Warfarin is superior to aspirin and placebo in preventing thromboembolic stroke in patients with atrial fibrillation.

True. Ample evidence exists to support the use of warfarin in preventing thromboembolic stroke in patients with atrial fibrillation. In SPAF trial (Stroke Prevention in Atrial Fibrillation Study), the primary event rate in placebo group was around 6%, which was reduced by 67% with warfarin. In the European Atrial Fibrillation Trial (EAFT), warfarin reduced stroke rate from 12% to 4% and was superior to aspirin.

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Ximelagatran is non-inferior to warfarin in preventing thromboembolic stroke in patients with atrial fibrillation.

True. The Stroke Prevention Using the Oral Direct Thrombin Inhibitor Ximelagatran in Patients With Nonvalvular Atrial Fibrillation (SPORTIF III) trial was performed to determine the safety and efficacy of a novel, oral direct thrombin inhibitor ximelagatran versus warfarin for prevention of stroke and systemic embolic events in patients with atrial fibrillation (AF) and at least one additional risk factor for stroke. It was found that ximelagatran was noninferior for the primary end point of stroke or systemic embolic events (Fig. 1). Unlike warfarin, ximelagatran does not require coagulation monitoring, and is delivered in a fixed oral dose. The elevations in liver enzymes, although transient, may require monitoring in patients treated with ximelagatran. Although this trial was open-label, the recently presented SPORTIF V trial was a double-blind trial of ximelagatran versus warfarin, which showed similar, noninferior primary endpoint results (Fig. 2). Ximelagatran is not yet commercially available. (Source of information and image from ACC Foundation).

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Aspirin plus Clopidogrel is non-inferior to warfarin in preventing thromboembolic stroke in patients with atrial fibrillation.

False. In the ACTIVE-W trial (Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events), treatment with clopidogrel and aspirin was compared with oral anticoagulant therapy among patients with atrial fibrillation and at least one risk factor for stroke. The trial was discontinued early at the recommendation of the data safety monitoring board due to evidence of superiority on the primary endpoint with oral anticoagulant therapy over clopidogrel plus aspirin (3.93% per year vs 5.64% per year, relative risk [RR] 1.45, p=0.0002) (Fig. 3). This study confirms the current gold standard in using warfarin for stroke prevention I patients with atrial fibrillation. (Source of information and image from ACC Foundation).

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What are the diagnosis and differential diagnoses?

The diagnosis is erysipelas. Differential diagnoses include deep vein thrombosis, infected stasis dermatitis, infected contact dermatitis.

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What is the usual etiologic agent?

Erysipelas is usually caused by group A Streptococcus. It is a superficial type of cellulitis involving lymphatics. Margin of lesion is raised, sharply demarcated from the adjacent normal skin. The sites of predilection are face, lower legs, area of pre-existing lymphedema and umbilical stump.

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What are the possible complications?

Possible complications include post-streptococcal glomerulonephritis, endocarditis, septicaemia, streptococcal toxic shock syndrome and carvenous sinus thrombosis.

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What is the management?

Rest, immobilization, elevation, moist heat and analgesic are useful. In mild cases, the patients can be treated on an out-patient basis. Procaine penicillin G or penicillin V can be used and erythromycin is also effective in patients with penicillin allergy. Alternative choices are cephalosporins, vancomycin, clarithromycin, azithromycin or clindamycins. Treatment should be given for 10-14 days.

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What is the prophylactic management for recurrent cases?

Support stockings, antiseptics to skin should be used especially in sites of chronic lymphedema. Chronic antimicrobial prophylaxis (e.g. penicillin G, dicloxacillin or erythromycin) may be used for severe and recalcitrant cases. Tinea pedis, if present, should be treated accordingly. A 50 year old man presented with a painful rash over his left lower leg for five days. There was no precipitating factor and no history of trauma. His general health was good. Physical examination showed a raised sharply demarcated tender red plaque over his left calf. He was afebrile and there was no systemic upset.

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