[The effects of post coronary stenting triple antiplatelet therapies on platelet functions].

Zhonghua Nei Ke Za Zhi

Department of Cardiology, Shenyang General Hospital, the Cardiovascular Research Institute, PLA, Shenyang 110016, China.

Published: August 2006

AI Article Synopsis

  • The study aimed to investigate how triple antiplatelet therapy affects platelet aggregation and activation in patients who had coronary stenting, comparing it with dual antiplatelet therapy.
  • It involved 120 patients who were divided into two groups, with one group receiving aspirin and clopidogrel plus cilostazol while the other received only aspirin and clopidogrel.
  • Results indicated that while some measures of platelet activation (such as CD62p and PAC-1) were significantly higher in the triple therapy group, the differences in platelet aggregation rates were not statistically significant between the two groups.

Article Abstract

Objective: To explore the effects of triple antiplatelet therapy on platelet aggregation and activation in patients who underwent coronary stenting.

Methods: 120 in-hospital coronary heart disease patients with coronary stenting were randomized to two groups receiving either triple antiplatelet drugs of aspirin and clopidogrel combined with cilostazol or dual antiplatelet drugs of aspirin and clopidogrel. On the first day after stenting cilostazol was added to the triple group patients who were previously administered aspirin and clopidogrel. Expressions of PAC-1 and CD62p which indicate platelet activation were assessed with flow cytometry and the maximal platelet aggregation rate (MPAR) induced by 5 and 20 micromol/L ADP was measured at the day before receiving cilostazol and the fifth day after stenting, respectively.

Results: The baseline clinical characteristics did not differ significantly between the two groups. There were no significant differences in the baseline level of MPAR CD62p and PAC-1 at the first day after stenting between the two groups. The margins between the two measurements were [(6.44 +/- 14.44)% vs (5.41 +/- 13.77)%, P > 0.05] for DeltaMPAR induced by 5 micromol/L ADP, [(8.50 +/- 15.50)% vs (7.84 +/- 14.21)%, P > 0.05] for DeltaMPAR induced by 20 micromol/L ADP, [(5.12 +/- 11.25)% vs (1.08 +/- 4.97)%, P < 0.05] for DeltaCD(62)p and [(12.12 +/- 12.30)% vs (2.22 +/- 15.15)%, P < 0.01] for DeltaPAC-1 in the triple and dual group patients, respectively. Among the above measurements, DeltaCD62p and DeltaPAC-1 in the triple group patients were significantly higher than those in the dual group patients although DeltaMPAR did not significantly differ between the two groups at the fifth day after stenting. Subgroup analysis for patients with acute coronary syndrome (ACS) showed that DeltaMPAR induced by 5 micromol/L ADP [(8.68 +/- 10.35)% vs (2.92 +/- 13.06)%, P = 0.018], DeltaMPAR induced by 20 micromol/L [(11.05 +/- 11.14)% vs (5.16 +/- 13.27)%, P = 0.019], DeltaCD62p [(5.57 +/- 12.08)% vs (1.35 +/- 4.42)%, P = 0.028] and DeltaPAC-1 [(11.62 +/- 12.73)% vs (1.29 +/- 15.73)%, P = 0.001] in triple group were significantly higher than that in dual group. At 3-month clinical follow-up, the rate of major adverse cardiac and cerebral events was 0 in the triple group and 3.3% (2/60) in the dual group, and the rate of hemorrhage was 5% (3/60) in the triple group and 3.3% (2/60) in the dual group, the differences were not statistically significant.

Conclusions: Compared with dual antiplatelet regimen with aspirin plus clopidogrel, triple antiplatelet therapy with aspirin and clopidogrel combined with cilostazol is more efficient in inhibiting platelet activation and aggregation after coronary stent implantation. Large scale clinical trials are needed to confirm efficacy and safety of the triple antiplatelet regimen.

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