From the Guidelines
Nearly all patients (approximately 90-95%) should receive aspirin therapy after an ischemic stroke unless contraindicated, as it reduces the risk of early recurrent ischemic stroke and death or functional dependence. The standard recommendation is to start aspirin within 24-48 hours of stroke onset at a dose of 81-325 mg daily, with most clinicians prescribing 81 mg daily for long-term secondary prevention, as supported by the Canadian stroke best practice recommendations for acute stroke management, 6th edition, update 2018 1. This therapy should be continued indefinitely unless the patient develops a contraindication or is switched to an alternative antithrombotic regimen. Aspirin works by inhibiting platelet aggregation through the irreversible inhibition of cyclooxygenase-1, thereby reducing the risk of recurrent stroke by approximately 20-25%. Some key points to consider when prescribing aspirin therapy include:
- The results of a Cochrane review indicated that aspirin at doses of 160 and 300 mg, initiated within 48 h of stroke onset, was associated with a significant reduction in the odds of recurrent ischemic/unknown stroke and death or functional dependence 1.
- For every 1000 people treated with aspirin, 13 fewer people were dead or dependent, 9 fewer were dead, and 7 fewer experienced a recurrent stroke 1.
- Dual therapy using clopidogrel plus aspirin has also been evaluated for the prevention of recurrent stroke following minor events, but the generalizability of the results in a North American population was questioned, and the risk of major hemorrhage was significantly increased 1. Contraindications include hypersensitivity to aspirin, active peptic ulcer disease, recent gastrointestinal bleeding, or hemorrhagic stroke. For patients who cannot tolerate aspirin, alternative antiplatelet agents like clopidogrel (75 mg daily) may be considered. In certain cases, such as cardioembolic strokes due to atrial fibrillation, anticoagulation rather than antiplatelet therapy may be indicated, which would replace aspirin therapy.
From the Research
Aspirin Use After Ischemic Stroke
- The use of aspirin after an ischemic stroke is a common practice to prevent further strokes and other cardiovascular events 2, 3, 4, 5, 6.
- Studies have shown that aspirin can reduce the risk of stroke, myocardial infarction, and vascular death in patients with ischemic stroke 2, 3, 6.
- The recommended dose of aspirin for stroke prevention varies, but low doses (50-81 mg daily) may be insufficient for some indications, such as acute ischemic stroke treatment, which requires 160-325 mg 6.
- Combining aspirin with other antiplatelet agents, such as clopidogrel, may be more effective in reducing stroke recurrence and major adverse cardiovascular events than aspirin alone 3, 4.
- However, dual antiplatelet therapy (DAPT) with aspirin and clopidogrel may also increase the risk of moderate or severe bleeding 3.
Patient Characteristics and Aspirin Use
- Patients who experience a new ischemic stroke while taking aspirin may require a different approach to prevention strategies, as aspirin failure may be associated with a higher prevalence of lacunar stroke, comorbidities, and/or adverse interactions with other drugs 5.
- Factors associated with aspirin failure include hypertension, hypercholesterolemia, smoking, diabetes, and coronary artery disease 5.
- Aspirin users with first or recurrent ischemic strokes may also be more likely to be receiving statins and antihypertensive drugs 5.
Treatment Strategies
- Switching to or adding alternative antiplatelet agents, such as clopidogrel, may be a better strategy than maintaining aspirin monotherapy for patients who experience a new ischemic stroke while taking aspirin 4.
- The combination of aspirin and dipyridamole may also be effective in stroke prevention, particularly in patients with transient ischemic attack (TIA) or ischemic stroke of noncardiac origin 2.
- Anticoagulation with an International Normalized Ratio (INR) of 2.0 to 3.0 may be recommended for patients with a cardiac source of embolism, but its use in patients with noncardiac TIA or stroke is not well established 2.