salicylates and Embolism

Topics: Albumins; Barbiturates; Carbon; Cellulose; Collodion; Creatinine; Embolism; Hemadsorption; Microscopy, Electron, Scanning; Poisoning; Salicylates; Thrombocytopenia; Uremia

This trial evaluated the efficacy and safety of the combination of antiplatelet and moderate-intensity anticoagulation therapy in patients with atrial fibrillation associated with recognized risk factors or mitral stenosis.. Warfarin was more effective than aspirin in preventing stroke in these patients; combined therapy with low anticoagulant intensity was ineffective. Mitral stenosis patients were not investigated.. We performed a multicenter randomized trial in 1,209 patients at risk. The intermediate-risk group included patients with risk factors or age >60 years: 242 received the cyclooxygenase inhibitor triflusal, 237 received acenocumarol, and 235 received a combination of both. The high-risk group included patients with prior embolism or mitral stenosis: 259 received anticoagulants and 236 received the combined therapy. Median follow-up was 2.76 years. Primary outcome was a composite of vascular death and nonfatal stroke or systemic embolism.. Primary outcome was lower in the combined therapy than in the anticoagulant arm in both the intermediate- (hazard ratio [HR] 0.33 [95% confidence interval (CI)0.12 to 0.91]; p = 0.02) and the high-risk group (HR 0.51 [95% CI 0.27 to 0.96]; p = 0.03). Primary outcome plus severe bleeding was lower with combined therapy in the intermediate-risk group. Nonvalvular and mitral stenosis patients had similar embolic event rates during anticoagulant therapy.. The combined antiplatelet plus moderate-intensity anticoagulation therapy significantly decreased the vascular events compared with anticoagulation alone and proved to be safe in atrial fibrillation patients.

Topics: Acenocoumarol; Aged; Anticoagulants; Atrial Fibrillation; Cause of Death; Dose-Response Relationship, Drug; Drug Therapy, Combination; Embolism; Female; Follow-Up Studies; Hemorrhage; Humans; International Normalized Ratio; Intracranial Embolism; Male; Middle Aged; Mitral Valve Stenosis; Platelet Aggregation Inhibitors; Proportional Hazards Models; Salicylates; Survival Analysis; Treatment Outcome

Few trials have studied platelet activity during oral anticoagulation and all show a tendency for platelet aggregation to increase. This adverse effect has also been shown in some patients treated with unfractionated heparin, the so-called white clot syndrome. We studied platelet aggregation in patients with atrial fibrillation enrolled in the NASPEAF study and receiving antiaggregant, anticoagulant and both treatments.. 15 healthy control subjects (group C) and 99 patients were enrolled, the latter receiving 4 different antithrombotic regimens for platelet aggregation: group 1, 600 mg of the antiplatelet drug triflusal; group 2, anticoagulation for an INR of 2-3; and both treatments with 2 different levels of anticoagulation, mean INR of 1.85 (group 3) and of 2.15 (group 4). The same amounts of the agonists ADP, arachidonic acid and collagen were used in all tests. For statistical analysis we used the interval in min, from the addition of the agonist to the beginning of aggregation and the % of aggregation at 5 and 8 min.. After arachidonic acid was given, the interval to the beginning of aggregation was shorter in group 2 than in group C: 0.6 +/- 0.21 and 1.1 +/- 1.2, and in both was significantly shorter than in the other three receiving antiplatelet drugs alone: group 1 = 1.58 +/- 1.4 or combined with anticoagulants: group 3 = 1.7 +/- 1.7 and group 4 = 2.4 +/- 2.1. The % of aggregation at 5 min, in groups C, 2, 1, 3 and 4 was respectively 48 +/- 24, 43.2 +/- 19, 29.6 +/- 17, 34.8 +/- 22 and 23.2 +/- 22.5. The data showed significantly increased platelet activity in groups C and 2 compared to groups 1, 3 and 4. Group 3 with a low anticoagulation level (mean INR = 1.85) showed a tendency to greater platelet activity than group 1 and 4 with p value = 0.08.. The antiplatelet drug triflusal alone or combined with a therapeutic level of anticoagulation effectively reduces platelet aggregation and is not influenced by anticoagulant treatment. A low level of anticoagulation (INR < 2) shows a tendency to increase platelet activity.

Topics: Acenocoumarol; Adenosine Diphosphate; Aged; Analysis of Variance; Anticoagulants; Arachidonic Acid; Atrial Fibrillation; Blood Platelets; Collagen; Embolism; Female; Humans; Male; Platelet Aggregation; Platelet Aggregation Inhibitors; Salicylates; Time Factors

Topics: Adsorption; Aldehydes; Animals; Capsules; Charcoal; Creatinine; Drug Compounding; Electrophoresis, Polyacrylamide Gel; Embolism; Gels; Glutaral; In Vitro Techniques; Methylmethacrylates; Microscopy, Electron, Scanning; Particle Size; Renal Dialysis; Salicylates; Serum Albumin, Bovine; Sheep; Thrombocytopenia

Topics: Adsorption; Aged; Blood Flow Velocity; Blood Platelets; Capsules; Charcoal; Creatinine; Embolism; Female; Glutethimide; Guanidines; Humans; Kidney Failure, Chronic; Kidneys, Artificial; Membranes, Artificial; Pentobarbital; Perfusion; Poisoning; Salicylates; Urea; Uric Acid; Water-Electrolyte Balance