[Evaluation of anti-thrombosis treatment in patients with chronic non-valvular atrial fibrillation]. / Valoración del tratamiento antitrombótico en pacientes con fibrilación auricular crónica no valvular.

OBJECTIVES: To assess both the indications of anti-thrombosis treatment in patients in our ambit with chronic non-valvular atrial fibrillation, and its observance in Primary Care. DESIGN: A descriptive, crossover, observational study of consecutive cases. SETTING: Third-level referral hospital in our Health District. PATIENTS: 132 adults first diagnosed with chronic atrial fibrillation between July 1st and December 31st 1996. MEASUREMENTS AND MAIN RESULTS: Patients' clinical records were used to assemble data on risk factors of embolism and counter-indications to prescribing antithrombosis treatment. A logistic regression model was performed to analyse the variables affecting the treatment at the time it was first given. 65 men (mean age 68.3) and 67 women (mean age 74.6) were included in the study. 87.9% of the patients had embolism risk factors; and 30.3% had at least one absolute or relative counter-indication to anti-coagulation. 79 patients had risk factors but no counter-indication, of whom 28% took anticoagulants, 39% had anti-aggregates prescribed and the remaining 33% received no anti-thrombosis treatment at all. Only 3 patients taking anticoagulants were referred to the Primary Care doctor. The regression model worked out signalled age under 75 and a previous embolism as factors associated with the indication and anticoagulants: We found no coherent regression model for the indication of anti-aggregates. CONCLUSIONS: Anti-thrombosis treatment is underused in Primary Care. An antecedent of an embolism is the most weight criterion for giving anticoagulants to patients. Age is shown to be the main reason for therapeutic reluctance to give anticoagulants to patients without counter-indications. There should be more patients being treated with anticoagulants in Primary Care.

Effects of S-adenosyl-L-methionine on hepatic and renal oxidative stress in an experimental model of acute biliary obstruction in rats.

We used an animal model of extrahepatic biliary obstruction of 7 days' duration to study the production of thiobarbituric acid reactive substances (TBARS), total glutathione (TG), reduced glutathione (GSH), and oxidized glutathione (GSSG), and the enzymatic activities of GSH-peroxidase, GSSG-reductase, and GSH-transferase. Four groups of six rats each were treated with saline, drug solvent, S-adenosyl-L-methionine (SAM) 5 mg/kg/d, subcutaneously, or SAM 10 mg/kg/d, subcutaneously. Extrahepatic biliary obstruction increased TBARS. SAM had the dose-dependent effects of inhibiting TBARS production and increasing TG content, mainly as a result of the increase in GSH. The activity of GSH-peroxidase and GSH-transferase was also significantly increased. In renal tissue these effects were statistically significant only in animals given the higher dose of SAM. In liver we found a reduction in biochemical values indicative of liver damage. We conclude that effect of SAM on hepatorenal function is strongly influenced by the drug's ability to reestablish equilibrium after oxidative tissue stress.

Effects of S-adenosyl-L-methionine on platelet thromboxane and vascular prostacyclin.

We therefore designed the present study to evaluate the effect of S-adenosyl-L-methionine (SAMe) on the synthesis of platelet thromboxane and vascular prostacyclin. The experimental materials were human blood and aortic rings from untreated Wistar rats; and platelets and aortic rings from Wistar rats treated for 7 days with SAMe at 5 or 10 mg/kg/day s.c. The administration of 10 mg/Kg/day of SAMe to rats significantly increased vascular production of 6-keto-PGF1alpha. In vitro vascular production of 6-keto-PGF1alpha increased in a concentration-dependent manner when SAMe was incubated in the range of 10(-7) to 10(-4) M. The greatest increase was 167 +/- 15%, obtained in samples incubated with 5 x 10(-5) M SAMe. In aortic rings, lipid peroxidase production was inhibited in a concentration-dependent manner in the SAMe range of 10(-7) to 10(-5) M. Maximum inhibition (75.3 +/- 6.2%) was obtained with SAMe at 1.5 x 10(-5) M. Vascular 6-keto-PGF1alpha production showed a significant inverse linear correlation with vascular lipid peroxide production (Y = -0.04x + 18.1, r = 0.7309, P < 0.0001).