Key Points
- To evaluate the clinical evidence, biological mechanisms, prevalence estimates, and diagnostic measurement tools associated with aspirin resistance.
- Reviewed published literature examining reported prevalence rates, dosage effects, and intrapatient variability in responsiveness to aspirin.
- Evaluated proposed molecular and physiological mechanisms alongside commercially available laboratory assays designed to detect aspirin resistance.
- Estimated prevalence of aspirin resistance ranges widely from 5% to 60%, showing marked intrapatient variability over time and potential dose dependence.
- Multiple putative mechanisms remain unconfirmed, including reduced compliance, impaired absorption, elevated isoprostane production, platelet hypersensitivity, and polymorphisms in COX-1 and platelet glycoprotein IIIa.
- Commercial assays currently marketed to identify aspirin resistance lack sufficient sensitivity, specificity, and convincing clinical trial data to reliably predict therapeutic failure.
Aspirin resistance remains an enigma requiring further investigation to identify and treat resistant patients, as current commercial assays lack convincing clinical data.