Eated with warfarin.

Eated%20with%20warfarin.%20Methyl 6-bromo-5-fluoropicolinateMethyl 6-bromo-5-fluoropicolinate An echocardiographic Doppler scan showed obstruction of the popliteal bypass. Therapy with aspirin, clopidogrel, and warfarin was initiated. Out-patient follow-up was arranged, and eight months later the patient did not report any further embolization.Discussion Our patient presented with recurrent overt episodes of peripheral embolization and subclinical pulmonary and spleen embolism. The first reported episode of peripheral embolism in our patient was associated with left atrial appendange thrombosis as a consequence of atrial fibrillation that was not anti-thrombotic prophylaxis. Atrial fibrillation is the most prevalent cardiac dysrhythmia and is a strong independent risk factor for both systemic embolism and stroke [2]. Systemic embolic events associated with atrial fibrillation are cerebral in 85 of cases and peripheral in 15 [3]. According to the current guidelines [4], the patient presented here should have been treated with aspirin or warfarin. In our patient, the subsequent embolization occurred after we initiated anti-coagulation therapy. This therapy was associated with PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/9625274 the resolution of atrial thrombosis and the appearance of a mural thrombus localized in the descending aorta as a consequence of the underlying thrombocytosis and, eventually, some degree PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 of atherosclerosis. Peripheral embolization is of cardiac origin or due to atherosclerosis of the abdominal aorta in 85 of cases [5]. Peripheral embolisms associated with atherosclerosis of the abdominal aorta generally occur in the presence of advanced and complicated lesions. The angiogram in our case, however, did not show appreciable atherosclerosis of the abdominal aorta. The initiation of anti-coagulation therapy is not sufficient to fully prevent further episodes of embolization from the atrial thrombus. Patients with atrial fibrillation and dense spontaneous echocontrast have a high likelihood of cerebral embolism (22 ) or death, despite the use of oral anti-coagulation therapy [6]. In the first days after initiation of anti-coagulation treatment, the risk of embolization remains high. A transient pro-thrombotic state can be induced by excessive doses of warfarin, which rapidly depletes circulating protein C [7]. On the other hand, embolectomy is associated with a recurrence rate of thrombosis of 4 to 7 [8]. Recurrent thromboembolism under warfarin treatment should prompt the clinician to search for other factors,including a hypercoagulable state or vasculitis. In addition, trans-esophageal echocardiography should be repeated to assess the state of the previously recognized atrial thrombosis. The only relevant alteration, in the blood analysis results in our patient, was the marked increase in the number of platelets, which was not present at the first admission.Thrombocytosis is per se complicated by major thrombosis, with a rate as high as approximately 50 [9]. Two possible explanations could account for our patient's normal platelet count at admission: either this was a reactive thrombocytosis or thrombocytosis was misdiagnosed at admission for the eventual occurrence of artefactual platelet count [10]. In the 5-Fluoro-3-nitropyridin-2(1H)-one event of preexisting thrombocytosis, we tested the patient for positivity for the JAK2 V617F mutation to establish whether it was essential thrombocytosis according to the recently revised diagnostic criteria [11]. Essential thrombocytosis, which is one of the conditions of myelo-proliferative disorders, is associated with JAK2 mut.