Secondary Prevention After Cardioembolic Stroke

Abstract

Cardiac causes of ischemic stroke usually lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is nonvalvular atrial fibrillation (AF), which has an increasing incidence with age. Other less common causes of cardioembolic stroke include myocardial infarction, left ventricular thrombus, reduced left ventricular ejection fraction, valvular abnormalities, and endocarditis. Patent foramen ovale (PFO) is a common finding on echocardiograms in patients with and without stroke (up to 20 % of the population), and a controversial source of cryptogenic stroke. AF stroke trials demonstrate that anticoagulation is superior to antiplatelet therapy in terms of ischemic stroke and systemic embolism prevention. Recently, warfarin has been compared with a number of drugs with different mechanisms of anticoagulation, namely direct thrombin (Factor II) inhibitors and Factor Xa inhibitors, which are collectively referred to as the novel or new oral anticoagulants (NOAC). Overall, the NOACs were found to be at least equally effective in reducing ischemic stroke with less intracranial bleeding risk. NOACs are attractive because of warfarin’s narrow therapeutic index, requirement for frequent blood monitoring, multiple drug interactions, and a higher rate of intracranial bleeding as compared to NOACs in randomized trials. The best way to prevent cardioembolic stroke remains early detection and treatment of AF in eligible patients, and treating the underlying stroke mechanism.