Background-Hyperuricemia is common in chronic heart failure (CHF), and it is a strong independent marker of prognosis. Upregulated xanthine oxidase (XO) activity and impaired renal excretion have been shown to account for increased serum uric acid (UA) levels in CHF. Therapeutic interventions with allopurinol to reduce UA levels by XO inhibition have been shown to be beneficial. Discussions are ongoing whether UA itself is actively involved or it is a mere marker of upregulated XO activity within CHF pathophysiology. Therefore, the aim of this study was to test the effect of lowering UA by uricosuric treatment without XO inhibition on hemodynamic and metabolic characteristics of CHF. Impaired renal excretion of UA was taken into account. Methods and Results-Serum UA (SUA), urinary UA (uUA) excretion, and renal clearance test for UA (Cl UA ) were measured in 82 patients with CHF. SUA was significantly increased compared with controls of similar age (control, 5.45Ϯ0.70 mg/dL; New York Heart Association I, 6.48Ϯ1.70 mg/dL; New York Heart Association II, 7.34Ϯ1.94 mg/dL; New York Heart Association III, 7.61Ϯ2.11 mg/dL; PϽ0.01). Patients with CHF showed lower uUA excretion and Cl UA . On multivariate analysis, insulin, brain natriuretic peptide (PϽ0.01), and creatinine levels (Pϭ0.05) showed independent correlation with SUA. The treatment effect of the uricosuric agent benzbromarone was tested in 14 patients with CHF with hyperuricemia in a double-blind, placebo-controlled, randomized crossover study design. Benzbromarone significantly decreased SUA (PϽ0.01). Brain natriuretic peptide, left ventricular ejection fraction, and dimensions in echocardiographic assessment did not change after benzbromarone therapy. In contrast, fasting insulin (placebo, 18.8Ϯ8.9 U/mL; benzbromarone, 11.0Ϯ6.2 U/mL; PϽ0.05), homeostasis model assessment of insulin resistance index (placebo, 5.4Ϯ2.6; benzbromarone, 3.0Ϯ1.7; PϽ0.05), and tumor necrosis factor-␣ (placebo, 2.59Ϯ0.63 pg/mL; benzbromarone, 2.14Ϯ0.51 pg/mL; PϽ0.05) improved after benzbromarone, and the changes in tumor necrosis factor-␣ levels were correlated with reduction of SUA (PϽ0.05). Conclusions-These results show that UA lowering without XO inhibition may not have an effect on hemodynamic impairment in CHF pathophysiology. To the extent that these data are correct, this finding suggests that upregulated XO activity rather than UA itself is actively involved in hemodynamic impairment in CHF. Clinical Trial Registration-clinical trials.gov. Identifier: NCT00422318.(Circ Heart Fail. 2010;3:73-81.)

Our data show that the long-term patient and graft survival rates after donation after cardiac death lung transplantation were equivalent to those after brain-dead donor lung transplantation. Our findings suggest that the use of donation after cardiac death donors can safely and substantially expand the donor pool for lung transplantation.

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The best recovery was observed in the non-beating donor hearts resuscitated by continuous myocardial perfusion when the initial controlled reperfusion with lukewarm blood cardioplegic solution at 40 mm Hg lasted for 20 minutes.

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This study was undertaken to evaluate outcomes for single (SLT) vs. bilateral lung transplantation (BLT) in patients with interstitial lung disease (ILD). One hundred and eleven patients with ILD who underwent lung transplantation between January 1993 and March 2009 were evaluated. Recipients with BLT were younger (43 ± 12 vs. 57 ± 7 years), and significantly more patients with non-idiopathic pulmonary fibrosis (IPF) received BLT (50%) vs. patients with IPF (18%). BLT recipients had a significantly longer mean waitlist time (240 vs. 125 days), significantly higher systolic (51 ± 18 vs. 40 ± 11 mmHg) pulmonary artery pressures, were placed on cardiopulmonary bypass more frequently (67 vs. 31%), had a higher incidence of primary graft dysfunction (63 vs. 17%), more frequently were given prolonged peri-operative inhaled nitric oxide and more frequently required prolonged post-operative mechanical ventilatory support (6.0 vs. 1.7 days). Additionally, BLT recipients had a significantly longer intensive care unit (8 vs. 4 days) and hospital (24 vs. 15 days) length of stay. We did not detect a difference in survival (Kaplan-Meier) for SLT vs. BLT. Our findings suggest that outcomes for SLT for patients with ILD are comparable or somewhat superior to those for BLT, and short- and long-term survival are not significantly different for the two procedures.

PTHrP is produced in a wide variety of different cells, including cardiomyocytes. Its production is augmented by mechanical and neurohumoral stimulation, and PTHrP has positive chronotropic and vasodilatory effects. Thus, in the heart, PTHrP has the potential to serve as a mechano-sensitive regulatory molecule. We evaluated peripheral and central levels of PTHrP in patients with congestive heart failure (CHF) and tested the hypothesis that PTHrP is released from the heart in patients with CHF. Intact full-length PTHrP (i-PTHrP) and C-terminal PTHrP (c-PTHrP) levels were measured in the plasma of 64 patients with CHF and 12 controls. Plasma PTHrP concentrations in the coronary sinus and aortic root were also measured in 18 CHF patients and 10 controls. Both plasma i-PTHrP and c-PTHrP levels in CHF patients were significantly higher than control levels and increased as a function of New York Heart Association classification. There were significant correlations between c-PTHrP levels and plasma norepinephrine, brain natriuretic peptide, angiotensin II, and endothelin-1 levels. Plasma i-PTHrP was significantly correlated with left ventricular ejection fraction and end-diastolic and end-systolic dimensions. Plasma i-PTHrP levels were significantly higher in the coronary sinus than in the aortic root in CHF patients, but among controls concentrations of i-PTHrP were indistinguishable at these two sites. This is the first report demonstrating that PTHrP is produced in the myocardium and is increased in CHF; these findings suggest that PTHrPs levels might be modulated by cardiac performance in patients with CHF.

MCI-186 exerts a cardioprotective action at least partly by inhibition of lipid peroxidation. Antioxidant therapy at the initial reperfusion is essential to successful resuscitation of nonbeating hearts by continuous myocardial perfusion.