Clinical and Applied Thrombosis/Hemostasis最新文献

Background: Carotid artery stenosis (CAS) may cause many cerebrovascular diseases, and a biomarker for screening and monitoring is needed. This study focused on the clinical significance of long-chain non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) in patients with CAS and aimed to search for potential biomarkers of CAS.

Methods: Eighty-six asymptomatic patients with CAS and 60 healthy individuals were enrolled, with corresponding clinical data and serum samples collected. The expression of NORAD was detected by reverse transcription-quantitive PCR (RT-qPCR). All patients were followed up for 2 years to collected the occurrence data of cerebrovascular events, and Kaplan-Meier and Cox regression were used for data analysis. Receiver operator characteristic curve was used to analyze the diagnostic value of NORAD in distinguishing CAS patients from healthy people, and to evaluate the prediction accuracy of NORAD.

Results: NORAD is overexpressed in the serum of CAS patients, and associated with patients' hypertension, TC, LDL-C levels and stenosis degree. NORAD has high sensitivity (88.37%) and specificity (80.00%) in the identification of CAS patients (AUC = 0.917). NORAD was independently related to the occurrence of cerebrovascular events (HR = 2.435, P = .003). a logistic regression risk model for predicting cerebrovascular events was constructed with the parameters including NORAD, TC and LDL.

Conclusion: NORAD can be used as a diagnostic and prognostic biomarker for CAS, and NORAD, total cholesterol (TC), and low density lipoprotein cholesterol (LDL-C) can be independently correlated to predict cerebrovascular events.

Gender sensitive medicine refers to the need to individualize epidemiology, diagnosis, knowledge of disease presentation, and therapy based also on sex and gender. An impressive amount of scientific literature deals now with sex and gender differences in disease. Not so much, yet, on individualized therapeutic approaches. Part of the reason lies in how studies that deal with the pharmacology, efficacy and safety of drugs are conducted. Often women are under-represented, and/or no gender specific analysis of outcomes is performed. As a consequence, in many fields of medicine, not as much is known about important and life-saving drug dosage, safety and efficacy in women as in men. Oral anticoagulants are not the exception, even if new regulations are operative regarding inclusion of women in all phases of drug studies. The result is that there are many areas of uncertainty or outright confusion regarding the efficacy and safety of oral anticoagulants in women that need to be addressed.

ObjectiveEnzyme-linked immunosorbent assay (ELISA) is the established method for detecting antiphospholipid antibodies (aPL) in the diagnosis of antiphospholipid syndrome (APS) but is labor-intensive compared with the newer automated chemiluminescent assay (CLIA). This study aims to evaluate CLIA versus ELISA for aPL, correlate each method with clinical manifestations and perform a comprehensive literature review.MethodsPatient samples were concurrently tested by ELISA (QUANTA Lite^®) and CLIA (ACL AcuStar^®) for anti-cardiolipin antibody (aCL) and anti-β2-glycoprotein-I (aβ2GPI) IgG and IgM. Assay results were correlated with any of the revised Sapporo APS clinical criteria.ResultsOf the 107 patients, 67% fulfilled at least one clinical criterion. 38 patients (35.5%) had APS. For aCL IgG, aCL IgM and aβ2GPI IgM, CLIA showed above 77% concordance and fair to excellent agreement (Cohen's kappa 0.39-0.86) with moderate/high positive ELISA of ≥40 units. Both methods showed good correlation (Spearman's r 0.60-0.80, p < 0.0001) that was non-linear over the range of titers. CLIA sensitivity and specificity was 46%-100% and 68%-95%, with AUROC ranging from 0.80-0.93. For aβ2GPI IgG, concordance was 36.7% and agreement was low (kappa -0.23). Correlation with clinical criteria revealed no statistically significant difference in the occurrence of clinical manifestations in ELISA-positive versus CLIA-positive groups.ConclusionsaPL detection by CLIA showed close but incomplete concordance with ELISA. CLIA positivity correlated well with moderate/high ELISA positivity, but antibody titers should not be directly compared across systems. CLIA is an acceptable alternative to ELISA in the routine non-research setting. Our findings are congruent with the reviewed literature.

BackgroundCystatin C is a cysteine protease inhibitor, synthesized by nucleated cells, and released into various body fluids. Lots of studies have reported an association between cystatin C and atherosclerotic cardiovascular disease. However, the association of cystatin C with high-risk patients with acute coronary syndrome(ACS) has not been well studied. In this study, we investigated potential association of cystatin C with high-risk patients with ACS, and assessed whether cystatin C provide discriminating power of clinical risk stratification in patients with ACS.MethodsWe enrolled 219 patients with ACS in the present study. The cystatin C concentration was measured in clinical laboratory. The global registry of acute coronary events (GRACE) scores was calculated to assess risk stratification. The high-risk patients with ACS were defined based on GRACE scores and killip classification.ResultsThe cystatin C levels were significantly higher in high-risk patients compared to non-high-risk patients, both in the overall ACS group and its subtypes, including non-ST elevation ACS (NSTE-ACS) and ST elevation ACS (STE-ACS)(P < 0.05). The receiver operating characteristic (ROC) curve analysis showed that cystatin C had a discriminative performance for identifying high-risk patients across these groups(P < 0.05). After adjusting for potential confounders, multivariate logistic regression confirmed that the elevated cystatin C levels were independently associated with high-risk patients with ACS(P < 0.05).ConclusionsThe cystatin C was obviously elevated in high-risk group in the patients with ACS and its subgroups. Cystatin C appears to be a valuable biomarker for distinguishing and predicting high-risk patients with ACS, suggesting its relevance in clinical risk stratification.

Multimorbidity defined as the co-occurrence of two or more chronic comorbidities, is becoming increasingly burdensome and is a big challenge for healthcare systems all over the world. Venous thromboembolism (VTE) is a potentially lethal disease and is the third most common cardiovascular disease. Multimorbidity is closely associated with VTE, and the VTE risk is approximately fourfold higher in individuals with multimorbidity compared to those without. Notable and consistent evidences show a significant association between multimorbidity and VTE. Plausible mechanisms for the observed associations between multimorbidity and VTE have been outlined, including higher prevalence of identified VTE risk factors, organ function and coagulation function disorders, reduced physical activity, older age, low cognitive level of VTE, and complications following the multimorbidity. Worse therapeutic and prophylactic anticoagulation efficacy, and safety are suggested by the studies, and the VTE recurrence and bleeding risk are higher in patients with multimorbidity compared to those without. Management of the therapeutic and prophylactic anticoagulation for VTE in patients with multimorbidity is difficult, and a balanced and detailed evaluation of the risks of VTE and bleeding is needed, and antiplatelet medications, increased doses or alternative direct oral anticoagulants (DOACs), thromboelastography (TEG), and physical activity may be helpful.

BackgroundThe purpose of this prospective observational study was to predict plaque vulnerability, stenosis, and hemodynamic problems based on coronary CT angiography (CCTA) using the Fat Attenuation Index (FAI) as a marker.MethodsPatients with stable coronary artery disease (CAD) who underwent CCTA between January 2021 and January 2023 were included in this study. Data on basic patient information, plaque parameters, and Fractional Flow Reserve (FFR) were collected and analyzed. Multiple linear analysis was performed to explore the association between FAI and FFR. Additionally, regression models were developed to predict dependent variables such as FFR, plaque vulnerability, and the degree of stenosis based on FAI values. We also explored specific thresholds of FAI to classify plaques into vulnerable and non-vulnerable categories.ResultsA total of 62 patients with 84 coronary arteries were included in the final analysis. Based on FAI levels, the study subjects were divided into FAI-negative group (FAI ≤ -70.1 HU, 52 cases) and FAI-positive group (FAI > -70.1 HU, 32 cases). Patients in the FAI-positive group had significantly lower FFR values compared to those in the FAI-negative group, and the proportion of vulnerable plaques was significantly higher in the FAI-positive group. Furthermore, as the degree of stenosis observed on CCTA increased, FAI values showed a significant increase. Analysis of plaque types revealed that FAI in vulnerable plaques was significantly higher than in other plaque types. In the multiple linear analysis, lesion length, TPB and FFR was negatively correlated with FAI (β = -0.25, -0.13 and -41.72).ConclusionThe results support the use of FAI as a valuable tool in clinical practice. Its predictive capabilities regarding hemodynamic dysfunction and plaque susceptibility make it an essential component of modern cardiovascular risk assessment strategies.

Limited available evidence comparing DOACs with warfarin suggests efficacy and safety of DOACs for CVT. We aimed to evaluate whether a specific DOAC is preferred for the treatment of CVT. This retrospective cohort study included adult patients with CVTs between September 2018 and September 2022 treated with a DOAC. The primary outcome was rate of partial or complete recanalization. Secondary outcomes included rate of recurrent VTE, CVT extension, major or clinically relevant non-major bleeding, and death within 180 days after DOAC initiation. Of 31 patients with CVT, 21 received apixaban, 7 received rivaroxaban, and 3 received dabigatran. Among those with repeat imaging, the primary composite outcome occurred in 100%, 80%, and 100% for each group, respectively (P = 0.34). One patient had extension of CVT while on apixaban and one patient had increased midline shift while on rivaroxaban. No other secondary outcomes were observed. There do not appear to be significant efficacy or safety differences between DOACs when used for CVT treatment, though larger studies are needed to validate these findings.

BackgroundHemophilia A (HA) occurs due to the deficiency of factor VIII (FVIII). Individuals with HA generally present with elevated activated partial thromboplastin time (aPTT) and normal prothrombin time (PT). The only possible treatment for this bleeding condition is factor concentrate.AimThe aim of this study is to compare the effect of recombinant factor VIII (rFVIII) and recombinant factor VII (rFVII) on prothrombin time (PT), activated partial thromboplastin time (aPTT), FVIII and FVII in severe HA.MethodologyA mixing study was conducted on 30 samples of severe HA patients to assess the correction of PT, aPTT, FVIII, and FVII values using biosimilars of rFVIII (NovoEight and Kogenate FS) and rFVII (NovoSeven and AryoSeven) using a fully automated coagulation analyser 'Ceveron alpha'.ResultsAll the four drugs demonstrated a significant alteration for both PT (P < .0001) and aPTT (P < .0001) values. A significant, notable increase of FVIII levels were observed for FVIII biosimilars. Further investigation into the effect of rFVII biosimilars on inhibitor-positive patients revealed a significant alteration in PT (P < .0001) and aPTT (P < .001) values.ConclusionTo the best of our knowledge, this is the first study to compare the effect of all four drugs on PT, aPTT, FVIII, and FVII. Two different groups of biosimilars were found to have a high potential to alter the PT and aPTT values. The FVIII biosimilars are efficient in increasing the FVIII levels.

Convalescent plasma (CP) therapy for COVID-19 infection may have favorable safety but varying efficacy, with concerns about its procoagulant impact. We investigated whether administration of CP to hospitalized patients affects their coagulation profile. Fifty-four patients randomized in a double-blinded fashion received either placebo, low-titer CP (LCP) or high-titer CP (HCP). Donor blood samples were obtained at the time of the plasmapheresis, while recipient blood samples were collected before infusion, one day post-infusion and between two and six days after infusion. Routine laboratory follow-up, coagulation biomarkers, antiphospholipid antibodies, and thrombin generation (TG) were assessed. CP donors had normal blood cell counts and coagulation profiles, without differences between LCP and HCP donors at the baseline. All CP recipients were on low-molecular-weight heparin thromboprophylaxis at the time of the infusion. Despite randomization, the HCP group had lower baseline (p = 0.004) and Day 1 platelet counts (p = 0.019) than the LCP group. Von Willebrand antigen (VWF:Ag) levels clearly exceeded normal without differences at baseline. At Day 1, LCP recipients had higher VWF:Ag (mean ± SD 224 ± 15%) than HCP recipients (210 ± 8%) (p = 0.012). In all groups, overall 80% lupus anticoagulant was positive. Baseline TG variables were comparable, but again LCP recipients exhibited higher endogenous thrombin potential (ETP) (1313 ± 535 nM.min) (p = 0.038) and peak TG (184 ± 106 nM) (p = 0.037) than the HCP group (870 ± 425 nM.min and 86 ± 54 nM). Our findings show that LCP increases VWF:Ag levels and enhances TG despite the thromboprophylaxis. These results suggest that HCP induces less hypercoagulability than LCP, which may contribute to the variability in CP efficacy.