Aspirin
ASA · Bayer · Ecotrin
Irreversible COX-1/COX-2 inhibitor — antiplatelet / NSAID
Irreversibly acetylates COX-1 → blocks thromboxane A2 for the platelet's lifespan (~7–10 days). Antiplatelet effect at low dose; analgesic/anti-inflammatory at high dose.
Indications
- •Secondary CV prevention
- •ACS
- •Post-stent (with P2Y12 inhibitor)
- •Analgesia/antipyresis (higher dose)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Antiplatelet | 81 mg PO daily (loading 162–325 mg in ACS) | — |
Pharmacokinetics
Onset ~30–60 min (chewed faster). Platelet effect lasts the platelet lifespan despite short plasma half-life.
Side effects
- !GI bleeding/ulcer
- !Bleeding
- !Bronchospasm (AERD/Samter's triad)
- !Reye syndrome (children with viral illness)
- !Tinnitus (toxicity)
Contraindications
- ×Aspirin-exacerbated respiratory disease
- ×Active peptic ulcer bleeding
- ×Children with viral illness
Clinical pearls
- ★ASRA neuraxial: aspirin/NSAIDs ALONE are NOT a contraindication to neuraxial anesthesia — no hold required.
- ★Irreversible — effect persists ~7–10 days until new platelets are made; often CONTINUED perioperatively for cardiac patients.
- ★AERD/Samter's triad: asthma + nasal polyps + ASA sensitivity → bronchospasm.
Other drugs in Antiplatelets
- Clopidogrel
Prodrug → active metabolite (CYP2C19) irreversibly blocks the platelet P2Y12 ADP receptor for the platelet lifespan.
- Prasugrel
Prodrug → active metabolite irreversibly blocks P2Y12. More potent + more consistent than clopidogrel (not CYP2C19-limited), but more bleeding.
- Ticagrelor
Directly and REVERSIBLY inhibits P2Y12 (not a prodrug, not thienopyridine). Faster onset/offset than clopidogrel.
- Ticlopidine
Irreversibly blocks P2Y12. Largely replaced by clopidogrel due to hematologic toxicity.
- Abciximab
Fab fragment that irreversibly blocks the platelet GP IIb/IIIa receptor → prevents fibrinogen cross-linking (final common pathway of aggregation).
- Eptifibatide
Reversibly blocks GP IIb/IIIa (final common pathway of platelet aggregation). Short-acting.
- Dipyridamole
Inhibits platelet PDE (↑ cAMP) and adenosine reuptake (↑ adenosine → vasodilation). Weak antiplatelet; also a coronary vasodilator used in stress testing.
