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- Title
Effects of diltiazem on platelet activation and cytosolic calcium during percutaneous transluminal coronary angioplasty.
- Authors
Dai H; Chen J; Tao Q; Zhu J; Zhang F; Zheng L; Qiu Y; Dai, H; Chen, J; Tao, Q; Zhu, J; Zhang, F; Zheng, L; Qiu, Y
- Abstract
<bold>Aims: </bold>To evaluate effects of diltiazem on platelet hyper-reactivity in situations associated with endothelial injury and their possible relationship to cytosolic calcium concentration.<bold>Methods: </bold>Blood samples were collected at seven time points from 35 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) who received combined diltiazem and aspirin/ticlopidine therapy or aspirin/ticlopidine therapy alone. Platelet expression of glycoprotein IIb/IIIa and P-selectin, production of thromboxane B(2), and cytosolic calcium concentration were measured, respectively, by whole blood flow cytometry, radioimmunoassay, and fluorospectrophotometry. The effects of diltiazem of different concentrations on expression of glycoprotein IIb/IIIa and P-selectin were also studied in vitro in blood samples from patients with chronic stable angina.<bold>Results: </bold>Of the two treatments, aspirin/ticlopidine therapy did not prevent an acute increase of expression of glycoprotein IIb/IIIa and P-selectin and plasma thromboxane B(2) five minutes and 10 minutes after first inflation and 10 minutes after PTCA, whereas combined diltiazem and aspirin/ticlopidine therapy had a significant inhibitory effect. In the group receiving aspirin/ticlopidine therapy, there was a short term increase of platelet [Ca(2+)](i) immediately after PTCA which was significantly reduced by diltiazem treatment. Expression of glycoprotein IIb/IIIa and P-selectin was significantly inhibited in vitro by diltiazem in the concentration of 200 ng/ml or higher, but not 50 ng/ml.<bold>Conclusions: </bold>Combined diltiazem and aspirin/ticlopidine therapy significantly inhibited platelet activation that continued in the presence of conventional aspirin/ticlopidine treatment. Antiplatelet effects of diltiazem were probably a consequence of reduction of platelet [Ca(2+)](i) and may only be achieved in higher than therapeutic concentrations.
- Subjects
DRUGS; ENDOTHELIUM; WOUNDS &; injuries; CALCIUM; ASPIRIN; CALCIUM antagonists; CALCIUM metabolism; CORONARY heart disease prevention; TICLOPIDINE; PLATELET aggregation inhibitors; DILTIAZEM; ANTIGENS; BLOOD platelets; BLOOD platelet activation; COMBINATION drug therapy; CLINICAL trials; COMPARATIVE studies; GLYCOPROTEINS; RESEARCH methodology; MEDICAL cooperation; MYOCARDIAL revascularization; RESEARCH; THROMBOXANES; TRANSLUMINAL angioplasty; EVALUATION research; THERAPEUTICS
- Publication
Postgraduate Medical Journal, 2003, Vol 79, Issue 935, p522
- ISSN
0032-5473
- Publication type
journal article
- DOI
10.1136/pmj.79.935.522