A 62-year-old obese woman with prior history of type 2 diabetes, hypertension, and a pack-a-day smoking habit presented to the emergency department (ED) for acute onset of right-side weakness and sensory loss noted on awakening from sleep.
She reports taking a baby aspirin daily to “prevent heart attacks” prior to her stroke. Her electrocardiogram demonstrates a left bundle branch block and frequent premature atrial contractions. She recovers with mild hemiparesis and is ready for discharge. What is the best medical therapy for secondary prevention of stroke?
Cerebrovascular accident (CVA) represents an important diagnosis for the hospitalist, with 700,000 people suffering a stroke in the U.S. each year.1 This translates to a stroke every 45 seconds. About 200,000 of these strokes are recurrent events.
Cardioembolism is the largest cause of ischemic strokes, representing 29% of all infarcts.2 Stasis from impaired contractile function, atrial fibrillation, or mechanical valves are significant risk factors. More rarely, a paradoxical embolus arising in the venous system may pass through a patent foramen ovale.
Large-artery atherosclerosis and lacunar infarcts each account for 16% of strokes. Risk factors for these forms of strokes are the same as those for atherosclerosis and include hypertension and diabetes. Rarer causes such as vasculitis, dissection, hypercoagulability, or hematological disorders account for 3% of strokes. Work-up for these should be driven by historical and atypical features such as young age, family history, or unusual distribution of ischemic zones. Despite appropriate work-up, the mechanism remains uncertain in 36% of strokes.
Regardless of the manifestation and residua of the index event, the hospitalist must initiate appropriate therapy to prevent a disabling CVA. While antithrombotic drugs are the mainstay of secondary prevention, it is a mistake to miss other opportunities for risk modification. Optimal management requires a tailored evaluation for etiology, identification of modifiable risk factors, and initiation of antiplatelet or anticoagulant therapy.
Treatment of stroke depends on the etiology of the original infarct. Evidence is strong that the optimal therapy for cardioembolic stroke is anticoagulation with warfarin.
The European Atrial Fibrillation Trial found that warfarin reduces the risk for second strokes in patients with atrial fibrillation by two-thirds and is superior to antiplatelet agents for preventing cardioembolic strokes.3 Warfarin increases the risk of extracranial bleeding, but not severely enough to negate the benefit of reducing stroke death and disability. The target international normalized ratio (INR) for non-valvular atrial fibrillation is generally two to three, although this may be higher for certain prosthetic valves.
For large-vessel atherosclerotic and lacunar cerebral ischemia, the oldest—and still effective—treatment for recurrent stroke is aspirin. The use of low-dose aspirin after transient ischemic attack (TIA) or stroke reduces second strokes or death by approximately 15%-18%.4-5 Larger doses do not appear to be more effective, although the rate of gastrointestinal complaints is greater with increased dosage. The use of either 325 mg or 1,200 mg of aspirin produced the same 15% reduction in second ischemic events. Similar efficacy has been seen in comparisons between 30 mg and 283 mg dosing.6