Arterioscler Thromb Vasc Biol Research Articles

Correction to: EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 43, No. 6Correction to: EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy Originally published24 May 2023https://doi.org/10.1161/ATV.0000000000000163Arteriosclerosis, Thrombosis, and Vascular Biology. 2023;43:e230This article corrects the followingEVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of AutophagyIn the article by Canham et al, “EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy,” which published in the April 2023 issue of the journal (Arterioscler Thromb Vasc Biol. 2023;43:547–561. doi: 10.1161/ATVBAHA.122.318110), a correction was needed.An additional affiliation was added for Paul C. Evans: William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.122.318110. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesEVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of AutophagyLindsay Canham, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2023;43:547-561 June 2023Vol 43, Issue 6 Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000163 Originally publishedMay 24, 2023 PDF download Advertisement

Correction to: How Irritating! Electronic Cigarettes Not "95% Safer" Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial Dysfunction.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 43, No. 1Correction to: How Irritating! Electronic Cigarettes Not “95% Safer” Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial Dysfunction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: How Irritating! Electronic Cigarettes Not “95% Safer” Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial Dysfunction Originally published21 Dec 2022https://doi.org/10.1161/ATV.0000000000000160Arteriosclerosis, Thrombosis, and Vascular Biology. 2023;43:e65This article corrects the followingHow Irritating! Electronic Cigarettes Not “95% Safer” Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial DysfunctionIn the article by Conklin, “How Irritating! Electronic Cigarettes Not ‘95% Safer’ Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial Dysfunction,” which published in the November 2022 issue of the journal (Arterioscler Thromb Vasc Biol. 2022;42:1351–1354. doi: 10.1161/ATVBAHA.122.318468), a correction was needed.The first sentence on the “Constituents” section has been revised as follows: “As in their published studies of E-cig–derived aerosols, the article by Nabavizadeh et al2 shows FMD is impaired following acute exposures of anesthetized rats to individual constituent gases (ie, acrolein or acetaldehyde) as well as Marlboro Red smoke when compared with the air control.”The author apologizes for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.122.318468. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesHow Irritating! Electronic Cigarettes Not “95% Safer” Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial DysfunctionDaniel J. Conklin,Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42:1351-1354 January 2023Vol 43, Issue 1 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000160PMID: 36542727 Originally publishedDecember 21, 2022 PDF download Advertisement

Unbiased Identification of Thrombosis Risk Factors in Polycythemia Vera (PV) Using Machine Learning and Rich Data from Automated Extraction of Medical Records Generates Dynamic Models Highly Predictive for Thrombosis in PV

Background: Thrombosis is a leading cause of early morbidity and mortality in patients (pts) with polycythemia vera (PV)1. Thrombosis risk informs treatment decisions in PV but current risk stratification relies upon two non-modifiable factors - Age(</≥ 60) and thrombosis history (hx)2 - thereby offering no potential to monitor changes in risk. We used a rich dataset and machine learning (ML) methods to identify clinically available data useful for dynamic prediction of individualized thrombosis risk in PV. Methods: Under Weill Cornell Medicine (WCM) institutional board approval, we identified in our research repository (RDR) 470 eligible pts with PV diagnosis (Dx) and annotated thrombosis outcomes, as previously described3. We queried electronic medical records using our RDR, Observational Medical Outcomes Partnership, Structured Query Language, and novel workflows implemented in R and Python, to automate extraction of all available clinical data for pts at every clinical visit. Over 2100 clinical parameters were available for ~8400 hematology clinic visits yielding ~1.4 million data elements. These data included all laboratory measures, molecular studies, pathology reports, vitals, medications and clinical hx. Data completeness varied across data types with 283 parameters available in >90% of visits for all pts. In total, 292 parameters with over 50% availability were assessed while others were excluded from analysis. Multivariate imputation by chained equations (MICE) was used to impute missing data. To address potential artifacts from imputation, all analyses were performed on 10 separately imputed datasets and results were aggregated. AutoGluon infrastructure was used to identify the best performing ML algorithms. We then used our dataset to train random forest (RF) ML models that classify, at each clinic visit, the likelihood of thrombosis within a year. Parameters were ranked by Gini feature importance to identify a practical clinical model comprised of a few core parameters (eg 3-7) and interrogated the performance of >2x105 of these models (every combination of top 20 parameters in groups of 3-7) compared to the full model. Model performance was evaluated using the F1 score, which is considered highly predictive when >0.8. Results: Of 470 PV pts, Dx at median age of 54 (range 20-94), 64 (14%) had a thrombosis hx at Dx (8.1% venous, 6.6% arterial). Over a median follow-up of 10 years (yr), 159 thromboses occurred in 115 pts (88 venous, 71 arterial). Cumulative incidence of thrombosis was non-linear, as previously appreciated1. Annual incidence rate (IR) of thrombosis was higher shortly after diagnosis (IR of 4.4% vs 1%, 2yr cutoff), and following a thrombotic event (IR of 9.7% vs 1.8%, 2 yr cutoff). Consistent with this observation, ML models identified time from Dx, and time from prior thrombosis among the top 20 most predictive parameters as assessed by Gini feature importance (Figure 1). Most predictive parameters also included risk factors previously implicated in PV thrombosis (age, blood counts, JAK2 allele burden) as well as known thrombosis risk factors under-recognized in PV (blood type4, BMI, creatinine), and parameters not previously thought to contribute to thrombosis risk (MCV, uric acid, LDH). The full ML model was highly predictive of thrombosis with an F1 of 0.82 (Figure 2). We then identified simplified models (combinations of 4-5 variables) that performed similarly to the full model with an F1 > 0.8. One example combines age, time since Dx, time since prior thrombosis, and BMI. These models are being validated against external datasets and an online risk calculator will be developed. Discussion: We used ML and deep datasets for unbiased identification of the clinical parameters most predictive of near-term thrombosis risk in PV pts. These models address dynamic changes to patient risk due to intrinsic factors (e.g. age, blood type), life events (e.g. time since Dx/thrombosis) and clinical changes (e.g. ANC, BMI) that can be used to tailor risk mitigation strategies. Validation of models with at least core variables of age, time since Dx, time since prior thrombosis, and BMI against external datasets would likely establish a universal model to dynamically predict individualized risk of thrombosis in PV pts. References 1 Hultcrantz. et al. Ann Intern Med. 2018 2 Barbui T, et al.Leukemia 2018 3 Abu-Zeinah G, et al. Leukemia 2021 4 Groot H, et al. Arterioscler Thromb Vasc Biol 2020 Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

A gain‐of‐function filamin A mutation in mouse platelets induces thrombus instability

BackgroundFilaminopathies A are rare disorders affecting the brain, intestine, or skeleton, characterized by dominant X‐linked filamin A (FLNA) gene mutations. Macrothrombocytopenia with functionally defective platelets is frequent. We have described a filaminopathy A male patient, exhibiting a C‐terminal frame‐shift FLNa mutation (Berrou et al., Arterioscler Thromb Vasc Biol. 2017;37:1087–1097). Contrasting with female patients, this male patient exhibited gain of platelet functions, including increased platelet aggregation, integrin αIIbβ3 activation, and secretion at low agonist concentration, raising the issue of thrombosis risk. ObjectivesOur goal is to assess the thrombotic potential of the patient FLNa mutation in an in vivo model. MethodsWe have established a mutant FlnA knock‐in mouse model. ResultsThe mutant FlnA mouse platelets phenocopied patient platelets, showing normal platelet count, lower expression level of mutant FlnA, and gain of platelet functions: increased platelet aggregation, secretion, and αIIbβ3 activation, as well as increased spreading and clot retraction. Surprisingly, mutant FlnA mice exhibited a normal bleeding time, but with increased re‐bleeding (77%) compared to wild type (WT) FlnA mice (27%), reflecting hemostatic plug instability. Again, in an in vivo thrombosis model, the occlusion time was not altered by the FlnA mutation, but arteriolar embolies were increased (7‐fold more frequent in mutant FlnA mice versus WT mice), confirming thrombus instability. ConclusionsThis study shows that the FlnA mutation found in the male patient induced gain of platelet functions in vitro, but thrombus instability in vivo. Implications for the role of FLNa in physiology of thrombus formation are discussed.

Vascular Imaging Follow‐Up in Carotid Webs: Is There Vascular Remodeling?

Vascular Imaging Follow‐Up in Carotid Webs: Is There Vascular Remodeling?

Retraction.

The following Arteriosclerosis, Thrombosis, and Vascular Biology article is being retracted: Xu J, Xie Z, Reece R, Pimental D, Zou MH. Uncoupling of Endothelial Nitric Oxidase Synthase by Hypochlorous Acid Role of NAD(P)H Oxidase-Derived Superoxide and Peroxynitrite. Arterioscler Thromb Vasc Biol. 2006;26:2688-2695. doi: 10.1161/01.ATV.0000249394.94588.82. The editors received a request from the University of Oklahoma Health Sciences Center to retract the above referenced article due to data irregularities in Figures 2C and 3B that affect the results and conclusions reported in the manuscript. In addition, lanes 1 and 4 of Figure 3B "dimer and monomer" Western blot are duplicates. The editors are retracting this article in agreement with the University of Oklahoma. The authors do not agree to the retraction.

Retraction.

The following Arteriosclerosis, Thrombosis, and Vascular Biology article is being retracted: Song P, Zhou Y, Coughlan KA, Dai X, Xu H, Viollet B, Zou MH. Adenosine monophosphate-activated protein kinase-α2 deficiency promotes vascular smooth muscle cell migration via S-phase kinase associated protein 2 upregulation and E-cadherin downregulation. Arterioscler Thromb Vasc Biol. 2013;33:2800-2809. doi: 10.1161/ATVBAHA.113.301869 The editors received a request from the University of Oklahoma Health Sciences Center to retract the above referenced article due to data irregularities and image reuse in Figures 4 and 6 that affect the results and conclusions reported in the manuscript. Specifically, the following irregularities were found: -Lanes 4-6 of Figure 4A "GAPDH" blot lane spacing is inconsistent with lanes 1-3 of same blot and the authenticity of that blot related to the rest of the data in the figure could not be confirmed. -Figure 6D "E-cadherin" was duplicated with Online Figure 1B "HDAC3" blot. The editors are retracting this article in agreement with the University of Oklahoma. The authors do not agree to the retraction.

Correction to: Macrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis Development.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 42, No. 8Correction to: Macrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis Development Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: Macrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis Development Originally published27 Jul 2022https://doi.org/10.1161/ATV.0000000000000156Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42:e252This article corrects the followingMacrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis DevelopmentIn the article by Zhang et al, “Macrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis Development,” which published in the June 2022 issue of the journal (Arterioscler Thromb Vasc Biol. 2022;42:700–716. doi: 10.1161/ATVBAHA.121.317204), corrections were needed.The ORCID logo in the author byline should have been associated with Dr Feng Xu.In the Figure 7 legend, “acute coronary syndromes (ACs)” should have been “apoptotic cells (ACs)”.The publisher apologizes for the errors.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.121.317204. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesMacrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis DevelopmentJian Zhang, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42:700-716 August 2022Vol 42, Issue 8 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000156PMID: 35895806 Originally publishedJuly 27, 2022 PDF download Advertisement

Correction to: Sex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial Infarction

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 41, No. 12Correction to: Sex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial Infarction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: Sex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial Infarction Originally published23 Nov 2021https://doi.org/10.1161/ATV.0000000000000148Arteriosclerosis, Thrombosis, and Vascular Biology. 2021;41:e528This article corrects the followingSex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial InfarctionIn the article by Soo Kim et al, “Sex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial Infarction,” which published in the January 2021 issue of the journal (Arterioscler Thromb Vasc Biol. 2021;41:390–400. DOI: 10.1161/ATVBAHA.120.315033), a correction was needed.In transitioning the color scheme in the figures prior to submission, Figure 1E, which measures cAMP inside the platelets of healthy men, had the color notation for men and women inadvertently switched.The authors apologize for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.120.315033. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesSex-Specific Platelet Activation Through Protease-Activated Receptors Reverses in Myocardial InfarctionBeom Soo Kim, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2021;41:390-400 December 2021Vol 41, Issue 12 Advertisement Article InformationMetrics © 2021 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000148PMID: 34813348 Originally publishedNovember 23, 2021 PDF download Advertisement

A Randomized Open-Label Clinical Trial of Lipid-Lowering Therapy in Psoriasis to Reduce Vascular Endothelial Inflammation

In psoriasis, immune systemic activation and cardiometabolic abnormalities, including dyslipidemia, play a role in promoting impaired endothelial health and increased cardiovascular (CV) risk ( Greb et al., 2016 Greb J.E. Goldminz A.M. Elder J.T. Lebwohl M.G. Gladman D.D. Wu J.J. et al. Psoriasis. Nat Rev Dis Primers. 2016; 2: 16082 Crossref PubMed Scopus (427) Google Scholar ). Patients with psoriasis have elevated brachial vein endothelial proinflammatory transcript expression (impaired vascular endothelial health), with the degree of impairment directly correlated with skin activity and circulating biomarkers of systemic inflammation ( Garshick et al., 2019 Garshick M.S. Barrett T.J. Wechter T. Azarchi S. Scher J.U. Neimann A. et al. Inflammasome signaling and impaired vascular health in psoriasis. Arterioscler Thromb Vasc Biol. 2019; 39: 787-798 Crossref PubMed Scopus (34) Google Scholar ). In psoriasis, TNF and IL-17A synergism promote inflammasome (IL-1β) signaling and downstream IL-6 production (driver of CRP) ( Verma et al., 2021 Verma D. Fekri S.Z. Sigurdardottir G. Bivik Eding C. Sandin C. Enerbäck C. Enhanced inflammasome activity in patients with psoriasis promotes systemic inflammation. J Invest Dermatol. 2021; 141: 586-595.e5 Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar ), which associates with vascular endothelial inflammatory transcript expression, suggesting a pathogenic (immune-mediated) mechanism of atherosclerosis development ( Garshick et al., 2019 Garshick M.S. Barrett T.J. Wechter T. Azarchi S. Scher J.U. Neimann A. et al. Inflammasome signaling and impaired vascular health in psoriasis. Arterioscler Thromb Vasc Biol. 2019; 39: 787-798 Crossref PubMed Scopus (34) Google Scholar ). Is It Prime Time for Statin Therapy in Psoriasis?Journal of Investigative DermatologyVol. 142Issue 6PreviewIt has been over a decade and a half since the first large-scale study of the accelerated risk of myocardial infarction in psoriasis (Gelfand et al., 2006). Since then, a broad range of scientific approaches has determined that psoriasis itself is associated with a higher-risk subclinical vascular disease (Naik et al., 2015), high-risk coronary plaque (Lerman et al., 2017), and major adverse cardiovascular (CV) events (Mehta et al., 2010) and mortality (Noe et al., 2018). Although these studies have established that the risk of CV disease (CVD) is independent of traditional CV risk factors, psoriasis also has complex interactions with metabolic disease. Full-Text PDF

Anti-HNA-3a Alloantibodies Can Cause Differential Endothelial Damage through a Direct Neutrophil Activation Pathway

INTRODUCTIONThe human neutrophil antigen (HNA) 3a/b is associated with a single amino acid substitution (R 154Q polymorphism) on the first extracellular loop of choline transporter-like protein 2 (CTL2). Antibodies against HNA-3a have been associated with severe and fatal transfusion-related acute lung injury (TRALI). Epitope mapping suggests the existence of two types of HNA-3a antibodies. Type I antibodies only require first extracellular loop of the CTL2 for expression of the antigen, type II antibodies require at least the first 3 extracellular loops of CTL2 in a native configuration (i.e. expressed on a cell membrane). This study aimed to evaluate the activity of type I and type II anti-HNA-3a antibodies in an in vitro TRALI model.STUDY DESIGN & METHODS: The granulocyte agglutination test (GAT) and granulocyte immunofluorescence test (GIFT) were used to confirm anti-HNA-3a activity in two donor sera (Q49 and Q50). Flow cytometry was used to confirm antibody binding to freshly isolated human or mouse neutrophils. A rabbit polyclonal antibody against an epitope in the third extracellular loop of CTL2's was coated onto the wells of an ELISA plate and neutrophil HNA-3a antigen was captured and sera tested. For the TRALI model, human lung microvascular endothelial cells (HLMVECs) were grown to confluence before being treated with lipopolysaccharide (LPS). Freshly isolated neutrophils from HNA-3aa homozygote donors were then added with 10% Q49 or Q50. Microscopic counting of Trypan blue staining was used to measure rate HLMVEC death. Significance was determined using a one-way ANOVA (p<0.05), followed by Dunnett's post-hoc test. RESULTS AND DISCUSSIONGAT and GIFT confirmed that both Q49 and Q50 contained an anti-HNA-3a antibody, and that neither contained antibodies against any other HNA or HLA molecules. In flow cytometry, both Q49 and Q50 bound to human neutrophils, but only Q49 bound to mouse neutrophils. In the ELISA, signal was detected only for Q49. These data provided evidence that Q49 was a type I antibody and Q50 was a type II antibody. Within the TRALI model, HLVMEC death was observed with both Q49 and Q50 only in the presence of LPS and neutrophils (Table 1). Previously reported HLMVEC permeability in the absence of neutrophils (Bayat et al. Arterioscler Thromb Vasc Biol. 2013) was not observed as in this study the outcome measured was HLMVEC death. In the present study, the effect for Q49 (type I) was significantly larger than for Q50 (type II; Table 1; p-value <0.0001). CONCLUSIONSIn this model, LPS and neutrophils were required for anti-HNA-3a mediated HLMVEC death thought to reflect events involved in the initiation of TRALI. The observation that type I antibodies elicited a stronger response provides a direction for further research. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Clinical Research on Antioxidant-Based Modalities in 2020

Clinical Research on Antioxidant-Based Modalities in 2020

Other and All-Cause Mortality among Men Diagnosed with Prostate Cancer in the PLCO Trial

Men with prostate cancer have high cause-specific survival, and most deaths are from other causes. This study aimed to investigate other and all-cause mortality in a large cancer screening cohort. From the PLCO (Prostate, Lung, Colorectal and Ovarian) Cancer Screening Trial cohort, we selected men diagnosed with prostate cancer from 1994-2014. We examined other and all-cause survival by prostate cancer risk level, defined as the D'Amico categories for localized disease (low, intermediate and high risk) plus nonlocalized disease. We developed 3 Cox proportional hazards models to assess the relationship between risk level and survival. Model I controlled for age, race, study arm and diagnosis year. Model II additionally controlled for other demographic and medical history factors. Model III additionally controlled for initial treatment. Of 76,672 men in PLCO and 10,859 prostate cancer cases, 9,248 (85.2%) had known prostate cancer risk level (mean±SD age 70.4±6.2 years). Median followup time from diagnosis was 10.8 years (IQR 6.8-15.0). Of 3,318 deaths 81% were from other causes. Compared to the low risk group, other-cause mortality HRs were 1.13 (95% CI 1.04-1.23), 1.35 (95% CI 1.21-1.50) and 1.63 (95% CI 1.35-1.97) for intermediate risk, high risk and advanced disease, respectively, in model II. Model III HRs were similar to model II except for advanced disease, where the HR decreased to 1.35. Other-cause survival was greater in lower vs higher risk disease, even after controlling for lifestyle characteristics and comorbidities. Further research is needed to identify factors contributing to this higher other-cause mortality to help mitigate the risk.

Функциональное состояние сосудистой стенки и плазменного звена гемостаза у женщин раннего постменопаузального периода на фоне длительной менопаузальной гормональной терапии

Цель исследования: оценка изменений функциональной активности сосудистой стенки и плазменного звена гемостаза у женщин раннего постменопаузального периода на фоне длительной низкодозовой менопаузальной гормональной терапии (МГТ). Материалы и методы: Обследовано 162 женщины в ранней постменопаузе. В основную группу вошли 84 пациентки, которым была назначена низкодозовая МГТ: 1 мг 17β-эстрадиола (E2) и 2 мг дроспиренона (ДРСП) — препарат Анжелик® (Байер Фарма, Германия). Контрольную группу составили 78 женщин, не получавших МГТ. Длительность наблюдения составила 5,2 [4,8; 5,7] лет. Исследовали антитромбогенную активность сосудистой стенки, лабораторные маркеры эндотелиальной дисфункции. Результаты: Несмотря на увеличение агрегационной активности тромбоцитов и более низкие значения активности антитромбина III у женщин на фоне МГТ, не было отмечено увеличения риска развития венозного тромбоза и эмболий, ишемического инсульта и случаев острого коронарного синдрома. К окончанию наблюдения установлено снижение антиагрегационного потенциала сосудистой стенки, более выраженное у женщин группы кон-троля. У женщин, принимавших МГТ, выявлено снижение концентрации фибриногена крови к окончанию исследования. На фоне МГТ отмечено значимое возрастание уровня метаболитов оксида азота, снижение уровней эндотелина-1 и асимметричного диметиларгинина к 12 мес наблюдения, но в дальнейшем отмечено повышение их уровней, не достигшее исходных значений. Заключение: Изменения функциональной активности эндотелия свидетельствуют об отсутствии негативного влияния на эндотелий сосудов длительной низкодозовой МГТ (1 мг E2/2 мг ДРСП). Objectives: to assess changes in the functional activity of the vascular wall and plasma hemostasis in women of early postmenopausal period under long-term low-dose menopausal hormone therapy (MHT). Patients/Methods: We examined 162 women in early postmenopause. The main group included 84 patients; they were prescribed a low-dose MHT: 1 mg of 17β-estradiol (E2) and 2 mg of drospirenone (DRSP) — Angelique® (Bayer Pharma, Germany). The control group consisted of 78 women did not taking MHT. The duration of observation was 5.2 [4.8; 5.7] years. Antithrombogenic activity of the vascular wall and laboratory markers of endothelial dysfunction were examined. Results: In women taking MHT we found increasing of platelet aggregation activity and lower antithrombin III activity, but did not reveal increased risk of venous thrombosis and embolism, ischemic stroke, and cases of acute coronary syndrome. By the end of observation decreasing of antiplatelet potential of the vascular wall, more expressed in women of the control group, was noted. In women taking MHT, blood fi brinogen concentration decreased by the end of the study. After 12 months of observation in women taking MHT we revealed significant increasing of nitric oxide metabolites, decreasing of endothelin-1 and asymmetric dimethylarginine; later their levels increased but did not reach the initial values. Conclusions: Changes in endothelial functional activity showed no adverse effect of long-term low-dose MHT (1 mg E2/DRSP 2 mg) on the vascular endothelium.

Correction to: Causal Associations Between Serum Bilirubin Levels and Decreased Stroke Risk: A Two-Sample Mendelian Randomization Study.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 40, No. 4Correction to: Causal Associations Between Serum Bilirubin Levels and Decreased Stroke Risk: A Two-Sample Mendelian Randomization Study Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: Causal Associations Between Serum Bilirubin Levels and Decreased Stroke Risk: A Two-Sample Mendelian Randomization Study Originally published25 Mar 2020https://doi.org/10.1161/ATV.0000000000000095Arteriosclerosis, Thrombosis, and Vascular Biology. 2020;40:e118This article corrects the followingCausal Associations Between Serum Bilirubin Levels and Decreased Stroke RiskIn the article by Choi et al, “Causal Associations Between Serum Bilirubin Levels and Decreased Stroke Risk: A Two-Sample Mendelian Randomization Study,” which published in the February 2020 issue of the journal (Arterioscler Thromb Vasc Biol. 2020;40:437-445. doi: 10.1161/ATVBAHA.119.313055), a correction was needed.The following funding source was erroneously omitted: Wellcome Trust grant number 108902/B/15/Z.The authors apologize for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.119.313055. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesCausal Associations Between Serum Bilirubin Levels and Decreased Stroke RiskYoonjeong Choi, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2020;40:437-445 April 2020Vol 40, Issue 4 Advertisement Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000095PMID: 32208995 Originally publishedMarch 25, 2020 PDF download Advertisement

Correction to: Shear Stress and VE-Cadherin: The Molecular Mechanism of Vascular Fusion.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 40, No. 2Correction to: Shear Stress and VE-Cadherin: The Molecular Mechanism of Vascular Fusion Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: Shear Stress and VE-Cadherin: The Molecular Mechanism of Vascular Fusion Originally published22 Jan 2020https://doi.org/10.1161/ATV.0000000000000092Arteriosclerosis, Thrombosis, and Vascular Biology. 2020;40:e36This article corrects the followingShear Stress and VE-CadherinIn the article by Caolo et al, “Shear Stress and VE-Cadherin: The Molecular Mechanism of Vascular Fusion,” which published in the September 2018 issue of the journal (Arterioscler Thromb Vasc Biol. 2018;38:2174-2183. doi: 10.1161/ATVBAHA.118.310823), a correction was needed.In the “Cell Culture and Shear Stress Experiments” section, there was an error with a catalog number and in the basement membrane protein that was used for coating slides. The section has been revised as follows: “Human microvascular endothelial cells (Promocell, C-12210) were cultured in endothelial growth medium 2MV (EGM-2MV, Lonza, CC-3202) according to manufacturer’s protocol. Endothelial cells were seeded on glass slides (VWR, MENZJ5800AMNZ) coated with fibronectin (VWR, 734-0085).”The authors apologize for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.118.310823. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesShear Stress and VE-CadherinVincenza Caolo, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2018;38:2174-2183 February 2020Vol 40, Issue 2 Advertisement Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000092PMID: 31967902 Originally publishedJanuary 22, 2020 PDF download Advertisement

Correction to: SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 40, No. 1Correction to: SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization Originally published23 Dec 2019https://doi.org/10.1161/ATV.0000000000000091Arteriosclerosis, Thrombosis, and Vascular Biology. 2020;40:e21In the article by Kim et al, “SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization,” which published in the October 2019 issue of the journal (Arterioscler Thromb Vasc Biol. 2019;39:2120–2131. doi: 10.1161/ATVBAHA.119.313179), a correction was needed.The fourth author’s name has been corrected to Jaetaek Kim.The authors apologize for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.119.313179. Previous Back to top Next FiguresReferencesRelatedDetails January 2020Vol 40, Issue 1 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000091PMID: 31869268 Originally publishedDecember 23, 2019 PDF download Advertisement

Correction to: 18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 39, No. 12Correction to: 18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection to: 18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus Originally published26 Nov 2019https://doi.org/10.1161/ATV.0000000000000090Arteriosclerosis, Thrombosis, and Vascular Biology. 2019;39:e292This article corrects the following18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes MellitusIn the article by Raggi et al, “18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus,” which published in the February 2019 issue of the journal (Arterioscler Thromb Vasc Biol. 2019;39:276–284. DOI: 10.1161/ATVBAHA.118.311711), a correction was needed.The seventh author’s name should be spelled as Roseanne O. Yeung.The authors apologize for the error.This correction has been made to the current online version of the article, which is available at www.ahajournals.org/doi/10.1161/ATVBAHA.118.311711. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articles18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes MellitusPaolo Raggi, et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2019;39:276-284 December 2019Vol 39, Issue 12 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/ATV.0000000000000090PMID: 31770026 Originally publishedNovember 26, 2019 PDF download Advertisement

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

Potential Anti-Thrombotic Effect without Accompanying Hemorrhage with Fostamatinib Use in Patients with Immune Thrombocytopenia

Potential Anti-Thrombotic Effect without Accompanying Hemorrhage with Fostamatinib Use in Patients with Immune Thrombocytopenia