioners are often the first doctors to take care of organ transplant recipients (before they will present at outpatient transplant clinics or hospital transplant units); therefore, knowledge about the disturbances in iron metabolism in this specific population would be useful for better diagnosis and treatment both before and after transplantation.

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