Aim. Assessment within the multi-marker panel applied to patients with NSTEMI of admission levels of the main markers of cardiovascular pathology in order to disentangle the pathogenetic interface and identify diagnostic predictors. Material and methods. The research was carried out on a group of 87 patients with NSTEMI, exposed to angioplasty, in which the admission values of 2 morphofunctional markers of endothelial dysfunction were determined, as well as the serum levels of 53 biochemical markers with reference to: inflammation, oxidative stress, endothelial dysfunction, cell injury, hemostasis disorder, myocardial and extracellular matrix (ECM) remodeling. The control group has consisted of 40 apparently healthy people. Results. The analysis of the multi-makrer panel revealed significant deviations of the majority of the explored markers compared to the control level. Endothelial dysfunction was marked by the increase of thickness of the medial-intima complex of the carotid artery and the decrease of the flow-mediated dilation of brachial artery in association with a 7694% raise of endothelial cell fragments (EF), phospholipase A2 (PhA2) and angiopoietin 2 (Ang 2). Among 16 markers of inflammation, the elevation of myeloperoxidase (MPO) by 156% is remarkable as a specific marker of NETosis. Activated oxidative stress is the result of the impairment of the antioxidant defense, and hemostasis disorder must be underlined by double increase of fibrin monomers (FM). From a pathogenetic point of view, the multiple increase (more than 8 times) of cardiac myosin-binding protein (cMyBP-C) is important and understandable, and the markers of myocardial and ECM remodeling basically demonstrated an activation of several types of metalloproteinases. Conclusion. From the spectrum of the multi-marker panel applied to patients with NSTEMI, markers with plausible diagnostic value due to inteligibly reflected pathogenetic mechanism are highlighted as: MPO, PhA2, Ang 2, EF, FM, and cMyBP-C.
Background: Coronary thrombosis is the key pathogenic mechanism of acute heart attack, including non-ST segment elevation (NSTEMI). Given that, the detection of reliable markers of hemostasis disorders is important in the process of optimizing the diagnosis of NSTEMI. Material and methods: The study was conducted on 54 patients with NSTEMI (average age 69.7±1.5 years). In 60% of cases, 3-vessel disease was noted; 56% of patients had ejection fraction >50%, and Killip class I of heart failure was revealed in 78% of patients. With the help of the STA-Liatest (France) equipment, the blood tests determined the following hemostasis markers: fibrin monomers (FM), thrombotic complex activity of factors II, VII and X. Additional markers like Procoag, the coagulation indicator dependent on circulating phospholipids or SPA, D-dimers, as well as factors C, S and antithrombin III were appreciated. The values of these markers determined by the same method in 20 healthy persons (control group) were used as normal values. Results: Circulating level of FM on admission was increased twice, while the values of Procoag and SPA were significantly decreased by 35.3% compared to the control. Factors C, S and antithrombin III were 54-80% of the control value range, and D-dimers were within the permissible values. In the acute phase of the heart attack, a deterioration of hemostasis indicators was noted, excepting the D-dimers. The levels of FM determined 24 and 72 hours after revascularization were consistently increased (up to 3.8 times) compared to the control, while Procoag and SPA decreased by 54-57%. Further reduction of factors C, S and antithrombin III accounted for 42-54% of normal indicators. After 5 days, an improvement in hemostasis markers was observed, but a significant difference still remained comparing to the control group. Conclusions: The hemostasis particularities discovered in patients with NSTEMI indicate the features of an activated prothrombotic status, and FM could be an important diagnostic marker of NSTEMI, due to its most significant deviation from the normal value (>100%). It can reliably reflect the thrombin level, which triggers the last enzymatic phase of thrombus formation.
Purpose. Evaluation of circulating levels of lipopolysaccharide and zonulin in conjunction with markers of endothelial dysfunction, inflammation, and oxidative stress in patients with microvascular angina (MА). Material and methods. The study was carried out in a group of 58 patients with MA hospitalized in the Institute of Cardiology. The determination of circulating levels of 20 biomarkers was carried out in cooperation with the laboratory investigation center of Sapienza University (Italy). All functional and biochemical markers were also determined in 48 apparently healthy people (control group) with the values of which the markers of MA patients were compared. Results. Endothelial dysfunction in patients with MA excelled by increasing the thickness of the intima-media complex of the carotid artery by 41%, as well as by reducing of flow-mediated brachial artery dilatation (FMD) by 31,6%. The presence of dysbiosis was manifested by an 80% increase in the serum content of lipopolysaccharides (LPS) and by doubling of zonulin (1,8±0,3 vs 3,6±0,7 ng/ml). Endothelial dysfunction and dysbiosis evolved in association with oxidative stress activation estimated by means of 6 markers and increased serum content of 6 important pro-inflammatory markers (hsCRP, IL-6, TNF-α, etc.) Conclusions. 1. In patients with MA, elevated circulating levels of LPS and zonulin more than twice compared to the control value were found, which indicates the presence of intestinal dysbiosis. 2. LPS and zonulin correlate robustly with morphofunctional and biochemical markers of endothelial dysfunction, as well as with markers of its main pathogenetic factors, - inflammation and oxidative stress.
Scop. Evaluarea rolului morții neutrofilelor (NET-ozei) în evoluția infarctului miocardic acut fără elevarea segmentului ST (NSTEMI) prin aprecierea nivelurilor circulante de admitere în staționar ale markerilor care au în plan fiziopatologic tangență la acest fenomen. Material și metode. Cercetarea s-a realizat pe un lot de 54 de pacienți cu NSTEMI, supuși angioplastiei coronariene în laboratorul de cardiologie intervențională în cadrul proiectului științific din cadrul Programului de stat, la care prin metoda ELISA s-a determinat conținutul seric al 7 markeri biochimici: Selectina E, moleculei de adeziune intercelulare 1(ICAM-1), fosfolipaza 2(PhA2), interleukina 8 (IL-8), elastaza neutrofilelor ( EN), mieloperoxidaza (MPO) și metaloproteinaza 8 (MMP-8). Lotul de control a fost format din 30 de persoane aparent sănătoase. Rezultate. Rezultatele obținute indică prezența devierilor incrementale semnificative ale tuturor markerilor explorați la pacienții cu NSTEMI în comparație cu nivelul control. Markerii mai specifici ai NETozei (MPO, EN și MMP-8) au excelat prin rata maximă de elevare în ser, decelată în limitele 88-151%. Ceilalți markeri au avut o rată de creștere a nivelurilor lor circulante de 50-74%. Concluzie. La pacienții cu NSTEMI nivelurile circulante de admitere ale markerilor specifici ai NET-ozei, mieloperoxidaza, elastaza neutrofilelor și MMP-8 sunt elevate cu 88-151% față de control, fapt ce indică asupra rolului patogenetic al NET-ozei și, totodată, invocă plauzibil acestor markeri valoare predictivă diagnostică și prognostică.
Background. Fatty liver disease (FLD) is composed of a wide spectrum including metabolic associated fatty liver disease (MAFLD). Cardiovascular disease (CVD) is the leading cause of mortality in this populational group. Many risk estimation systems are in existence for improving the management of population groups, but currently, none of the available risk prediction models are authenticated in patients with hepatic steatosis. Materials and methods. Transversal, observational, prospective, case control study has been included 680 patients with MAFLD and 96 control subjects without MAFLD. Experimental group was divided in tree subgroups: A - overweight or obesity (BMI ≥ 25 kg/m2 ) N= 498; B – lean/normal weight (BMI <25kg/m2 ) N= 58 and C – Type 2 diabetes mellitus N= 156. For each patient, cardiovascular risk was estimated using the Framingham equation (risk ≥ 20% – high), SCORE risk chat (risk ≥ 10% – high) and Atherosclerotic Cardiovascular Disease Risk Algorithm from the American College of Cardiology and the American Heart Association (AHA/ACC) (risk ≥ 20% – high). Results. Model Risk SCORE and Risk ACC/AHA had identified the low proportion of patients with high risk, however, Risk FRS determined the highest proportion of the patients as being ‘at high-risk’ (Risk SCORE -7% vs Risk ACC/AHA - 15% vs Risk FRS - 38%, p <0.001). Statistically significant correlations were found between the scoring systems Risk FRS and Risk ACC/AHA (Pearson’s r = 0.939, p = 0.0001, Spearman`s rho=0.960, p <0.001). The highest proportion of the patients as being ‘at high-risk’ from group C – DMT2 was found by model RiskFRS – 82.7%, with statistically significant difference between group A and B – 28.1 % vs 6.8%, p < 0.001. The same tendency was observed for RiskSCORE and Risk ACC/AHA (RiskSCORE DMT2 – 26.3% vs Risk ACC/AHA DMT2 – 46.8%), bur these scores have identified the low proportion of patients with high risk in this populational group. Conclusions. The study shows that RiskFRS appeared to be most useful CVD risk assessment model in hepatic steatosis, RiskFRS is likely to identify a greater number of patients at ‘high-risk’ as compared to Risk SCORE and Risk ACC/AHA.
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