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Early detection of platelet activation after coronary angioplasty
1Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan.
Insights
Percutaneous transluminal coronary angioplasty (PTCA) activates platelets, indicated by increased CD62P and CD63 expression and thrombomodulin levels in the coronary sinus. Minimizing vascular injury during PTCA is crucial to inhibit this platelet activation.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Interventional Cardiology
Background:
- Platelet activation is a known response to percutaneous transluminal coronary angioplasty (PTCA).
- Direct in vivo detection of activated platelets post-PTCA remains challenging.
Purpose of the Study:
- To detect early-stage platelet activation following PTCA.
- To investigate the relationship between platelet activation markers and thrombomodulin levels post-PTCA.
Main Methods:
- Blood samples were collected from the coronary sinus and aorta in patients undergoing PTCA.
- Flow cytometry analyzed platelet surface expression of CD62P (P-selectin) and CD63.
- Plasma thrombomodulin levels were measured.
Main Results:
- Platelet CD62P and CD63 expression significantly increased in the coronary sinus post-PTCA.
- Plasma thrombomodulin levels also rose in the coronary sinus after PTCA.
- Coronary angiography alone did not alter these parameters.
- Post-PTCA, thrombomodulin levels correlated strongly with CD62P and CD63 expression in the coronary sinus.
Conclusions:
- PTCA induces circulatory platelet activation, likely due to balloon-induced vascular endothelial injury.
- Careful procedural technique to minimize vascular injury is recommended to inhibit platelet activation.
Background:
Although platelet activation has been considered an important reaction after percutaneous transluminal coronary angioplasty (PTCA), it is still difficult to detect the activated platelets in vivo directly.
Methods:
To detect platelets activated at an early stage after PTCA, blood samples were take from the coronary sinus and the aorta in 22 patients with coronary artery disease, who underwent PTCA for a lesion of the left anterior descending artery. Ten patients with coronary artery disease, who underwent diagnostic coronary angiography only, were compared with them. The expression of activation-dependent granular protein, CD62P (P-selectin) and CD63, on the platelet membrane surface was analysed using flow cytometry. The plasma thrombomodulin level was also measured.
Results:
The percentage of platelets positive for CD62P (0.53 +/- 0.04 to 0.80 +/- 0.11%, P < 0.01) and CD63 (16.0 +/- 1.4 to 19.8 +/- 2.0%, P < 0.05) increased after PTCA in the coronary sinus, although it did not change in the aorta. The plasma thrombomodulin level also increased after PTCA in the coronary sinus (16.7 +/- 1.0 to 20.4 +/- 2.0 mu/ml, P < 0.05). However, these parameters did not change after coronary angiography only. After PTCA, the plasma thrombomodulin level was correlated with the percentage of platelets positive for CD62P (r = 0.88, P < 0.001) and with that for CD63 (r = 0.69, P < 0.001) in the coronary sinus.
Conclusions:
PTCA produced activation of circulatory platelets, which might have been caused by balloon-induced vascular endothelial injury. One should take care to avoid needless vascular injury during the PTCA procedure to inhibit the platelet activation.