10 research outputs found

    Prevalence of left atrial abnormalities in atrial fibrillation versus normal sinus patients

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    BACKGROUND: Atrial fibrillation (AF) may be the cause or sequela of left atrial abnormalities and variants. PURPOSE: To determine the prevalence of left atrial (LA) abnormalities in AF patients compared to normal sinus rhythm (NSR) patients. MATERIAL AND METHODS: We retrospectively reviewed 281 cardiac CT examinations from 2010 to 2012, excluding patients with prior pulmonary vein ablation, known coronary artery disease, prior coronary stent placement, or coronary artery bypass grafts. The first group consisted of 159 AF patients undergoing cardiac CT prior to pulmonary vein ablation and the second group consisted of 122 NSR patients evaluated with coronary CT angiography. Demographic data were collected. LA abnormalities were analyzed. Left atrial diameter was measured on an axial view. RESULTS: A total of 281 patients were included. The male gender has significantly higher prevalence of AF than female gender, P value <0.001. Patients with AF were significantly older (mean age, 57.4 years; standard deviation [SD], 11.8 years) than NSR patients (mean age, 53.4 years; SD, 13.6 years), P value, 0.01. The left atrial diameter was greater in the AF patients (mean diameter, 4.3 cm; SD, 0.82 cm) versus the NSR patients (3.4 cm; SD, 0.58 cm), P value, <0.0001. LA diverticulum was the most prevalent variant, occurring in 28.4% of the entire patient population followed by LA pouch, occurring in 24%. There was no significant between group differences in the prevalence of these or the remainder of the LA variants. CONCLUSION: AF patients differed significantly from NSR patients in LA size, gender, and mean age. There was no statistical significance between the two groups with regard to the LA morphologic abnormalities other than size

    Plasma xanthine oxidase activity in patients with adult respiratory distress syndrome

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    Oxygen metabolites have been implicated in the pathogenesis of various types of acute tissue injury. One biologic source of oxygen metabolites is the reaction catalyzed by the enzyme xanthine oxidase. Because we previously demonstrated that the substrates for xanthine oxidase (hypoxanthine and xanthine) are elevated in the plasma of critically ill patients, we questioned whether the enzyme itself might also be present. We therefore measured hypoxanthine concentration and xanthine oxidase activity in the plasma of 15 patients with ARDS and in 13 non-ARDS critically ill patients. Plasma xanthine oxidase activity in our ARDS group (1,514 +/- 975 mlU/L, mean +/- SE) was higher than that seen in the non-ARDS group (17 +/- 4 mlU/L, P [pre] .05). Plasma hypoxanthine was elevated in both groups, and there was no difference between the ARDS and non-ARDS groups (22.0 +/- 9.2 [mu]mol/L and 11.8 +/- 4.3 [mu]mol/L, respectively). The presence of both circulating xanthine oxidase and its substrate demonstrates the potential for intravascular oxygen metabolite production. These toxic products may then cause tissue injury in ARDS.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26777/1/0000333.pd

    Absence of xanthine oxidase or xanthine dehydrogenase in the rabbit myocardium

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    We directly measured the activity of the enzymes xanthine oxidase and xanthine dehydrogenase in rabbit and rat hearts, using a sensitive radio-chemical assay. Neither xanthine oxidase activity nor xanthine dehydrogenase activity was detected in the rabbit heart. In the rat heart, xanthine oxidase activity was 9.1 [plus-or-minus sign] 0.5 mIU per gram wet weight and xanthine dehydrogenase activity was 53.0 [plus-or-minus sign] 1.9 mIU per gram wet weight. These results argue against the involvement of the xanthine oxidase/xanthine dehydrogenase system as a mechanism of tissue injury in the rabbit heart, and suggest that the ability of allopurinol to protect the rabbit heart against hypoxic or ischemic damage must be due to a mechanism other than inhibition of these enzymes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25939/1/0000001.pd

    Invited Commentary

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    OXIDANT ACTIVITY IN EXPIRED BREATH OF PATIENTS WITH ADULT RESPIRATORY DISTRESS SYNDROME

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    Hydrogen peroxide levels were measured in the breath condensate of 43 patients receiving mechanical ventilation. In 16 patients the mean breath condensate peroxide level was 1[middle dot]68+/-0[middle dot]35 [mu]mol/l on the day they met diagnostic criteria for adult respiratory distress syndrome (ARDS). The peak breath condensate peroxide level in the 27 patients in whom ARDS did not develop was significantly lower (0[middle dot]34+/-0[middle dot]08 [mu]mol/l). Plasma lysozyme, a measure of in-vivo neutrophil turnover, was significantly higher in ARDS than in non-ARDS patients (9[middle dot]2+/-2[middle dot]2 U/ml v 3[middle dot]4+/-1[middle dot]1 U/ml). These findings support the hypothesis that neutrophil activation and oxidant production are involved in the pathogenesis of ARDS.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26303/1/0000388.pd
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