Antiplatelet agents · Cardiovascular
Aspirin (acetylsalicylic acid)
ASA · acetylsalicylic acid · Aspirin® · Entrophen®(brand names vary by market)
One irreversible acetylation, and the platelet never recovers.
Also: modified release, suppository
Mechanism
Irreversibly acetylates cyclooxygenase-1 in the platelet, abolishing thromboxane A2 production for the platelet's entire life. Platelets have no nucleus and cannot make more enzyme, which is why a low daily dose achieves total inhibition.
Indications
- Secondary prevention after myocardial infarction or ischemic stroke
- Acute coronary syndrome
- After coronary stenting
- Peripheral arterial disease
Formulations
Dosing concepts
Antiplatelet versus analgesic dose
The antiplatelet dose is a small fraction of the analgesic one. Higher doses add gastrointestinal toxicity without adding antiplatelet effect, because COX-1 inhibition is already complete.
Acute chest pain
Chewed rather than swallowed, because dissolution rather than absorption is what limits the speed of onset.
Concepts, not prescribing instructions. Practice numbers live in current references and local protocols.
Pharmacokinetics
- Bioavailability
- ~50 to 70%, lower for enteric-coated products
- Half-life
- Aspirin itself 15 to 20 min; the platelet effect lasts 7 to 10 days
- Elimination
- hepatic: Rapidly hydrolysed to salicylate; the antiplatelet effect long outlives the drug
Adverse effects
- Gastrointestinal bleeding and ulcerationcommon & serious
- Dyspepsiacommon
- Bruising and prolonged bleedingcommon
- Bronchospasm in aspirin-exacerbated respiratory diseaseserious
- Reye syndrome in children with viral illnessserious
Contraindications & precautions
Contraindications
- Active peptic ulceration or bleeding
- Aspirin-exacerbated respiratory disease
- Children under 16 with a febrile illness
- Severe hepatic or renal impairment
Precautions
- Prior gastrointestinal bleeding
- Concurrent anticoagulation or NSAIDs
- Uncontrolled hypertension
- Gout: it raises urate at low doses
Interactions
- SSRIs + NSAIDs / anticoagulantsmonitorUpper GI bleeding risk roughly doubles versus either alone.
- ACE inhibitor / ARB + diuretic + NSAID (the 'triple whammy')avoidAcute kidney injury, classically in a dehydrated older adult who bought ibuprofen for a sore knee.
- Warfarin + NSAIDs (e.g. ibuprofen, naproxen)avoidMajor GI bleeding risk multiplies while the INR looks reassuring.
Monitoring
Dyspepsia and bleeding symptoms
The main harm, and largely preventable
Hemoglobin in anyone at risk
Chronic occult loss
Whether the indication still exists
Primary-prevention aspirin has largely been withdrawn from guidance
Counselling points
- Take it with food.
- Tell us about indigestion or black stools rather than treating it yourself.
- Do not add ibuprofen or naproxen without asking; the combination multiplies stomach risk and ibuprofen can block aspirin's effect.
- Keep taking it before dental work unless specifically told otherwise.
Clinical pearls
- Ibuprofen taken shortly before aspirin occupies the COX-1 site reversibly and blocks the irreversible acetylation. In a patient who takes both, timing genuinely matters and aspirin should come first.
- Enteric coating reduces dyspepsia but not the bleeding risk, because that risk is systemic prostaglandin inhibition rather than local contact.
- For primary prevention in someone who has never had an event, the modern evidence puts net benefit near zero. Finding it on a list is a deprescribing conversation.
References & review
- Acetylsalicylic acid product monograph (consult the current version for your market) (monograph)
- Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed. (reference-work)
Last reviewed 2026-08-16 · jurisdiction: global · drug information changes; verify against current references before practice use.