Monitoring the Antiplatelet Effect of Cilostazol with Light Transmission Aggregometer: Two Cases of Possible Cilostazol Resistance.
- Author:
Hyoeun SHIM
1
;
Seongsoo JANG
;
Chan Jeoung PARK
;
Hyun Sook CHI
;
Seung Whan LEE
;
Seong Wook PARK
Author Information
- Publication Type:Original Article
- Keywords: Antiplatelet; Cilostazol; Light transmission aggregometry
- MeSH: Adenosine Diphosphate; Adult; Alprostadil; Aspirin; Cause of Death; Coronary Artery Disease; Healthy Volunteers; Humans; In Vitro Techniques; Methods; Platelet Aggregation; Platelet Aggregation Inhibitors; Stents; Thrombosis; Volunteers
- From:Laboratory Medicine Online 2016;6(4):214-220
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Coronary artery disease is an important cause of death in adults and stent insertion is one of the treatment modalities. The most severe adverse effect of a stent insertion is the formation of a thrombus; therefore, antiplatelet agents are used. The addition of cilostazol to low-dose aspirin and clopidogrel results in a better antiplatelet effect. However, laboratory tests to monitor the effect of cilostazol are insufficient. METHODS: We tested the inhibitory effect of cilostazol using maximal platelet aggregation in 20 healthy volunteers. Conditions for incubation and concentrations of cilostazol and prostaglandin E1 (PGE1) were established and aggregation was induced by 5'-adenosine diphosphate (ADP) and measured with light transmission aggregometry (LTA). Blood samples were incubated with 1 µM and 2 µM cilostazol for 10 minutes at room temperature, and 80 nM PGE1 was added and incubated for an additional 10 minutes. Aggregation was induced by ADP and reactivity was evaluated. RESULTS: The average maximum aggregation (MA) was 58.1% at 1 µM cilostazol and 22.0% when PGE1 was added. The average MA was 42.8% when cilostazol concentration was increased to 2 µM and 21.2% when PGE1 was added. Average inhibition of aggregation at 1 µM cilostazol was not statistically significant (P=0.085), but was significant (P=0.004) at 2 µM cilostazol. Aggregation was not inhibited even with 2 µM cilostazol and PGE1 in 2 volunteers, which suggests possible resistance to cilostazol. CONCLUSIONS: We designed a method to monitor the effect of cilostazol using in vitro incubation with PGE1.
