Key result
STA2 stimulation drives greater platelet aggregation and intracellular calcium increases in IHD patients versus controls.
Why the study?
Does stimulation with a thromboxane A2 analog increase platelet aggregation and intracellular calcium concentrations differently in patients with ischemic heart disease compared to controls?
Case-Control
Does stimulation with a thromboxane A2 analog increase platelet aggregation and intracellular calcium concentrations differently in patients with ischemic heart disease compared to controls?
Platelets from patients with ischemic heart disease show enhanced aggregation and calcium influx in response to a thromboxane A2 analog, suggesting an abnormality in the platelet membrane.
May reflect platelet membrane Ca2+ influx abnormality in IHD; hypothesis-generating and should not yet change practice.
We compared platelet aggregation and intracellular free calcium concentrations [( Ca2+]i) following stimulation with STA2, an analog of thromboxane A2 between patients with ischemic heart disease (IHD) showing significant stenosis in coronary angiograms and controls. In the presence of extracellular calcium, platelet aggregation and intracellular Ca2+ increase were enhanced by STA2 stimulation in a dose-dependent fashion and were higher in the IHD patients than in the controls. However, in the absence of extracellular calcium, no difference in intracellular Ca2+ increase was observed due to its total dependence on release from intracellular stores. These results suggest that thromboxane A2 increases platelet intracellular Ca2+-inducing aggregation, and this increase and aggregation, which is enhanced by thromboxane A2 in IHD patients, is due to promotion of Ca2+ influx by thromboxane A2. IHD patients appear to have an abnormality in the platelet membrane which may explain such thromboxane A2-dependent increased permeability to Ca2+.
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Kobayashi et al. (1989) conducted a case-control in Ischemic heart disease. STA2 (thromboxane A2 analog) stimulation vs. Controls was evaluated on Platelet aggregation and intracellular free calcium concentrations. STA2 stimulation enhanced platelet aggregation and intracellular Ca2+ increase, which was higher in IHD patients than controls in the presence of extracellular calcium.
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