Cardiovascular Toxicology最新文献

{"title":"Impact of Proton Pump Inhibitors on Osimertinib-Induced Cardiotoxicity in NSCLC Patients.","authors":"Haitao Wang, Sinan Ma, Weijia Huang, Keyu Chen, Jiao Xie, Na Wang, Youjia Li, Qianting Yang, Xin Yang, Yan Wang","doi":"10.1007/s12012-025-10012-8","DOIUrl":"10.1007/s12012-025-10012-8","url":null,"abstract":"<p><p>There is a lack of comprehensive research investigating the relationship between proton pump inhibitors (PPIs) and osimertinib combination therapy concerning cardiotoxicity. We conducted a retrospective analysis of adverse event reports from the US Food and Drug Administration Adverse Event Reporting System (FAERS). In this analysis, we used patients with non-small cell lung cancer (NSCLC) who did not receive osimertinib or PPIs as a control group to assess the association between cardiotoxicity occurrence in patients receiving osimertinib with PPIs and those without PPIs. We employed disproportionality analysis along with both additive and multiplicative models. The reporting odds ratios (ROR) for cardiac events, including torsade de pointes/QT prolongation, cardiomyopathy, cardiac arrhythmias, cardiac failure, ischaemic heart disease, and embolic and thrombotic events, were significantly higher in patients using PPIs with osimertinib (14.11, 9.04-22.04; 4.67, 2.67-8.16; 4.43, 3.17-6.20; 3.67, 2.53-5.34; 2.24, 1.31-3.84; 1.92, 1.43-2.56, respectively) compared to osimertinib alone (4.87, 3.91-6.07; 2.50, 2.02-3.09; 1.59, 1.37-1.84; 2.00, 1.74-2.29; 0.65, 0.50-0.84; 1.01, 0.91-1.11). Our investigation unveiled an elevated risk of cardiotoxicity in NSCLC patients when osimertinib was combined with PPIs, compared to osimertinib monotherapy. Therefore, vigilant monitoring for cardiotoxicity is paramount in NSCLC patients undergoing these combined treatments.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1084-1093"},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Urinary Metals and Polycyclic Aromatic Hydrocarbon Levels and Cardiovascular Disease Among Adult Americans: Data from NHANES 2011 to 2016.","authors":"Minyao Zhao, Sijie Gu, Tingchao Liu, Shipeng Gao, Zheng Qiao, Kui Wang, Qiang Niu, Rulin Ma, Heng Guo, Shuxia Guo, Jia He","doi":"10.1007/s12012-025-10009-3","DOIUrl":"10.1007/s12012-025-10009-3","url":null,"abstract":"<p><p>Previous studies have inconclusively examined the associations of metals or polycyclic aromatic hydrocarbons (PAHs) with cardiovascular disease (CVD) separately, highlighting the need to explore their combined association with CVD. Based on the 2011-2016 National Health and Nutrition Examination Survey, the association of 12 metals and six PAHs in urine with CVD was analyzed using weighted logistic regression, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR). Crucial metals and PAHs were screened, and dose-response, subgroup, interactions, and mediation analyses were conducted. 4306 participants were included, of whom 406 had CVD. Weighted logistic regression showed that cadmium (OR = 1.41, 95% CI 1.11-1.78), tin (OR = 1.63, 95% CI 1.03-2.60), and 1-hydroxypyrene (1-PYR) (OR = 1.40, 95% CI 1.15-1.69) were positively correlated with CVD. These factors also showed a linear relation with CVD. The WQS and BKMR models indicated that the combined association of 12 metals and six PAHs was positively associated with CVD. Cadmium, cesium, tin, uranium, and 1-PYR played critical roles (all weights > 0.050). Subgroup analysis revealed that these substances were mostly positively associated with CVD in young and middle-aged people, smokers, drinkers, and those who were overweight. There was an interaction between tin and smoking status (P for interaction < 0.05). Cadmium and tin mediated 18.40% and 6.90% of the association of 1-PYR with CVD, respectively, whereas the proportions of the mediating effects of 1-PYR in the association of cadmium and tin with CVD were 8.10% and 7.90%, respectively. Overall, higher levels of urinary metals and PAHs mixtures may be associated with higher CVD prevalence. Cadmium, cesium, tin, uranium, and 1-PYR played crucial roles in this association. Cadmium and tin played mediating roles in the association between 1-PYR and CVD. Meanwhile, 1-PYR also played a mediating role in the association between cadmium and tin and CVD.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"929-943"},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Maternal/In Utero Exposure of Novel Tobacco Products on the Offspring Cardiovascular Health.","authors":"Shelby S Umphres, Precious O Badejo, Fadi T Khasawneh, Fatima Z Alshbool","doi":"10.1007/s12012-025-10023-5","DOIUrl":"10.1007/s12012-025-10023-5","url":null,"abstract":"<p><p>Novel tobacco products (NTPs) have recently been on the rise appealing to a variety of users, including pregnant women and women of childbearing age, who deem these products to be a safe/safer alternative to traditional smoking. To this end, several studies have made advances toward proving the invalidity of these claims, especially in the context of cardiovascular disease. However, an area that has yet to be extensively explored is maternal/in utero exposure to these devices and the cardiovascular health outcomes on the offspring into their adult life. Herein, our aim is to critically assess the literature to identify and discuss the cardiovascular health risks that the offspring exhibits as a result of in utero exposure to NTPs. These studies have been summarized as a comprehensive review.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF9-Mediated Transcriptional Promotion of HMGB2 Accelerates Cardiomyocyte Apoptosis, Inflammation, and Ferroptosis in Myocardial Ischemia/Reperfusion Injury.","authors":"Haijuan Cheng, Aiping Jin, Qianrong Zhang, Sha Ye, Yuanyuan Zheng","doi":"10.1007/s12012-025-10028-0","DOIUrl":"https://doi.org/10.1007/s12012-025-10028-0","url":null,"abstract":"<p><p>High-mobility group protein B2 (HMGB2) has been confirmed to participate in regulating the process of myocardial ischemia/reperfusion (I/R) injury. However, the more roles and mechanisms of HMGB2 in myocardial I/R injury need to be further revealed. Cardiomyocytes (HL-1) were cultured under hypoxia/reoxygenation (H/R) conditions, and myocardial I/R injury mouse model was established by ligation of the left anterior descending coronary artery. The protein levels of HMGB2 and kruppel-like factor 9 (KLF9) were determined by western blot. Cell viability and apoptosis were examined by CCK8 assay and flow cytometry. The levels of inflammatory factors and ferroptosis-related markers were tested to assess cell inflammation and ferroptosis. The interaction between KLF9 and HMGB2 promoter was evaluated by ChIP assay and dual-luciferase reporter assay. HMGB2 was higher expressed in H/R-induced HL-1 cells and its silencing could suppress H/R-induced HL-1 cell apoptosis, inflammation, and ferroptosis. KLF9 had binding sites in HMGB2 promoter region, which could increase HMGB2 expression by enhancing its transcription. Silencing of KLF9 inhibited H/R-induced HL-1 cell apoptosis, inflammation, and ferroptosis, while these effects were reversed by overexpressing HMGB2. In addition, animal study revealed that interference of KLF9 alleviated myocardial tissues damage and fibrosis in I/R injury mice models by reducing HMGB2 expression. Collectively, our study indicated that KLF9 promoted myocardial I/R injury by aggravating cardiomyocyte apoptosis, inflammation, and ferroptosis through promoting HMGB2 transcription.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NLRP3-Mediated PANoptosis and Associated Interventions in Endothelial Injury.","authors":"Aiwei Yan, Ting Cao, Xiao Li, Xingchen Li, Chaochu Cui, Xianwei Wang","doi":"10.1007/s12012-025-10020-8","DOIUrl":"https://doi.org/10.1007/s12012-025-10020-8","url":null,"abstract":"<p><p>Endothelial cell (EC) injury is highly significant in both health toxicology and cardiovascular disease. In the context of environmental and occupational health, ECs are frequently the frontline responders to pathogens and toxicants. Upon exposure to such agents, endothelial dysfunction ensues, triggering a cascade of cellular fates including pyroptosis, apoptosis, and necroptosis, which together constitute PANoptosis. The NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome is a sentinel of cellular stress and is activated in response to environmental pollutants and chemical toxins. Notably, strategies aimed at suppressing NLRP3 activation, such as the potential deployment of specific antidotes or detoxifying agents, have shown promise in impeding endothelial injury and halting the progression of cardiovascular diseases (CVDs). In this review, we summarize the role of NLRP3 in endothelial injury, highlight its PANoptosis ramifications, and partially discuss its relationship with vascular toxicity, which may aid in the prevention and treatment of vascular disorders and toxicology.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association of Blood Cobalt Levels with Cardiovascular and Chronic Kidney Diseases: Mediating Role of Inflammatory Indicators (SII, NLR, PLR, NMLR, and LMR).","authors":"Bei-Bei Lu, Qian Luo, Xiao-Lin Yuan, Qing-Song Chen, Jing-Yang Ran, Xing-Wei Zhe, Xiao-Hui Liao","doi":"10.1007/s12012-025-10018-2","DOIUrl":"https://doi.org/10.1007/s12012-025-10018-2","url":null,"abstract":"<p><p>Cobalt is a prevalent environmental metal with known toxicological potential. Inflammation plays a key role in the pathophysiology of cardiovascular disease (CVD) and chronic kidney disease (CKD). However, the relationships between blood cobalt concentrations, inflammatory indicators, and their roles in CVD and CKD remain inadequately characterized. This study aimed to evaluate the associations between blood cobalt concentrations and the prevalence of CVD and CKD and to explore the mediating role of inflammatory indicators in these associations. Data from 6689 participants were obtained from the National Health and Nutrition Examination Survey 2015-2018. Restricted cubic splines and multivariate logistic regression models were used to assess the associations between blood cobalt exposure, CVD, CKD, and inflammatory markers. Generalized additive models were applied to investigate potential nonlinear relationships. The receiver operating characteristic analysis assessed the discriminatory ability of blood cobalt levels for CVD and CKD. Mediation analysis was conducted to examine whether inflammatory indicators mediate the association between blood cobalt and CVD/CKD. Multivariate logistic regression analysis showed that higher blood cobalt levels (OR = 1.50, 95% CI 1.22-1.85, P < 0.001) and NMLR (OR = 1.34, 95% CI 1.07-1.68, P = 0.010) were significantly associated with a higher prevalence of CVD. For CKD, blood cobalt (OR = 1.74, 95% CI 1.44-2.11, P < 0.001), SII (OR = 1.43, 95% CI 1.18-1.73, P < 0.001), NLR (OR = 1.73, 95% CI 1.42-2.10, P < 0.001), and NMLR (OR = 1.63, 95% CI 1.33-2.00, P < 0.001) were all significantly associated with a higher prevalence of CKD. Blood cobalt levels showed significant positive correlations with SII, NLR, PLR, and NMLR. Specifically, SII (β = 49.93, 95% CI 26.91-72.94, P < 0.001), NLR (β = 0.21, 95% CI 0.13-0.30, P < 0.001), and NMLR (β = 0.20, 95% CI 0.13-0.27, P < 0.001) exhibited significant increases. Mediation analysis indicated that SII, NLR, NMLR, and LMR significantly mediated the association between log_BCo and both CVD and CKD (P < 0.05). Notably, NMLR had the strongest mediating effect in both CVD and CKD, with a mediation effect percentage: 13.42% (P < 0.001) in CVD and 11.76% (P < 0.001) in CKD. Blood cobalt concentrations are significantly associated with the prevalence of cardiovascular disease and chronic kidney disease. Inflammation may play a mediating role in these associations. These findings highlight the potential contribution of inflammation to cobalt-related cardiovascular and kidney disease risks.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal Electronic Cigarette Inhalation Exposure During Gestation: Impacts on Prolactin and Xanthine Oxidase.","authors":"Julie A Griffith, Kallie J Schafner, Krista L Garner, Evan DeVallance, Sara E Lewis, Timothy R Nurkiewicz, Eric E Kelley, Brooke A Maxwell, William T Goldsmith, Elizabeth C Bowdridge","doi":"10.1007/s12012-025-10022-6","DOIUrl":"https://doi.org/10.1007/s12012-025-10022-6","url":null,"abstract":"<p><p>Pregnancy requires metabolic and endocrine changes that must occur to support fetal growth and development. Aberrations in these necessary modifications can impact maternal health and fetal growth. Exposure to toxicants during pregnancy can negatively affect fetal health and development, but studies on electronic cigarette (e-cig) exposure is limited. We hypothesized that maternal e-cig exposure during gestation leads to hormonal and redox imbalance and negatively impacts fetal development. Pregnant Sprague-Dawley rats were exposed to e-cig aerosols (1227 ± 131 mg/m³) or HEPA-filtered air for 90 min from gestational day (GD) 10-19 for a total of 6 days. Dams were euthanized on GD 20 and dam serum, liver, lung, ovaries, and placental tissue were collected for analysis. Fetal mass, placental mass, and sex ratios were assessed. Fetal and placental mass were significantly decreased in e-cig exposed compared to sham-control (2.61 ± 0.19 g vs. 3.37 ± 0.09 g and 0.62 ± 0.03 g vs. 0.70 ± 0.02 g, respectively). Placental xanthine oxidase (XO) activity was significantly increased in e-cig exposed compared to sham-control (5.29 ± 0.27 µU/mL vs. 4.28 ± 0.36 µU/mL). Circulating prolactin (PRL) levels of e-cig exposed dams were significantly decreased compared to sham-control (2.40 ± 0.06 ng/mL of plasma vs. 3.83 ± 0.64 ng/mL of plasma). Maternal e-cig inhalation exposure during gestation negatively impacted fetal growth, increased placental XO activity, and decreased circulating PRL levels. These data demonstrate two potential mechanisms that could lead to the observed reduction in fetal growth following maternal exposure: potential redox imbalance within the placenta and/or hormonal imbalance directly affects fetal growth and potentially influences growth later in life.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renin-Angiotensin System Role in Cardiovascular Effects of Plasticizers: A Systematic Review.","authors":"Guilherme Dos Santos Reis, Luiza Mazzali Ferraz, Maria Eduarda Lima da Silva, Luiza da França Losito, Gabriel Ximenes de Oliveira, Antonio Claudio Lucas da Nóbrega, D 'Angelo Carlo Magliano, Eliete Dalla Corte Frantz, Beatriz Alexandre-Santos","doi":"10.1007/s12012-025-10016-4","DOIUrl":"https://doi.org/10.1007/s12012-025-10016-4","url":null,"abstract":"<p><p>Plasticizers, particularly bisphenols and phthalates, are prevalent additives in plastic products that enhance durability, shape, and flexibility. However, bisphenols and phthalates have been associated with adverse health effects. Recent studies linked these plasticizers to cardiovascular diseases, implicating the Renin-Angiotensin System (RAS) as a potential mediator of these effects. This review explores the relationship between plasticizer exposure and RAS modulation, focusing on cardiovascular outcomes. A systematic search was conducted in PubMed up to November 2024 according to the PRISMA guideline. The words used in this research were bisphenol, phthalates, angiotensin-converting enzyme, angiotensin II type 1 receptor, angiotensin, angiotensinogen, renin-angiotensin system, heart, cardio* (cardiovascular terms), hypertension, and blood pressure to find all relevant articles published. Thirty-one studies were screened based on inclusion and exclusion criteria, and thirteen articles were included in this systematic review. In different experimental models, several cardiovascular effects were associated with exposure to different doses of Bisphenol A (BPA) and phthalates due to the overactivation of the classical axis of the RAS. BPA exposure led to hypertension, vascular cell proliferation, and oxidative stress, and aggravated hypertensive and malnourishment conditions. In animal models, phthalates increased blood pressure, vascular thickening, and cardiac hypertrophy. These effects were partially reduced by ACE inhibition, highlighting the critical role of the RAS in plasticizer-induced cardiovascular outcomes (hypertension, smooth muscle cell proliferation, cardiac hypertrophy and fibrosis, and cardiovascular inflammation). The role of the counterregulatory axis of the RAS and the effects of emerging plasticizer analogs on cardiovascular health should be addressed by future investigations.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Not 'Inactive' After All: Cardiotoxic Mechanisms of Catecholamine Metabolism by Monoamine Oxidase.","authors":"Rachel M Crawford, Ethan J Anderson","doi":"10.1007/s12012-025-10021-7","DOIUrl":"https://doi.org/10.1007/s12012-025-10021-7","url":null,"abstract":"<p><p>Monoamine oxidase (MAO) helps regulate catecholaminergic signaling via metabolism of neurotransmitters epinephrine, norepinephrine, and dopamine-in turn producing the metabolites hydrogen peroxide (H₂O₂), ammonia (NH₄⁺), and corresponding catecholaldehydes. While MAO has been a key facet of neuroscience and mood disorder research for > 60 years, MAO-generated metabolites have been largely overlooked until recently when reports have begun to illustrate the reactivity of these metabolites and their pathogenic contributions to disease (e.g., inflammation, fibrosis, cell death). These findings have extended MAO's biological relevance beyond the brain and, most notably, to the heart, where a large and growing body of literature clearly indicates a pathophysiologic role for MAO-mediated catecholamine metabolism in heart disease. Herein, we discuss the evidence connecting MAO to various cardiac injuries and disorders, as well as describe the known cardiotoxicity associated with MAO's reactive metabolites, specifically in connection to cardiac pathophysiology. Potential therapeutic strategies for targeting MAO and its metabolites to prevent and treat heart disease are also discussed, and important knowledge gaps highlighted.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of COVID-19 on Graft Vasculopathy and Postoperative Thromboembolism in CABG Patients: A Prospective Controlled Study.","authors":"İlknur Şahin, Şebnem Batur, Ahmet Üstündağ, Berk Arapi, Çiğdem Tel Üstünışık, Deniz Göksedef, Suat Nail Ömeroğlu, Gökhan İpek, Ozan Onur Balkanay","doi":"10.1007/s12012-025-10017-3","DOIUrl":"https://doi.org/10.1007/s12012-025-10017-3","url":null,"abstract":"<p><p>It is known that COVID-19 patients may experience endothelial cell inflammation, apoptosis, dysfunction, and systemic coagulation disorders. In CABG operations, graft patency plays a crucial role in survival and morbidity. Thrombosis and endothelial cell inflammation in grafts can pose challenges for CABG candidates with a history of COVID-19. This study aimed to evaluate the vasculitic effects of a history of COVID-19 among CABG patients. A total of 94 consecutive patients, including 34 with a history of COVID-19 and 60 without, who were scheduled for CABG at our clinic, were included in the study after informed consent was obtained. Patients with a history of COVID-19 underwent surgery at least 4 weeks after the recovery of infection. Thromboembolic events were monitored throughout the hospital stay, and vascular grafts obtained during surgery were pathologically evaluated for signs of vasculitis and inflammation. All COVID-19 (n = 34) cases were mild. Statistical analysis revealed no significant difference between the groups regarding vein thrombosis/thrombophlebitis (p = 0.626). Additionally, pathological evaluation showed no signs of vasculitis or inflammation. There were also no significant differences in postoperative mortality and morbidity between the two groups (p > 0.05). Based on our findings, undergoing CABG surgery after a four-week recovery period appears to be safe for patients with a history of mild COVID-19, at least in terms of early postoperative vascular outcomes.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}