Long-term albumin administration after first-onset ascites significantly improves patients' survival and decreases the risk of ascites recurrence.

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An increased release of nitric oxide (NO), a powerful vasodilating agent, has been proposed to play a role in the pathogenesis of vasodilation and hyperdynamic circulation associated with advanced cirrhosis. We evaluated NO synthase (NOS) activity in peripheral leukocytes of 12 cirrhotic patients and 9 healthy subjects together with plasma endotoxin levels and systemic hemodynamic (by a noninvasive echocardiographic method). NOS activity was evaluated by (1) measuring the capacity of isolated polymorphonuclear cells (PMNs) and monocytes to convert [3H]arginine to [3H]citrulline; (2) measuring the ability of neutrophils and monocytes to inhibit thrombin-induced platelet aggregation and to increase guanosine 3'-5'-cyclic monophosphate content in coincubated platelets, an expression of NO release from these cells. Both neutrophils and monocytes from cirrhotic patients produced significantly higher amounts of [3H]citrulline than cells obtained from healthy subjects (P < .001 and P < .02 for neutrophils and monocytes, respectively) and were more effective than control cells in inhibiting platelet aggregation (P < .05 and P < .001, respectively for 2 x 10(6) cells) and in increasing guanosine 3'-5'-cyclic monophosphate content in coincubated platelets (P < .05 and P < .001, respectively). The anti-aggregating activity expressed by leukocytes has a pharmacological profile similar to that described for NO, because it increased after addition of superoxide dismutase, a superoxide anion scavenger, and markedly decreased after inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine-methyl ester (L-NAME). Cirrhotic patients had significantly higher plasma endotoxin levels (P < .001) and cardiac index (P < .01) when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Numerous studies have pointed out the frequent association of tetralogy of Fallot (TF) with other cardiovascular defects and coronary tree anomalies. We found cardiac defects in 181 (68%) out of 265 patients with TF investigated by catheterization and selective coronary angiography. These anomalies were isolated in 88 cases (49%) and associated with others in 93 patients. In the case of an isolated anomaly associated with TF, the coronary tree was involved in 37.5% and the cardiovascular system in the remaining 62.5%; in the case of two anomalies, the coronary system was involved in 66% of the patients and the cardiovascular apparatus in 34%; in the case of three or more anomalies, the coronary arteries were involved in 71% and the cardiovascular system in 29%. Anomalies in the course and/or distribution of coronary arteries were present in 96 patients (36%): 10 had a single coronary ostium, 13 a left anterior descending artery arising from the right coronary artery, one a circumflex artery arising from the right coronary artery. Small fistulas between coronary arteries and the pulmonary artery were found in 20 cases; anastomoses between coronary and bronchial arteries or right atrium in 42. In 39 patients we observed a large conus artery or large anterior ventricular branches crossing the right ventricle. A right aortic arch was found in 56 patients (21%), a stenosis of the trunk and/or the peripheral pulmonary artery in 35 (13%) and pulmonary artery atresia in five. Four patients showed a complete atrioventricular canal, three an atrial septal defect (primum type) with cleft of the mitral valve, 61 (23%) an atrial septal defect (ostium secundum). Eleven patients had anomalies of the systemic venous return, 26 (10%) a patent ductus arteriosus. Four patients had valvular abnormalities. In our series, a large proportion of cardiac defects associated with TF consists of anomalies of coronary arteries. Our data confirm the usefulness of performing preoperatively routine coronary angiography in patients with complex congenital heart disease.