Addition of cilostazol reduces biological aspirin resistance in aspirin users with ischaemic stroke: a double-blind randomized clinical trial

• Published in: European journal of neurology Vol. 17; no. 3; pp. 434 - 442
• Main Authors: Lee, J.-H., Cha, J.-K., Lee, S. J., Ha, S.-W., Kwon, S. U.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-03-2010; John Wiley & Sons, Inc
• Subjects: Aspirin; Aspirin - administration & dosage; Aspirin - therapeutic use; aspirin resistance; Bleeding Time; Brain Ischemia - diagnosis; Brain Ischemia - drug therapy; Brain Ischemia - epidemiology; cilostazol; Double-Blind Method; Drug Resistance - drug effects; Drug Therapy, Combination; Female; Humans; Incidence; ischaemic stroke; Male; Middle Aged; Platelet Aggregation Inhibitors - administration & dosage; Platelet Aggregation Inhibitors - therapeutic use; Prognosis; Stroke; Stroke - diagnosis; Stroke - drug therapy; Stroke - epidemiology; Tetrazoles - administration & dosage; Tetrazoles - therapeutic use; Treatment Outcome
• ISSN: 1351-5101; 1468-1331
• DOI: 10.1111/j.1468-1331.2009.02837.x

Background and purpose:  Biological aspirin resistance (AR) has been recognized as an important cause of clinical AR. Recent studies have reported the beneficial effects of cilostazol for the prevention of cardiovascular diseases. This study investigated whether addition of cilostazol to aspirin in ischaemic stroke patients can reduce AR.
Methods:  In this double‐blind multicenter trial, 244 aspirin users with ischaemic stroke were randomly assigned to receive cilostazol 100 mg twice daily or to placebo. Antiplatelet function was assessed using the VerifyNow™ Aspirin system. The primary end‐point was the incidence of AR, which was measured as aspirin resistance unit (ARU) ≥550 after 4‐week treatment.
Results:  The incidence of AR after treatment in cilostazol group was not significantly different from that in placebo (8.8% vs. 10.9%, P = 0.578). However, AR decreased from 12.8% to 8.8% in cilostazol group, whereas it was not changed in the placebo group. The mean ARU after treatment were also lower in the cilostazol group (456.9 ± 56.0 vs. 470.7 ± 67.2, P = 0.081). Cilostazol addition did not prolong bleeding time.
Conclusions:  Although this was a negative study, our findings disclosed a trend toward enhanced antiplatelet effects when cilostazol was added to aspirin in ischaemic stroke patients. Combination of aspirin and cilostazol might be a treatment option in the ischaemic stroke patients with AR.