Mengshi Xie, Pan Jiang, Xiyang Yang, Dili Sun, Baoling Zhu, Xiaowei Zhu, Suling Ding, Jian Gao, Xiangdong Yang, Hongyu Shi
{"title":"Astemizole Exacerbates 5-Fluorouracil-Triggered Cardiotoxicity by Enhancing Ptgs2.","authors":"Mengshi Xie, Pan Jiang, Xiyang Yang, Dili Sun, Baoling Zhu, Xiaowei Zhu, Suling Ding, Jian Gao, Xiangdong Yang, Hongyu Shi","doi":"10.1007/s12012-024-09953-3","DOIUrl":"https://doi.org/10.1007/s12012-024-09953-3","url":null,"abstract":"<p><p>5-fluorouracil (5-FU), a commonly utilized antitumor agent for the treatment of colon cancer, is linked to an increased risk of cardiovascular diseases. Antihistamines including astemizole (AST) have been reported to present cardiovascular toxicity; however, it remains unclear how 5-FU-mediated cardiotoxicity is affected by AST during the treatment of colon cancer. This study explored the role of AST in 5-FU-induced cardiotoxicity in colon cancer. 5-FU was used to induce cardiotoxicity in cardiomyocytes (HL-1 cells) and BALBc mice, creating in vitro and in vivo models of chemotherapeutic drug-induced cardiotoxicity. In the mice model, we found that the blocking of histamine signal by AST aggravated 5-FU-induced cardiac function injury and cardiac fibrosis. In HL-1 cardiomyocyte cells, the increases of apoptosis and generation of mitochondrial reactive oxygen species (mtROS) were evaluated after the combination treatment of AST and 5-FU. Proinflammatory M1-like-type macrophages were dominant in the AST and 5-FU combination group compared to control groups. The protein expression of prostaglandin-endoperoxide synthase 2 (Ptgs2) was assessed both in vitro and in vivo using Western blot analysis. Clinically, altered Ptgs2 was closely associated with adverse cardiovascular outcomes. Overall, the combination of AST and 5-FU significantly enhanced cardiotoxicity by inducing cardiomyocyte apoptosis, inflammation, and the expression of Ptgs2.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945200","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":"SUZ12-Increased NRF2 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Apoptosis, Inflammation, and Ferroptosis.","authors":"Guoyong Zhang, Zhimin Ma, Zheng Ma, Peilin Liu, Lin Zhang, Zheng Lian, Caixia Guo","doi":"10.1007/s12012-024-09950-6","DOIUrl":"https://doi.org/10.1007/s12012-024-09950-6","url":null,"abstract":"<p><p>Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury. qRT-PCR and western blot assays were used to detect the levels of mRNAs and proteins. Cardiomyocyte injury was determined by detecting the levels of lactate dehydrogenase and creatine Kinase MB (CK-MB). Cell apoptosis was investigated by flow cytometry and related markers. Levels of IL-6, IL-10, and TNF-α were measured by ELISA. Cell ferroptosis was assessed by detecting the production of reactive oxygen species (ROS), malonaldehyde (MDA), reduced glutathione/oxidized glutathione disulfide (GSH/GSSG) ratio, Fe + content, and related regulators. The interaction between NRF2 and the suppressor of zest 12 (SUZ12) was analyzed by using dual-luciferase reporter and RNA immunoprecipitation assays. AMI rat models were established for in vivo analysis. NRF2 was lowly expressed in AMI patients and H/R-induced cardiomyocytes. Forced expression of NRF2 reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis. Moreover, NRF2 overexpression improved cardiac function and injury in vivo. Mechanistically, SUZ12 bound to the promoter of NRF2 and promoted its expression. Further functional analyses showed that SUZ12 overexpression reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis, which were reversed by NRF2 silencing. SUZ12-increased NRF2 suppressed H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis in vitro and improved cardiac functions in rats with I/R injury, suggesting the potential cardioprotective effect of NRF2 in cardiac injury during AMI.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892272","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}
Muhammad Fahad Tahir, Xiaofei Wu, Yuwei Wang, Qin Liu, Xizhou An, Daochao Huang, Lijing Chen, Lanling Chen, Xiaohua Liang
{"title":"Association Between Serum Essential Metal Elements and Blood Pressure in Children: A Cohort Study.","authors":"Muhammad Fahad Tahir, Xiaofei Wu, Yuwei Wang, Qin Liu, Xizhou An, Daochao Huang, Lijing Chen, Lanling Chen, Xiaohua Liang","doi":"10.1007/s12012-024-09948-0","DOIUrl":"https://doi.org/10.1007/s12012-024-09948-0","url":null,"abstract":"<p><p>A limited number of cohort studies have explored the impact of serum essential metal elements on blood pressure (BP) or glycolipids and their regulatory mechanism in children. This study aimed to investigate the relationship between serum metal concentrations of iron (Fe), zinc (Zn), calcium (Ca), copper (Cu), and magnesium (Mg) and BP in children, and explore the potential mediating effects of glycolipid profiles. This cohort study included 1993 children (3566 BP measurements) aged 6-14 years in Chongqing, China. Serum essential metals, BP, lipid profiles, and glucose and insulin levels were measured. The relationship between serum metal levels and BP was analyzed using generalized linear and regression models, and a mediation analysis was performed to examine the potential mediating role of glycolipids. After adjusting for confounders, positive associations were found between serum Fe and Zn levels and BP parameters (all P < 0.05). A \"U\" style relationship between Cu and BP was found. Stronger associations were found in children aged ≤ 10 years, with sex-specific differences for Fe, Zn, and Cu. The relationship between elevated BP and serum Mg and Ca was not found. Our study found that triglycerides showed a significant relationship with Fe and Zn levels (P < 0.005). Moreover, triglycerides, partially mediate the effects of Zn on elevated BP. Serum Fe, Zn, and Cu concentrations were associated with BP in children, and age and sex differences were observed. Triglycerides may play a mediating role. These findings highlight the importance of maintaining an optimal serum essential metal status for cardiovascular health in children and suggest potential early prevention strategies.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846145","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":"Metagenomic Analysis of Gut Microbiome of Persistent Pulmonary Hypertension of the Newborn.","authors":"Linli Han, Chuyang Lin, Yue Lan, Yimin Hua, Jinlin Wu, Zhenxin Fan, Yifei Li","doi":"10.1007/s12012-024-09949-z","DOIUrl":"https://doi.org/10.1007/s12012-024-09949-z","url":null,"abstract":"<p><p>Persistent pulmonary hypertension of the newborn (PPHN) is one of the most common diseases in the neonatal intensive care unit which severely affects neonatal survival. Gut microbes play an increasingly important role in human health, but there are rarely reported how gut microbiota contribute to PPHN. In our study, the metagenomic sequencing of feces from 12 PPHN's neonates and 8 controls were performed to expose the relation between neonatal gut microbes and PPHN disease. Firstly, we found that the abundance of Actinobacteria, Proteobacteria, Bacteroidetes were significantly increased in PPHN compared with controls, but the Firmicutes components was reduced. And some pathogenic strains (like Vibrio metschnikovii) were significantly enriched in the PPHN compared with controls. Secondly, functional annotation of genes found that PPHN up-regulated transmembrane transport, but down-regulated ribosome and ATP binding. Lastly, microbial metabolic pathway enrichment analysis indicated that some metabolic pathway in PPHN were conflicting and contradictory, showed that an abnormally increased metabolism, disturbed protein synthesis and genomic instability in the PPHN neonate. Our results contribute to understanding the changes in the species and function of gut microbiota in PPHN, thus providing a theoretical basis for the explanation and treatment of PPHN.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827535","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":"Thiolutin Alleviates Cardiotoxic Effects of Doxorubicin by Suppressing NLRP3 Inflammasome in the Mouse Model.","authors":"Wenyuan Cai, Tingting Teng, Xiaoyan Wang, Baihong Li, Xin Gu, Yafeng Zhou","doi":"10.1007/s12012-024-09947-1","DOIUrl":"https://doi.org/10.1007/s12012-024-09947-1","url":null,"abstract":"<p><p>Doxorubicin (DOX) has a limitation in clinical oncology due to its dose-dependent cardiotoxicity. Thiolutin (THL) can undermine DOX-induced cardiomyocyte injury by inhibiting the NLRP3 inflammasome activation, yet the efficacy of THL in DOX-induced cardiotoxicity (DOXIC) needs to be validated in animal models. DOX-induced mice were treated with THL to evaluate the efficacy of THL. Relative NLRP3 mRNA levels were determined by quantitative PCR. Blood samples were collected from diffuse large B-cell lymphoma (DLBCL) patients with or without DOXIC to validate serum levels of cTnT, IL-1β, CRP, BNP, and IL-18 by enzyme-linked immunosorbent assay. Apoptosis and pyroptosis-related protein levels were analyzed by western blot. Cardiac function and histopathological changes were determined by echocardiography, HE, Masson's, and wheat germ agglutinin staining. In clinical samples, NLRP3 mRNA and/or protein levels were also markedly heightened in peripheral blood mononuclear cells and serum samples from DOXIC patients, along with higher concentrations of IL-18, cTnT, and IL-1β. Importantly, cTnT possessed a positive correlation with NLRP3 mRNA, IL-1β, and IL-18. Moreover, cTnT possessed a positive correlation with NLRP3 mRNA, IL-1β, and IL-18 levels, suggesting a potential link between DOXIC and NLRP3 inflammasome. The outcomes demonstrated that THL reduced LVEF and LVFS, as well as elevated LVESD and LVEDD in DOX-challenged mice, accompanied by elevated serum concentrations of cTnT, CRP, and BNP. In addition, THL attenuated DOX-induced myocardial hypertrophy and cardiac fibrosis in mice, in conjunction with attenuation of DOX-induced upregulation of C-caspase3, Bax, NLRP3, C-caspase-1/Pro-caspase, GSDMD-N/GSDMD, IL-1β, and IL-18 in heart or serum samples. In conclusion, our data supported that THL alleviates the cardiotoxic effects of DOX and suppresses NLRP3 inflammasome in the mouse model, suggesting that THL as a potential drug for DOXIC.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812045","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}
Lei Yang, Tong Gao, Yu Huang, Pei-He Wang, Xin-Hao Han, Jie Wu, Lei Huang, Qing-En Da, Kun-Fu Ouyang, Zhen Han, Hai Tian, Lu Sun
{"title":"Ultrasound-Targeted β-Catenin Gene Therapy Improves the Cardiac Function in Mice After Myocardial Infarction.","authors":"Lei Yang, Tong Gao, Yu Huang, Pei-He Wang, Xin-Hao Han, Jie Wu, Lei Huang, Qing-En Da, Kun-Fu Ouyang, Zhen Han, Hai Tian, Lu Sun","doi":"10.1007/s12012-024-09946-2","DOIUrl":"https://doi.org/10.1007/s12012-024-09946-2","url":null,"abstract":"<p><p>Gene therapy has received great attention as a therapeutic approach to improve cardiac function post-myocardial infarction (MI), but its limitation lies in the lack of targeting. This study explored the use of ultrasound-targeted microbubble destruction (UTMD) technique to deliver β-catenin gene to the myocardium, aiming to evaluate its efficacy in preventing cardiac dysfunction post-MI. A cationic microbubble solution containing β-catenin gene pcDNA3.1 plasmid was injected through the tail vein at a rate of 0.6 mL/h, and ultrasound beams were delivered to the heart using GE Vivid 7 Medical Ultrasound System M3s Transducer. Bioluminescence imaging was used to analyze the efficiency of UTMD gene transfection into the myocardium. β-catenin levels were detected by real-time polymerase chain reaction and western blot. Additionally, MI was induced in mice by surgical ligation of the left coronary artery, and cardiac function was evaluated using echocardiography at 14 and 28 days post-surgery. Masson's trichrome staining was employed to determine infarct size. Blood vessel density was also measured. TUNEL assay was used to measure cardiomyocyte apoptosis. Furthermore, mouse cardiac stem cells were isolated using flow cytometry, and Giemsa stain was applied to evaluate the colony adhesion. UTMD delivered the gene to the heart with high efficiency and specificity in vivo. The β-catenin expression was significantly increased in the myocardium (P < 0.01). After MI, the β-catenin group exhibited a notable improvement in the gene therapy-induced neovascularization in the border zone (P < 0.01) and the number and function of cardiac stem cells (P < 0.01), and a significant decrease in cardiomyocyte apoptosis in the heart tissue (P < 0.01). β-catenin gene pre-treated with UTMD can reduce the impact of myocardial injury and promote cardiac self-repair after MI.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799444","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}
Yue Ge, Maliha S Nash, Witold M Winnik, Maribel Bruno, William T Padgett, Rachel D Grindstaff, Mehdi S Hazari, Aimen K Farraj
{"title":"Proteomics Reveals Divergent Cardiac Inflammatory and Metabolic Responses After Inhalation of Ambient Particulate Matter With or Without Ozone.","authors":"Yue Ge, Maliha S Nash, Witold M Winnik, Maribel Bruno, William T Padgett, Rachel D Grindstaff, Mehdi S Hazari, Aimen K Farraj","doi":"10.1007/s12012-024-09931-9","DOIUrl":"10.1007/s12012-024-09931-9","url":null,"abstract":"<p><p>Inhalation of ambient particulate matter (PM) and ozone (O<sub>3</sub>) has been associated with increased cardiovascular morbidity and mortality. However, the interactive effects of PM and O<sub>3</sub> on cardiac dysfunction and disease have not been thoroughly examined, especially at a proteomic level. The purpose of this study was to identify and compare proteome changes in spontaneously hypertensive (SH) rats co-exposed to concentrated ambient particulates (CAPs) and O<sub>3</sub>, with a focus on investigating inflammatory and metabolic pathways, which are the two major ones implicated in the pathophysiology of cardiac dysfunction. For this, we measured and compared changes in expression status of 9 critical pro- and anti-inflammatory cytokines using multiplexed ELISA and 450 metabolic proteins involved in ATP production, oxidative phosphorylation, cytoskeletal organization, and stress response using two-dimensional electrophoresis (2-DE) and mass spectrometry (MS) in cardiac tissue of SH rats exposed to CAPs alone, O<sub>3</sub> alone, and CAPs + O<sub>3</sub>. Proteomic expression profiling revealed that CAPs alone, O<sub>3</sub> alone, and CAPs + O<sub>3</sub> differentially altered protein expression patterns, and utilized divergent mechanisms to affect inflammatory and metabolic pathways and responses. Ingenuity Pathway Analysis (IPA) of the proteomic data demonstrated that the metabolic protein network centered by gap junction alpha-1 protein (GJA 1) was interconnected with the inflammatory cytokine network centered by nuclear factor kappa beta (NF-kB) potentially suggesting inflammation-induced alterations in metabolic pathways, or vice versa, collectively contributing to the development of cardiac dysfunction in response to CAPs and O<sub>3</sub> exposure. These findings may enhance understanding of the pathophysiology of cardiac dysfunction induced by air pollution and provide testable hypotheses regarding mechanisms of action.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1348-1363"},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458727","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}
Hao Wu, Yan-Nan Che, Qi Lan, Yi-Xiang He, Ping Liu, Ming-Tai Chen, Li Dong, Meng-Nan Liu
{"title":"The Multifaceted Roles of Hippo-YAP in Cardiovascular Diseases.","authors":"Hao Wu, Yan-Nan Che, Qi Lan, Yi-Xiang He, Ping Liu, Ming-Tai Chen, Li Dong, Meng-Nan Liu","doi":"10.1007/s12012-024-09926-6","DOIUrl":"10.1007/s12012-024-09926-6","url":null,"abstract":"<p><p>The Hippo-yes-associated protein (YAP) signaling pathway plays a crucial role in cell proliferation, differentiation, and death. It is known to have impact on the progression and development of cardiovascular diseases (CVDs) as well as in the regeneration of cardiomyocytes (CMs). However, further research is needed to understand the molecular mechanisms by which the Hippo-YAP pathway affects the pathological processes of CVDs in order to evaluate its potential clinical applications. In this review, we have summarized the recent findings on the role of the Hippo-YAP pathway in CVDs such as myocardial infarction, heart failure, and cardiomyopathy, as well as its in CM development. This review calls attention to the potential roles of the Hippo-YAP pathway as a relevant target for the future treatment of CVDs.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1410-1427"},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371053","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}
Mohammad Mahdi Dabbaghi, Hesan Soleimani Roudi, Rozhan Safaei, Vafa Baradaran Rahimi, Mohammad Reza Fadaei, Vahid Reza Askari
{"title":"Unveiling the Mechanism of Protective Effects of Tanshinone as a New Fighter Against Cardiovascular Diseases: A Systematic Review.","authors":"Mohammad Mahdi Dabbaghi, Hesan Soleimani Roudi, Rozhan Safaei, Vafa Baradaran Rahimi, Mohammad Reza Fadaei, Vahid Reza Askari","doi":"10.1007/s12012-024-09921-x","DOIUrl":"10.1007/s12012-024-09921-x","url":null,"abstract":"<p><p>Tanshinone, a natural compound found in the roots of Salvia miltiorrhiza, has been shown to possess various pharmacological properties, including anti-inflammatory, antioxidant, and cardiovascular protective effects. This article aims to review the literature on the cardiovascular protective effects of tanshinone and its underlying mechanisms. Tanshinone has been demonstrated to improve cardiac function, reduce oxidative stress, and inhibit inflammation in various animal models of cardiovascular diseases. Additionally, it has been shown to regulate multiple signaling pathways involved in the pathogenesis of cardiovascular diseases, such as the PI<sub>3</sub>K/AKT, MAPK, and NF-κB pathways. Clinical studies have also suggested that tanshinone may have therapeutic potential for treating cardiovascular diseases. In conclusion, tanshinone has emerged as a promising natural compound with significant cardiovascular protective effects, and further research is warranted to explore its potential clinical applications.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1467-1509"},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280634","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}
Paweł Gać, Wojciech Hajdusianek, Aleksandra Żórawik, Małgorzata Poręba, Rafał Poręba
{"title":"Extracellular Volume and Fibrosis Volume of Left Ventricular Myocardium Assessed by Cardiac Magnetic Resonance in Vaccinated and Unvaccinated Patients with a History of SARS-CoV-2 Infection.","authors":"Paweł Gać, Wojciech Hajdusianek, Aleksandra Żórawik, Małgorzata Poręba, Rafał Poręba","doi":"10.1007/s12012-024-09929-3","DOIUrl":"10.1007/s12012-024-09929-3","url":null,"abstract":"<p><p>Cardiac magnetic resonance (CMR) enables the assessment of tissue characteristics of the myocardium. Changes in the extracellular volume (ECV) and fibrosis volume (FV) of the myocardium are sensitive and early pathogenetic markers and have prognostic significance. The aim of the study was to assess ECV and FV of left ventricular myocardium in T1 mapping sequence in patients with a history of SARS-CoV-2 infection, considering vaccination status against COVID-19. The study group consisted of 97 patients (52.54 ± 8.31 years, 53% women and 47% men). The participants were divided into three subgroups: A) patients with a history of symptomatic SARS-CoV-2 infection, unvaccinated against COVID-19 (n = 39), B) patients with a history of symptomatic SARS-CoV-2 infection, with a full vaccination schedule against COVID-19 (n = 22), and C) persons without a history of SARS-CoV-2 infection constituting the control subgroup (C, n = 36). All patients underwent 1.5 T cardiac magnetic resonance. In subgroup A compared to subgroups B and C, both the ECV whole myocardium and ECV segments 2, 5-6, 8, and 10-11 were statistically significantly higher. In addition, the ECV segment 16 was statistically significantly higher in subgroup A than in subgroup C. Also, the FV whole myocardium was statistically significantly higher in subgroup A in comparison to subgroups B and C. There were no significant differences in ECV and FV between subgroups B and C. In summary, unvaccinated against COVID-19 patients with a history of symptomatic SARS-CoV-2 infection have higher myocardial ECV and FV values in the T1 mapping sequence, compared to those without COVID-19 and those suffering from COVID-19, previously vaccinated with the full vaccination schedule.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1455-1466"},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11564387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}