Relationship between the Antiplatelet Effect of Aspirin and Serum VCAM-1 Concentration in Patients at High Risk for Cardiovascular Events

Chen, Cheng-Nan
Chen, Heng Rong
Chang, Hsin-I
Yen, Chia-Kuang
Lai, Chu-Jen
Lee, Kaun-Hau
Wong, Shou-Liang
Sung, Mao-Lin

Received: December 23, 2009 Accepted: February 9, 2010

¹Department of Biochemical Science and Technology, National Chiayi University; ²Nursing Department, Chung Jen College of Nursing, Health Science and Management; ³Department of Cardiology, St. Martin De Porres Hospital, Chiayi 600; ⁴Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 404, Taiwan.

Address correspondence and reprint requests to: Dr. Mao-Lin Sung, Department of Cardiology, St. Martin De Porres Hospital, Chiayi 600, Taiwan. Tel: 886–5–275–6000 ext. 3501; Fax: 886–5–276–2905; E-mail: [email protected]

Acta Cardiologica Sinica 26(1):p 28-36, March 2010.

Background:

There are reports on the correlation of the variability of the anti-platelet effect of aspirin and the clinical outcomes. However, the mechanism of this correlation is still unknown. There is still no report on the relationship between the variability of anti-platelet effect of aspirin and the changes of sVCAM-1, hs-CRP and platelet monocyte aggregates.

Methods:

A total of 42 cases, 22 men and 20 women, aged between 41 and 81 years at high cardiovascular risk (because of the presence of cardiovascular diseases, diabetes or at least two classical cardiovascular risk factors) were enrolled randomly from outpatient clinics. The patients were in stable condition and under therapy of 100 mg enteric-coated aspirin preparation per day for at least 1 month. Serum levels of markers of inflammation (hs-CRP), endothelial activation (sVCAM-1), platelet activation and platelet monocyte aggregates were measured. In addition, an in vitro cell culture model was used to study the effect of aspirin on platelet-induced VCAM-1 mRNA expression and nuclear factor (NF)-κB activation in endothelial cells (ECs).

Results:

High-risk patients taking aspirin were divided into a high 50-percentile group and a low 50-percentile group according to their different degrees of platelet activation. No significant difference was found in hs-CRP and platelet monocyte aggregates between these two groups. However, the high-platelet activation group had significantly higher sVCAM-1 than did the low platelet-activation group. Aspirin not only inhibited platelet activation by adenodiphosphate (ADP), but also decreased the activated platelet-induced VCAM-1 expression and NF-κB activation in ECs.

Conclusion:

Inadequate inhibition of platelet activation by aspirin was associated with higher serum concentration of sVCAM-1 in subjects with high cardiovascular risk.