147 research outputs found

    Outcome of 200 patients after an extracardiac Fontan procedure

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    OBJECTIVES: Despite the known advantages of the extracardiac conduit Fontan procedure, the long-term outcomes related to the longevity of the conduit and anticoagulation therapy have not been determined. The purpose of this study was to evaluate the outcome of hospital survivors with an extracardiac Fontan circulation. METHODS AND RESULTS: Between 1996 and 2006, 200 patients had the extracardiac conduit Fontan operation. The median age at operation was 3.4 years. Most patients (89.5%) underwent a bidirectional cavopulmonary shunt. Fenestration was required in 85 patients. Overall, the 10-year survival was 92.4% +/- 2.1%. Multivariate analysis identified severe infection during the early postoperative period and a high pulmonary arterial pressure during the preoperative period as independent risk factors for patient mortality. The Kaplan-Meier estimate for freedom from reoperation was 82.4% +/- 4.1% at 10 years. Arrhythmia occurred in 32 patients after the Fontan operation; freedom from arrhythmia was 85.1% +/- 4.4% at 10 years. The risk factors for arrhythmia were the heterotaxy syndrome, follow-up duration, and age at Fontan operation. Freedom from thromboembolism at 10 years was 92.9% +/- 1.9%. Among all of the patients, 95.2% were classified in New York Heart Association class I. CONCLUSIONS: The results of this study showed that during 10 years of follow-up, the overall survival and the functional status of the survivors after an extracardiac Fontan procedure were satisfactory. We might infer that fenestration provided benefit inasmuch as the high-risk Fontan patients fenestrated had similar outcomes to those not fenestrated, who were presumably low risk. The incidence of late death, reoperation, obstruction of the cavopulmonary pathway, arrhythmias, and thromboembolism was low

    Pulmonary Venous Malformation in a 4-Year-Old Boy: a Case Report

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    We report a case of a pulmonary venous malformation in a 4-year-old boy who presented with recurrent pneumonia. A radiograph revealed a right infrahilar mass and a hyperlucent right lung. Computed tomography (CT) demonstrated a mass containing intensely enhancing areas and multiple phleboliths located in the right lower lobe and encasing the right bronchus and right inferior pulmonary vein. Magnetic resonance imaging (MRI) precisely revealed the mass demarcation. A right lower lobectomy was performed and a pathological examination confirmed the diagnosis of a venous malformation. To the best of our knowledge, a venous malformation in pulmonary tissue has not been reported in the English literature. Herein, we report a case of a pulmonary venous malformation, with the radiograph, CT, MRI, and blood pool scan findings, along with its pathologic correlation

    Dual Fistulas of Ascending Aorta and Coronary Artery to Pulmonary Artery

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    Coronary artery fistula to pulmonary artery is common. However, to the best of our knowledge, a case of coronary artery fistula to pulmonary artery associated with aortopulmonary fistula remains unreported. We herein report a 64-year-old female with a left anterior descending coronary artery and ascending aorta to pulmonary artery fistulas, and conduct a brief review of the literature

    Pharmacokinetics of Amitriptyline Demethylation;A Crossover Study with Single Doses of Amitriptyline and Nortriptyline

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    A single dose crossover pharmacokinetic study of amitriptyline and nortriptyline was done to find out the extent of first-pass metabolism to nortriptyline after amitripyline administration, and the contribution of nortriptyline during amitriptyline therapy. Six healthy male volunteers took part in this study and were given single doses (50 mg) of amitriptyline and nortriptyline at more than three-week intervals. Plasma concentrations of the drugs were measured up to 48 hours. Total area under the plasma concentration-time curve (AUe) of amitriptyline (744.6±258.4 ng/ml·hl was smaller than that of nortriptyline (l497.3±589.8 ng/ml'h), and the mean terminal half-life of amitriptyline (21.8±3.9 hr) was shorter than that of nortriptyline (36.8±5.9 h). The total area under the plasma concentration-time curve of nortriptyline produced by amitriptyline administration was 498.1 ±274.5 ng/ml·h, and the fraction produced by the first-pass of amitriptyline was 33.7 ± 10.5%. From this data, it can be estimated that the average nortriptyline concentration could be about 40% of the total tricyclic antidepressants present in the plasma of patients taking multiple amitriptyline therapy at steady state. About 34% of nortriptyline is produced by first- pass effect during gastrointestinal absorption of amitriptyline to systemic circulation resulting from N-demethylation of amitriptyline in the liver. Then, the rest of the nortriptyline is formed continuously at a rate proportional to the rate of amitriptyline elimination

    Prediction of Plaque Progression in Coronary Arteries Based on a Novel Hemodynamic Index Calculated From Virtual Stenosis Method

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    RationalePredicting the sites in coronary arteries that are susceptible to plaque deposition is essential for the development of clinical treatment strategies and prevention. However, to date, no physiological biomarkers for this purpose have been developed. We hypothesized that the possibility of plaque deposition at a specific site in the coronary artery is associated with wall shear stress (WSS) and fractional flow reserve (FFR).Background and ObjectiveWe proposed a new biomarker called the stenosis susceptibility index (SSI) using the FFR and WSS derived using virtual stenosis method. To validate the clinical efficacy of this index, we applied the method to actual pilot clinical cases. This index non-invasively quantifies the vasodilation effects of vascular endothelial cells relative to FFR variation at a specific coronary artery site.Methods and ResultsUsing virtual stenosis method, we computed maximum WSS and FFR according to the variation in stenotic severity at each potential stenotic site and then plotted the variations of maximum WSS (y-axis) and FFR (x-axis). The slope of the graph indicated a site-specific SSI value. Then we determined the most susceptible sites for plaque deposition by comparing SSI values between the potential sites. Applying this method to seven patients revealed 71.4% in per-patient basis analysis 77.8% accuracy in per-vessel basis analysis in percutaneous coronary intervention (PCI) site prediction.ConclusionThe SSI index can be used as a predictive biomarker to identify plaque deposition sites. Patients with relatively smaller SSI values also had a higher tendency for myocardial infarction. In conclusion, sites susceptible to plaque deposition can be identified using the SSI index

    pH-dependent modulation of intracellular free magnesium ions with ion-selective electrodes in papillary muscle of guinea pig

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    A change in pH can alter the intracellular concentration of electrolytes such as intracellular Ca2+ and Na+ ([Na+]i) that are important for the cardiac function. For the determination of the role of pH in the cardiac magnesium homeostasis, the intracellular Mg2+ concentration ([Mg2+]i), membrane potential and contraction in the papillary muscle of guinea pigs using ion-selective electrodes changing extracellular pH ([pH]o) or intracellular pH ([pH]i) were measured in this study. A high CO2-induced low [pH]o causes a significant increase in the [Mg2+]i and [Na+]i, which was accompanied by a decrease in the membrane potential and twitch force. The high [pH]o had the opposite effect. These effects were reversible in both the beating and quiescent muscles. The low [pH]o-induced increase in [Mg2+]i occurred in the absence of [Mg2+]o. The [Mg2+]i was increased by the low [pH]i induced by propionate. The [Mg2+]i was increased by the low [pH]i induced by NH4Cl-prepulse and decreased by the recovery of [pH]i induced by the removal of NH4Cl. These results suggest that the pH can modulate [Mg2+]i with a reverse relationship in heart, probably by affecting the intracellular Mg2+ homeostasis, but not by Mg2+ transport across the sarcolemma
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