[Platelet activation in unstable angina depending on troponin I concentration]

Abstract

Platelet activation as a result of atheromatous plaque rupture in ischaemic heart disease can be detected by assesses plasma concentration of beta-thromboglobulin (beta-TG) and indirectly by changes in platelet counts (PLT). At the same time myocardial ischaemia and local destruction of cardiomyocyte leads to the increase troponin I concentration. The aim of this study was an evaluation of correlation between markers of platelet activation in vivo (beta-TG and PLT) and the level of troponin I in patients with unstable angina.

Material and methods: In our study 54 patients were divided into three groups depending on the risk of myocardial infarction. The first group - 10 patients, moderate risk of infarction, troponin I plasma concentration below 0.1 ng/ml, the second group - 33 patients, high risk of infarction, troponin I level between 0.2-1.5 ng/ml, and the third group - 11 patients with myocardial infarction, troponin I level above 1.5 ng/ml. The control group - 26 healthy subjects free from cardiovascular diseases.

Results: In the present study we found a significant increase (p < 0.05) in the beta-TG concentration in group two (18.2 IU/microl) and group three (17.4 IU/microl) compared with control (10.9 IU/microl). The PLT was a significantly lower only in group two (181.2 x 10(3)/microl) compared with the control group (217.3 x 10(3)/microl).

Conclusions: We found that the plasma concentration of beta-TG as a marker of platelet activation increase depends on higher risk of myocardial infarction measured by troponin I plasma concentration. beta-TG may be also useful parameter to help estimate the risk of myocardial infarction.