scholarly journals Hypercholesterolemia as a factor in the risk stratification of patients with hypertension depending on the ITGA2 gene polymorphism

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
V Netiazhenko ◽  
A V Liakhotska
Keyword(s):  
Platelet Aggregation ◽  
Gene Polymorphism ◽  
Included Study ◽  
Control Group ◽  
Genotype Group ◽  
Coronary Syndrome ◽  
Funding Sources ◽  
Increased Risk ◽  
Angioplasty And Stenting ◽  
Induced Aggregation

Abstract   Mutation C807 in the ITGA2 gene is associated with the risk of early myocardial infarction, ischemic stroke, embolism, thrombosis after angioplasty and stenting of coronary arteries. Aim To study the relationship between ITGA2 gene polymorphism and increased risk of CAD in patients with hypertension and hypercholesterolemia Materials and methods 72 patients were included. Study involved patients with ACS, which developed on the background of hypertension, 32 patients also had coronary angiography and stenting. We used analysis of spontaneous and induced platelet aggregation, polymorphism of C807T of the ITGA2 gene was determined by polymerase chain reaction. Results At 82.5% of patients with ACS genotype ITGA 2 C/T was prevalent – 40.3%, T/T – 31.9%. Aggregation capability research in the studied groups has shown that patients of all groups had their degree of spontaneous aggregation significantly exceeding limits of control. Wherein, the highest indices were recorded in the T/T genotype group, which exceeded reference values by 3,02 times. AA-induced aggregation in the group of patients with T/T genotype exceeded indexes of the C/C group by 17.3%, while C/T group's rates-by 16.5% (p<0.05 in both cases). Studying the degree of collagen-induced aggregation, it was noted that the highest rates were recorded in T/T genotype group – 1.68 times higher than control group. Conclusion It is found that T allele of ITGA2 carrier is typical for 72.1% of patients with acute coronary syndrome and combined with spontaneous acceleration of platelet aggregation and increases sensitivity of platelets to ADP and collagen. Results allow us to consider the carrier of the T-allele as a marker of predisposition to thrombophilia. FUNDunding Acknowledgement Type of funding sources: None.

P328Is there evidence of a rebound increase in platelet aggregation following withdrawal of Aspirin or Ticagrelor in patients who have previously undergone PCI and coronary stenting?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
B W Hennigan ◽  
R Good ◽  
C Adamson ◽  
L Martin ◽  
L Anderson ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Rebound Effect ◽  
Group Versus ◽  
Coronary Stenting ◽  
Control Group ◽  
Monotherapy Group ◽  
Coronary Syndrome ◽  
Increased Risk ◽  
Rebound Increase ◽  
Induced Aggregation

Abstract Introduction In patients treated with coronary stents previous studies have demonstrated an increased risk of acute coronary syndrome in after discontinuation of clopidogrel. In this study, we recruited patients already randomised in the GLOBAL LEADERS study allocated to discontinue aspirin treatment, while remaining on ticagrelor, 1 month after coronary stenting (Ticag MonoRx group) and a control group discontinuing ticagrelor at 6–12 months while remaining on aspirin (ASA MonoRx group). Both groups underwent platelet studies at day 0, prior to discontinuation of aspirin or ticagrelor and then on day 2, 7 and 14 day post cessation with multiple electrode aggregometry. Purpose This study was designed to look for evidence of a rebound increase in platelet aggregation in response to collagen after withdrawal of either aspirin or ticagrelor in patients who have been treated with both drugs after PCI with DES implantation. We needed a sample size of 26 patients in each group for 90% power to detect a mean change in platelet aggregation of 100 AU/min with an alpha of 0.05. The primary outcome measure was change in platelet aggregation in response to collagen between baseline and day 2, day 7 and day 14 following cessation of DAPT. A rebound effect was defined as a >10% increase in collagen induced platelet aggregation on either day 2 or day 7 compared to day 14 post discontinuation of either aspirin or ticagrelor. Methods Patients provided written informed consent and underwent MEA using arachidonic acid (AA), adenosine diphosphate (ADP), thrombin receptor activator peptide (TRAP) and collagen in prespecified concentrations timed at 30 mins post phlebotomy. Results were calculated from the area under the curve and expressed as as whole number aggregation units (AU). Inbuilt QC analysis was used to determine the need for repeat assays. Results Collagen induced platelet aggregation was similar in both groups at day 0 (37 AU vs 34 AU; p=0.687) and at day 2 (55 AU vs 40 AU; p=0.12). By day 7, patients on ticagrelor monotherapy had higher collagen induced platelet aggregation (78 AU vs 37 AU; p=0.0001) and this difference was maintained at 14 days (80 AU vs 43 AU; p=0.0001). In patients, assigned to ticagrelor monotherapy after 1 month of DAPT, AA induced platelet aggregation progressively increased from day 0 to day 14. In the patients discontinuing ticagrelor and continuing on aspirin monotherapy, ADP induced platelet aggregation increased from day 0 to day 14. Rebound was seen in 6/17 (35%) patients in the ticagrelor monotherapy group versus 8/17 (47%) patients in the aspirin monotherapy group (p=0.728) with a mean peak of 21 AU (SD 6) and 10 AU (SD 6) respectively above baseline readings, p=0.003. There was no difference in TRAP induced aggregation at any time point. Figure 1 Conclusions Ticagrelor monotherapy was associated with higher collagen induced platelet aggregation than aspirin monotherapy at both 7 and 14 days post cessation of DAPT. Acknowledgement/Funding British Heart Foundation Project Grant PG/14/97/31263, AstraZeneca UK Limited

scholarly journals HEMOSTASIOLOGICAL PARAMETERS AND SEVERITY OF STROKE AMONG PATIENTS WITH ATHEROTROMBOTIC AND CARDIEMOBOLIC SUBTYPES

2021 ◽  
Vol 21 (2) ◽  
pp. 34-38
Author(s):  
Ya. Yu. Havlovska
Keyword(s):  
Ischemic Stroke ◽  
Platelet Aggregation ◽  
Cerebrovascular Disorders ◽  
Magnetic Resonance Tomography ◽  
Control Group ◽  
Stroke Severity ◽  
Thrombin Time ◽  
Increased Risk ◽  
Induced Aggregation ◽  
The Brain

The aim of this study is to investigate the differences in hemostasiological parameters among patients with atherotrombotic and cardiemobolic subtypes of ischemic stroke and the relationship between the parameters and the severity of the disease in the first day. The study included 68 patients who were examined on the first day of the disease with a diagnosis of acute cerebrovascular disorders on ischemic type, among them 47 (69%) men and 21 (31%) women aged from 42 to 75 years (the average age was 61,85 ± 2,33 years old). We quantified the stroke severity by using the National Institutes of Health Stroke Scale, findings of magnetic resonance tomography and / or computer tomography of the brain; ultrasound scan of intra- and extracranial vessels of the brain was performed to verify the diagnosis. Patients were divided into 2 groups: Group 1 included atherotrombotic subtype of ischemic stroke (n = 51 individuals), group 2 included cardiembolic subtype of ischemic stroke (n = 17 individuals. The state of the hemostasis system was studied by the analysis of complete coagulograms. The patients with ischemic stroke were found to have a thrombin time reduction compared to the control group. The dynamics of this indicator in the coagulogram points out an increased risk of thrombosis in the patients of both groups with a significant predominance among the patients with an atherotrombotic stroke. In both groups of the patients with ischemic stroke, there was a decrease in intensity, time and rate of aggregation in 30 seconds compared to the control group, indicating the imbalance of platelet response to adenosine diphosphate-induced aggregation. When the rate and intensity of aggregation (the lowering of platelet aggregation function) for 30 seconds decreased, the aggregation time (the activation of platelet function) also reduced. The analysis of coagulogram indicators points out the possibility of developing the syndrome of disseminated intravascular coagulation among patients with ischemic stroke. In this case, the decrease in the platelet aggregation properties indicates the development of thrombocytopathy under a preserved platelet number among the patients with ischemic stroke. The degree of the severity of atherotrombotic ischemic stroke is associated with indicators of coagulation hemostasis and platelet aggregation characteristics. The severity of cardioembolic ischemic stroke is associated with processes of platelet aggregation processes.

scholarly journals Association of endothelial constitutive nitric oxide synthase gene polymorphism with acute coronary syndrome in Koreans

Heart ◽  
2004 ◽  
Vol 90 (3) ◽  
pp. 282-285 ◽  
Author(s):  
K-W Park ◽  
K-H You ◽  
S Oh ◽  
I-H Chae ◽  
H-S Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gene Polymorphism ◽  
Allele Frequencies ◽  
Control Group ◽  
Genotype Group ◽  
Coronary Syndrome ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Genotype And Allele Frequencies

Objective: To examine the effects of two polymorphisms of the endothelial constitutive nitric oxide synthase (ecNOS) gene, 4a/4b(A:B) located in intron 4 and Glu298Asp(G:T) located in exon 7, on the development of acute coronary syndromes (ACS).Methods: 164 patients with ACS and 142 control participants were investigated for genotype and conventional risk factors. Genotype was determined by polymerase chain reaction and restriction fragment length polymorphism analysis.Results: Genotype and allele frequencies of the A:B polymorphism in the ACS group (0.15:0.85 for AA+AB:BB, 0.09:0.91 for A:B) differed from those in the control group (0.26:0.74 for AA+AB:BB, 0.15:0.85 for A:B). However, genotype and allele frequencies of the G:T polymorphism in the ACS group (0.22:0.78 for TT+TG:GG, 0.11:0.89 for T:G) were similar to those in the control group (0.17:0.83 for TT+TG:GG, 0.09:0.91 for T:G). Multiple logistic regression analysis showed that the non-BB (AA+AB) and the non-BB+GG genotypes were significant protective factors against ACS (odds ratios 0.49 and 0.34, 95% confidence intervals 0.26 to 0.93 and 0.14 to 0.83, respectively). In addition, linear association analysis showed that the percentage of ACS patients was significantly lower in the genotype group non-BB+GG than in the genotype group BB+non-GG (39.6% v 62.7%, p  =  0.01).Conclusions: The non-BB genotype of the ecNOS 4a/4b gene polymorphism is a protective factor against the development of ACS. The GG genotype of the ecNOS Glu298Asp polymorphism exerts a benefit in addition to the non-BB genotype in the Korean population.

scholarly journals Double-blind, placebo-controlled randomised clinical trial to evaluate the effect of ASPIRIN discontinuation after left atrial appendage occlusion in atrial fibrillation: protocol of the ASPIRIN LAAO trial

BMJ Open ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. e044695
Author(s):  
Mu Chen ◽  
Qunshan Wang ◽  
Jian Sun ◽  
Peng-Pai Zhang ◽  
Wei Li ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Left Atrial Appendage ◽  
Ethics Committee ◽  
Aspirin Therapy ◽  
Atrial Appendage ◽  
Control Group ◽  
Coronary Syndrome ◽  
Left Atrial Appendage Occlusion ◽  
Increased Risk

IntroductionIt is the common clinical practice to prescribe indefinite aspirin for patients with non-valvular atrial fibrillation (NVAF) post left atrial appendage occlusion (LAAO). However, aspirin as a primary prevention strategy for cardiovascular diseases has recently been challenged due to increased risk of bleeding. Therefore, aspirin discontinuation after LAAO in atrial fibrillation (ASPIRIN LAAO) trial is designed to assess the uncertainty about the risks and benefits of discontinuing aspirin therapy at 6 months postimplantation with a Watchman LAAO device in NVAF patients.Methods and analysisThe ASPIRIN LAAO study is a prospective, multicentre, randomised, double-blinded, placebo-controlled non-inferiority trial. Patients implanted with a Watchman device within 6 months prior to enrollment and without pre-existing conditions requiring long-term aspirin therapy according to current guidelines are eligible for participating the trial. Subjects will be randomised in a 1:1 allocation ratio to either the Aspirin group (aspirin 100 mg/day) or the control group (placebo) at 6 months postimplantation. A total of 1120 subjects will be enrolled from 12 investigational sites in China. The primary composite endpoint is stroke, systemic embolism, cardiovascular/unexplained death, major bleeding, acute coronary syndrome and coronary or periphery artery disease requiring revascularisation at 24 months. Follow-up visits are scheduled at 6 and 12 months and then every 12 months until 24 months after the last patient recruitment.Ethics and disseminationEthics approval was obtained from the Ethics Committee of Xinhua Hospital, Shanghai, China (reference number XHEC-C-2018-065-5). The protocol is also submitted and approved by the institutional Ethics Committee at each participating centre. Results are expected in 2024 and will be disseminated through peer-reviewed journals and presentations at national and international conferences.Trial registration numberNCT03821883.

Platelet reactivity and clinical outcomes in acute coronary syndrome patients treated with prasugrel and clopidogrel: a pre-specified exploratory analysis from the TROPICAL-ACS trial

2019 ◽  
Vol 40 (24) ◽  
pp. 1942-1951 ◽  
Author(s):  
Dániel Aradi ◽  
Lisa Gross ◽  
Dietmar Trenk ◽  
Tobias Geisler ◽  
Béla Merkely ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Clinical Outcomes ◽  
Independent Predictor ◽  
Platelet Reactivity ◽  
Academic Research ◽  
Study Groups ◽  
Cardiovascular Death ◽  
Control Group ◽  
Coronary Syndrome ◽  
Increased Risk

Abstract Aims The value of platelet function testing (PFT) in predicting clinical outcomes and guiding P2Y12-inhibitor treatment is uncertain. In a pre-specified sub-study of the TROPICAL-ACS trial, we assessed ischaemic and bleeding risks according to high platelet reactivity (HPR) and low platelet reactivity (LPR) to ADP in patients receiving uniform prasugrel vs. PFT-guided clopidogrel or prasugrel. Methods and results Acute coronary syndrome patients with PFT done 14 days after hospital discharge were included with prior randomization to uniform prasugrel for 12 months (control group, no treatment modification) vs. early de-escalation from prasugrel to clopidogrel and PFT-guided maintenance treatment (HPR: switch-back to prasugrel, non-HPR: clopidogrel). The composite ischaemic endpoint included cardiovascular death, myocardial infarction, or stroke, while key safety outcome was Bleeding Academic Research Consortium (BARC) 2–5 bleeding, from PFT until 12 months. We identified 2527 patients with PFT results available: 1266 were randomized to the guided and 1261 to the control group. Before treatment adjustment, HPR was more prevalent in the guided group (40% vs. 15%), while LPR was more common in control patients (27% vs. 11%). Compared to control patients without HPR on prasugrel (n = 1073), similar outcomes were observed in guided patients kept on clopidogrel [n = 755, hazard ratio (HR): 1.06 (0.57–1.95), P = 0.86] and also in patients with HPR on clopidogrel switched to prasugrel [n = 511, HR: 0.96 (0.47–1.96), P = 0.91]. In contrast, HPR on prasugrel was associated with a higher risk for ischaemic events in control patients [n = 188, HR: 2.16 (1.01–4.65), P = 0.049]. Low platelet reactivity was an independent predictor of bleeding [HR: 1.74 (1.18–2.56), P = 0.005], without interaction (Pint = 0.76) between study groups. Conclusion Based on this substudy of a randomized trial, selecting prasugrel or clopidogrel based on PFT resulted in similar ischaemic outcomes as uniform prasugrel therapy without HPR. Although infrequent, HPR on prasugrel was associated with increased risk of ischaemic events. Low platelet reactivity was a strong and independent predictor of bleeding both on prasugrel and clopidogrel.

Gene Polymorphisms of Costimulatory Molecules: CTLA-4/CD28/ICOS Are Associated with B-Cell Chronic Lymphocytic Leukemia (B-CLL).

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2074-2074 ◽  
Author(s):  
Irena Frydecka ◽  
Katarzyna Suwalska ◽  
Edyta Pawlak ◽  
Lidia Karabon ◽  
Anna Tomkiewicz ◽  
...  
Keyword(s):  
T Cell ◽  
Gene Polymorphism ◽  
Costimulatory Molecules ◽  
N Gene ◽  
Control Group ◽  
Stepwise Logistic Regression ◽  
Polymorphism Analysis ◽  
Cell Functions ◽  
Increased Risk ◽  
Risk Of Cancer

Abstract There are strong evidences that altered immunological function entails an increased risk of cancer. Cytotoxic T-lymphocyte antigen 4 (CTLA-4), CD28, and Inducible co-stimulator (ICOS) are costimulatory molecules provide regulatory signals for T-cell activation. CD28 and ICOS potently enhance T-cell functions, while activation of T-cells is subsequently downregulated by CTLA-4. The abnormal expression of costimulatory molecules may be caused by polymorphisms of genes encoding these molecules. The extended study was undertaken to evaluate the association between the polymorphisms: CTLA-4+49A/G, CTLA-4-319C/T, CTLA-4(AT)n, CD28+17C/T, ICOS(GT)n and susceptibility to B-CLL in a Polish population. All together 124 B-CLL patients and 202 controls were studied. Single nucleotide polymorphisms were typed by minisequencing. The microsatellite polymorphisms were studied by PCR and fuorescence based technique. The distribution of -319T/C alleles and genotypes differed significantly between groups. The frequency of T allele and T phenotype was increased in patients with respect to controls (p=0.01, OR=1.74, 1.13∼95%CI∼2.68; p=0.01, OR =1.85, 1.13∼95%CI∼3.04, respectively). CTLA-4+49A/G and CTLA-4 (AT)n did not correlate with B-CLL. The analysis of the CD28+17C/T showed that the presence of C allele and C phenotype increased the OR of B-CLL by 1.97 and 2.07, respectively (p=0.002, 1.28∼95%CI ∼3.03; p=0.003, 1.27∼95%CI ∼3.38). For ICOS(GT)n gene polymorphism analysis we combined the alleles into 3 groups: (s)- short-alleles with 8 and 9 repeats, (m) -middle- with 10 and 11 and (l)- long- 12 and more repeats. The global distribution of alleles and genotypes was significantly different in patients and controls (p=0.00008 and p=0.00006, respectively). Individuals possessing (s) alleles were 2.75 times more prone to B-CLL than others (p=0.0000, OR=2.75, 1.67∼95%CI∼4.55), while carrying (l) alleles were protected to B-CLL (p=0.004, OR=0.47, 0.29∼95%CI∼0.79). The genotype (s)/(m) was overrepresented in patients (p=0.004, OR=2.29, 1.28∼95%CI∼2.09), but (l)/(l) individuals appeared more frequently in controls (p=0.002, OR=0.07, 0.00 ∼95%CI∼0.44). The haplotype association study of three polymorphic sites: CTLA-4-319C/T and CD28+17C/T and ICOS (s)/(m)/(l), which correlated with B-PBL in univariante analysis, showed that the distribution of haplotypes was different in cases and control, global p value was p= 3 ×108. Remarkable, the haplotypes T/C/(s) and T/T/(s) were presented only in B-CLL (p=0.0004, OR=62072, 3540∼95%CI∼1088238; p=0.00003, OR=3447, 203∼95%CI∼58334, respectively) while the haplotype C/T/(l) was significantly more frequent in control group as compared to B-CLL (p=0.000003, OR=0.3, 0.18∼95%CI∼0.51). B-CLL patients and controls polymorphic features for CTLA-4-319C/T, CD28IVS3+17C/T, ICOS (GT)n were subjected to multivariate forward stepwise logistic regression analysis. It appeared that C phenotype at CD28 T17int3C site increased twice risk of B-CLL (p=0.004, OR=2.09; 1.26∼95%CI∼3.48), while genotype (m)/(l) or (l)/(l) for ICOS gene protected from disease (p=0,0009, OR=0,41; 0,24∼95%CI∼0,69). We reported for the first time that the gene polymorphism of costimulatory molecules: CTLA-4/CD28/ICOS contribute to susceptibility to B-CLL.

scholarly journals PECAM-1 gene polymorphism (rs668) and subclinical markers of carotid atherosclerosis in patients with type 2 diabetes mellitus

2016 ◽  
Vol 19 (1) ◽  
pp. 63-70 ◽  
Author(s):  
D Popović ◽  
J Nikolajević Starčević ◽  
M Šantl Letonja ◽  
J Makuc ◽  
A Cokan Vujkovac ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gene Polymorphism ◽  
Carotid Atherosclerosis ◽  
Control Group ◽  
Minor Effect ◽  
Initial Examination ◽  
Increased Risk

ABSTRACTThe platelet endothelial cell adhesion molecule 1 (PECAM-1) plays an important role in many inflammatory processes, including the development of atherosclerosis. Polymorphism rs668 of the PECAM-1 gene (373C/G) is functional, and it was reported to be associated with increased serum levels of PECAM-1. We investigated the association between the rs668 polymorphism of PECAM-1 and subclinical markers of carotid atherosclerosis in subjects with type 2 diabetes mellitus (T2DM). Five hundred and ninety-five T2DM subjects and 200 control subjects were enrolled. The carotid intima-media thickness (CIMT) and plaque characteristics (presence and structure) were assessed ultrasonographically. Biochemical analyses were performed using standard biochemical methods. Geno-typing of the PECAM-1 gene polymorphism (rs668) was performed using KASPar assays. The control examinations were performed 3.8 ± 0.5 years after the initial examination. Higher CIMT was found in patients with T2DM in comparison with subjects without T2DM. Statistically sig-nificantly faster progression of the atherosclerotic markers was shown in subjects with T2DM in comparison with the control group. When adjusted to other risk factors, the rs668 GG genotype was associated with an increased risk of carotid plaques in subjects with T2DM. We concluded that our study demonstrated a minor effect of the rs668 PECAM-1 on markers of carotid atherosclerosis in subjects with T2DM.

scholarly journals Is endothelial dysfunction a driving force of COVID-19 induced coagulopathy?

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
O Dukhin ◽  
A Kalinskaya ◽  
I Molodtsov ◽  
A Maltseva ◽  
D Sokorev ◽  
...  
Keyword(s):  
Growth Rate ◽  
Platelet Aggregation ◽  
Endothelial Dysfunction ◽  
Endothelial Damage ◽  
Reference Ranges ◽  
Test Results ◽  
Plasma Coagulation ◽  
Funding Sources ◽  
Significant Difference ◽  
Induced Aggregation

Abstract Background/Introduction There are numerous reports regarding the direct endothelial damage by the SARS-CoV-2 that can lead to activation of both plasma hemostasis and platelet aggregation. However, the mechanism of interaction between endothelium and haemostasis in COVID-19 remains unclear. Purpose The aim of our study was to assess the relationship between each link of clot formation process (endothelial function, plasma coagulation, platelet aggregation) with the severity of the disease. Methods 58 COVID-19 patients were included in our study. Patients were divided into moderate (n=39) and severe (n=18) subgroups. All patients underwent a flow-mediated dilation (FMD) test, impedance aggregation, rotational thromboelastometry, thrombodynamics and von Willebrand factor antigen (vWF: Ag) quantification. All measurements were repeated on days 3 (point 2) and 9 (point 3) of hospitalization. Results COVID-19 patients demonstrated the enhanced plasma coagulation (clotting time, s 613,0 [480; 820], clot growth rate, μm/min 32,75 [29,3; 38,7]). At point 1 no significant difference in parameters of plasma coagulation between patients' subgroups was noted. At point 2 a significant decrease in the size (CS, μm 1278.0 [1216.5; 1356.5] vs 965.0 [659.8; 1098.0], p<0,01) and clot growth rate (μm/min 32,4 [29,2; 35,0] vs 17,7 [10,3; 24,4], p<0,01) under the influence of anticoagulants in the moderate subgroup compared with point 1 was observed. We didn't observe such phenomenon in severe subgroup. There was no significant difference in platelet aggregation between subgroups at point 1. During the course of the disease the patients in the moderate and severe subgroups demonstrated a significant increase in platelet aggregation induced by arachidonic acid and ADP (severe: AUC ARA 48,0 [25,0; 59,0] vs 77,5 [55,8; 92,7], p=0,04; AUC ADP 44,0 [41,0; 56,0] vs 58,0 [45,5; 69,0], p=0,04; moderate: AUC ARA 31,5 [19,8; 50,7] vs 56,0 [39,0; 76,0], p=0,01; AUC ADP 43,0 [20,0; 59,0] vs 56,6 [50,3; 70,5], p=0,04;), in moderate subgroup the significant increase in TRAP-induced aggregation was also noted (AUC TRAP 58,0 [41,0; 69,5] vs 76,0 [58,3; 81,5], p=0,048). There were no significant differences in the FMD-test results between the patient subgroups. FMD-test results were predominantly within the reference ranges (7,1 [4,0; 8,8]). Patients in the severe subgroup had significantly higher levels of vWF: Ag (228,0 [205,3; 240,7] vs 232,0 [226,0; 423,0], p=0,03). Conclusion SARS-CoV-2 infection was characterized by increased levels of vWF:Ag, that could represent the local endothelial damage, meanwhile there was no generalized endothelial dysfunction assessed via FMD-test in moderate to severe patients. At the same time the enhanced plasma coagulation in COVID-19 patients was observed. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals C-Reactive Protein Level Predicts Cardiovascular Risk in Chinese Young Female Population

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Ruifang Liu ◽  
Fangxing Xu ◽  
Qian Ma ◽  
Yujie Zhou ◽  
Tongku Liu
Keyword(s):  
Cardiovascular Risk ◽  
Young Women ◽  
Young Female ◽  
Control Group ◽  
C Reactive Protein ◽  
Female Population ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
Increased Risk

Background. C-reactive protein (CRP) is one of the most common oxidative indexes affected by many diseases. In recent years, there have been many studies on CRP, but the relationship between CRP levels and the cardiovascular risk in the Chinese young female population is still unclear. The purpose of this work is to explore the predictive value of CRP for the cardiovascular risk in the Chinese young female population. Methods. The study is conducted by 1 : 1 case-control to retrospectively analyze 420 young women with acute coronary syndrome (ACS group) who underwent percutaneous coronary intervention (PCI) and 420 young women (control group) who underwent coronary angiography (CAG) to exclude coronary heart disease from January 2007 to December 2016. All patients are divided into three subgroups according to CRP values: subgroup 1: CRP < 1.0   mg / L ( n = 402 ); subgroup 2: 1.0   mg / L ≤ CRP ≤ 3.0   mg / L ( n = 303 ); subgroup 3: CRP > 3.0   mg / L ( n = 135 ). The levels of CRP were observed in the two groups and three subgroups. Results. A total of 840 patients were analyzed. The mean duration of follow-up was 66.37 ± 30.06 months. The results showed that the level of CRP in the ACS group was significantly higher than that in the control group ( 1.30 ± 1.70 vs. 3.33 ± 5.92 , respectively, p < 0.001 ), and patients with higher CRP levels were associated with a significantly increased rate of major adverse cardiovascular events (MACE) (7.0% vs. 8.9% vs. 19.30%, respectively, p < 0.05 ). After adjustment for baseline covariates, CRP level was still an independent predictor for the incidence of MACE, either as a continuous variable or as a categorical variable. There was a significantly higher rate of all-cause mortality and myocardial infarction in patients with higher CRP values during follow-up. Conclusions. The research results show that high CRP is associated with increased risk of ACS in the Chinese young female population. Risk stratification with CRP as an adjunct to predict clinical risk factors might be useful in the Chinese young female population.

scholarly journals CAUSES OF THE DEVELOPMENT OF CORONARY SYNDROME X IN WOMEN

2020 ◽  
Vol 20 (3) ◽  
pp. 148-152
Author(s):  
I.V. Tsiganenko ◽  
L.K. Ovcharenko
Keyword(s):  
Endothelial Cells ◽  
Platelet Aggregation ◽  
Vascular Endothelium ◽  
Density Lipoprotein ◽  
Biologically Active ◽  
Syndrome X ◽  
Control Group ◽  
Coronary Syndrome ◽  
Experimental Group ◽  
Active Substances

The work considers the causes of the coronary X syndrome development in women by assessing the experimental group and the control group with typical angina pectoris with angiographically altered vessels. Each group included 30 patients. When studingy medical records of the patients in the study group, we found out that in the reproductive period all of them had hyperestrogenemia, confirmed by the laboratory data, with the corresponding consequences in the form of various gynecological diseases, while the patients of the control group had unburdened gynaecological history. In terms of the lipid spectrum, the results turned out to be opposite. In the experimental group, the rates were within the normal range, and the control level of LDL-C significantly exceeded the required values. Despite the fact that estrogens increase the concentration of high density lipoprotein (HDL) in the blood and lower the content of low density lipoprotein (LDL) that are atherogenic, their surplus has a less negative effect than their lack, as the risk of developing atherosclerosis increases with decreasing concentration, and with an increase there is a risk of developing endothelial dysfunction, which provokes the development of coronary syndrome X. These date confirm the development of endothelial dysfunction in the patients of the experimental group with hyperestrogenemia in the history resulted from the impairment of the process of proliferation of endothelial cells with subsequent imbalance of secretion of biologically active substances. Among them, there is nitric oxide, which causes the relaxation of smooth myocytes, thus resulting in vasodilatation, and endothelins, providing the opposite, vasodilating effect. Prostacyclines and thrombomodulins secreted by the vascular endothelium in physiological conditions, counteract platelet aggregation. In the case of damage to the vascular wall, the production of prostacyclin and thrombomodulin is suppressed, but the release of thromboplastin, platelet activation factor and von Willerband factor activates that promote platelet aggregation and blood clotting. Under the participation of other physiologically active substances, selectins, endothelial cells promote adhesion to their surface and further penetration into the site of inflammation of neutrophils, blood acidophils. Selectin is accumulated in the cytoplasm of the endothelial cells in the form of specific electron-cellular inclusions, the so-called bodies of Weibel-Palade. Normally, vascular endothelium is impervious to blood components. However, being affected by a number of factors, and in particular histamine, endothelial cells lose contact with each other and decrease in number. This leads to the release of water and plasma proteins into the intercellular medium causing oedema. Due to the ability of the inner layer of vessels to produce a large number of biologically active substances, such changes can hardly be corrected by therapy.

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