Beta-thromboglobulin and platelets in unstable angina

Atheromatous plaque rupture is the main cause of platelet activation in ischaemic heart disease (IHD). Platelet activation is manifested by a release into circulation of the components of granules, including beta-thromboglobulin (beta-TG) - a marker of platelet activation in vivo. The platelet count (PLT), mean platelet volume (MPV) and the proportion of large platelets (L(PLT)) are indirect platelet activation markers. Data in literature on the role of these markers in patients with unstable angina are discordant.

To assess plasma concentration of beta-TG, PLT, MPV and LPLT in patients with unstable angina before and during standard pharmacological therapy.

The study group consisted of 54 patients (19 females and 35 males) with unstable angina who were divided into two groups: Group A - 45 patients with a history of angina, and group B - nine patients with a new onset unstable angina. beta-TG and platelet activation markers were measured at baseline (groups A and B) and after 8-10 days of standard medical therapy for unstable angina (group B). The control group consisted of 26 healthy subjects (13 females and 13 males).

The mean beta-TG concentration in groups A (16.2 IU/ml) and B (19.7 IU/ml - before and 21.8 IU/ml - after treatment) was significantly (p<0.05) higher than in controls (10.6 IU/ml). In patients with unstable angina, the PLT and MPV values were not affected by therapy and were similar to those obtained in controls, whereas the LPLT value was significantly higher than in controls.

Concentrations of beta-TG and L(PLT) are increased in patients with unstable angina due to platelet activation. The introduction of standard medical treatment for unstable angina did not significantly change beta-TG and platelet activation markers.