Despite knowledge of classical coronary artery disease (CAD) risk factors, the morbidity and mortality associated with this disease remain high. Therefore, new factors that may affect the development of CAD, such as the gut microbiome, are extensively investigated. This study aimed to evaluate gut microbiome composition in CAD patients in relation to the control group.
View Article and Find Full Text PDFIntroduction: Thrombotic and inflammatory mechanisms are involved in the pathophysiology of acute coronary syndrome (ACS). The aim of the study was the evaluation of inflammation (white blood cells count/WBC, C-reactive protein/CRP, interleukin-6/IL-6) and platelet (platelet count/PLT, mean platelet volume/MPV, large platelet/LPLT, beta-thromboglobulin/β-TG) biomarkers in the groups of ACS patients depending on the severity of signs and symptoms and compared to controls without coronary artery disease.
Materials And Methods: The study group included 93 patients categorized into 3 subgroups depending on the severity of signs and symptoms of ACS.
Unlabelled: 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.
View Article and Find Full Text PDFUnlabelled: Platelet activation is known to play a key role in pathogenesis of acute coronary syndrome (ACS). Platelet activation leads to increased numbers of glycoprotein (GP) IIb/IIIa complex on the platelet membrane. On the other side antiplatelet therapy in patient with unstable angina can suppress the actions of platelet.
View Article and Find Full Text PDFBackground: 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.
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