Gut Microbiome in Chronic Coronary Syndrome Patients.

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. We examined 169 CAD patients and 166 people in the control group, without CAD, matched in terms of age and sex to the study group. Both populations underwent a detailed health assessment. The microbiome analysis was based on the V3-V4 region of the 16S rRNA gene (NGS method). Among 4074 identified taxonomic units in the whole population, 1070 differed between study groups. The most common bacterial types were Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. Furthermore, a higher Firmicutes/Bacteroidetes ratio in the CAD group compared with the control was demonstrated. Firmicutes/Bacteroidetes ratio, independent of age, sex, CAD status, LDL cholesterol concentration, and statins treatment, was related to altered phosphatidylcholine concentrations obtained in targeted metabolomics. Altered alpha-biodiversity (Kruskal-Wallis test, p = 0.001) and beta-biodiversity (Bray-Curtis metric, p < 0.001) in the CAD group were observed. Moreover, a predicted functional analysis revealed some taxonomic units, metabolic pathways, and proteins that might be characteristic of the CAD patients' microbiome, such as increased expressions of 6-phospho-ß-glucosidase and protein-N(pi)-phosphohistidine-sugar phosphotransferase and decreased expressions of DNA topoisomerase, oxaloacetate decarboxylase, and 6-beta-glucosidase. In summary, CAD is associated with altered gut microbiome composition and function.

The utility of inflammation and platelet biomarkers in patients with acute coronary syndromes.

INTRODUCTION: 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/ß-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. PLT, MPV, LPLT, and WBC were determined on hematological analyzer, IL-6 and ß-TG were measured using the ELISA method. RESULTS: In the whole group of ACS patients WBC, CRP, IL-6, MPV, and ß-TG were significantly higher as compared to controls. Analyzing the inflammation and platelet biomarkers depending on the severity of signs and symptoms in comparison to controls, statistically significant differences for above-mentioned parameters were also found. There were no significant differences between the advancement of coronary artery changes and inflammation as well as platelet parameters, except for CRP concentrations. The AUCs for all inflammation parameters tested were similar, however the highest AUCs showed WBC and CRP. Among platelet parameters the highest AUC revealed ß-TG. CONCLUSION: Markers of inflammation and platelet activation may be associated to myocardial ischemia and myocardial injury. WBC, CRP and IL-6 as inflammation parameters and MPV and ß-TG as platelet biomarkers may be useful indicators of the presence of coronary artery disease.

[Platelets and platelet microparticles glycoprotein IIb/IIIa complex in patients with unstable angina]. / Kompleks glikoproteiny IIb/IIIa na plytkach krwi i mikroplytkach u chorych na niestabilna chorobe wiencowa.

UNLABELLED: 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. THE AIM: To estimate by flow cytometry GP IIb/IIIa expression on the platelets and platelet microparticles membrane. MATERIAL AND METHODS: The study involved 21 patients with unstable angina, before (group B1) and after treatment (group B2). All subjects received aspirin, heparin (Clexane) and b-blocker. The control group consisted of 24 healthy subjects. RESULTS: Patients with unstable angina in group B1 were by 12% higher expression of GP IIb/IIIa than control group (62.6 vs 55.1%). In group B2- before treatment- the percentage of platelet expressing GP IIb/IIIa was lower (60.1%) than in the group B1. In both groups, B1 and B2, percentage of platelet microparticles expressions GP IIb/IIIa was elevated 8.5% and it was significantly higher than in the control group (5.3%). CONCLUSIONS: Our study show that patients with unstable angina had a higher expression GP IIb/IIIa on the platelets membrane and elevated percentage of platelet microparticles confirm platelet activation. There was no significantly different in platelet GP IIb/IIIa expression after the antiplatelet therapy in patients with unstable angina.

[Platelet activation in unstable angina depending on troponin I concentration]. / Aktywacja plytek krwi w niestabilnej chorobie wiencowej w zaleznosci od stezenia troponiny I.

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. 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.

Beta-thromboglobulin and platelets in unstable angina.

BACKGROUND: 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. AIM: To assess plasma concentration of beta-TG, PLT, MPV and LPLT in patients with unstable angina before and during standard pharmacological therapy. METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.