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Intracoronary platelet activation in ischemic heart disease: effects of ticlopidine
Insights
Platelet activation occurs in coronary artery disease, increasing platelet factor 4 levels. The antiplatelet drug ticlopidine effectively prevents this activation in patients with coronary artery disease.
Area of Science:
- Cardiology
- Hematology
- Vascular Biology
Background:
- Platelet activation is implicated in the pathophysiology of coronary artery disease (CAD).
- Platelet factor 4 (PF4) is a marker of platelet activation released during aggregation.
Purpose of the Study:
- To investigate platelet activation in the coronary circulation of patients with and without coronary artery disease.
- To assess the effect of ticlopidine on platelet activation in patients with ischemic heart disease.
Main Methods:
- Measurement of plasma platelet factor 4 (PF4) levels in aortic and coronary sinus blood.
- Comparison of PF4 levels in three patient groups: normal coronary arteriograms, angiographically proven CAD, and ischemic heart disease treated with ticlopidine.
- Statistical analysis to determine significant differences in PF4 levels between groups.
Main Results:
- A significant increase in PF4 levels across the coronary circulation was observed in patients with coronary artery disease (27.4 +/- 21.9 ng/ml) compared to controls (-1 +/- 4.5 ng/ml).
- Patients with ischemic heart disease treated with ticlopidine showed normal PF4 levels in both aortic and coronary sinus samples.
- These findings indicate ongoing platelet activation in stable CAD, which is inhibited by ticlopidine.
Conclusions:
- Platelet activation is a continuous process in the coronary circulation of patients with stable coronary artery disease.
- Ticlopidine effectively prevents platelet activation in the coronary circulation of patients with ischemic heart disease.
Abstract:
Plasma levels of platelet factor 4 have been measured in the aortic and coronary sinus blood of 35 patients: group I (n = 12) with normal coronary arteriograms; group II (n = 15) with angiographically proven coronary artery disease; and group III (n = 8) composed of patients with ischemic heart disease who were being treated with the antiaggregant agent ticlopidine at the time of cardiac catheterization. The mean increase in platelet factor 4 levels through the coronary circulation was 27.4 +/- 21.9 ng/ml (mean +/- standard deviation) in group II, compared with -1 +/- 4.5 ng/ml in group I (p less than 0.01). In group III plasma levels of platelet factor 4 in aortic and coronary sinus samples were all within the normal range. Thus, we conclude that platelet activation constantly occurs in the coronary circulation of patients with stable coronary artery disease, and can be prevented with ticlopidine.