Pub Date : 2024-05-28DOI: 10.1016/j.carpath.2024.107663
Eleonora Nardi , Vincenzo Arena
Cardiac myxoma are the most common primary tumor of the heart in adults. In approximately 2-5%, glandular differentiation occurs within these tumors. In the presence of glandular features attention must be taken to exclude and prevent a misdiagnosis of cardiac metastases of adenocarcinoma. Nevertheless, the localization in the left atrium, the solitary disposition of the cardiac mass, the histological features and the immunohistochemistry performed, argued against the possibility of a metastatic nature of the tumor.
We report the case of an 80-year-old woman, with a prior medical history of breast cancer, that underwent surgery for a cardiac myxoma that histologically showed glandular features.
Herein, we highlight the importance of a careful diagnosis of this entity, as it can be easily confused for a metastasis, especially in patients with a history of malignancy.
{"title":"Glandular cardiac myxoma with intraepithelial ductal neoplasia features: Report of the first case","authors":"Eleonora Nardi , Vincenzo Arena","doi":"10.1016/j.carpath.2024.107663","DOIUrl":"10.1016/j.carpath.2024.107663","url":null,"abstract":"<div><p>Cardiac myxoma are the most common primary tumor of the heart in adults. In approximately 2-5%, glandular differentiation occurs within these tumors. In the presence of glandular features attention must be taken to exclude and prevent a misdiagnosis of cardiac metastases of adenocarcinoma. Nevertheless, the localization in the left atrium, the solitary disposition of the cardiac mass, the histological features and the immunohistochemistry performed, argued against the possibility of a metastatic nature of the tumor.</p><p>We report the case of an 80-year-old woman, with a prior medical history of breast cancer, that underwent surgery for a cardiac myxoma that histologically showed glandular features.</p><p>Herein, we highlight the importance of a careful diagnosis of this entity, as it can be easily confused for a metastasis, especially in patients with a history of malignancy.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107663"},"PeriodicalIF":3.7,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1054880724000590/pdfft?md5=4cc1c06346addedf307cd9f7064983d7&pid=1-s2.0-S1054880724000590-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-25DOI: 10.1016/j.carpath.2024.107661
Bryan G. Pearson , David H. Walker , Alfred S. Lea , Wissam Khalife , Karen K. Kislingbury , Scott D. Lick , Paul J. Boor
The epidemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has had a significant global impact, especially on immunosuppressed populations such as heart transplant recipients. While SARS-CoV-2 initially infects the respiratory system, cardiovascular complications induced by coronavirus disease 2019 (COVID-19) include cardiac arrest, myocardial infarction, heart failure, myocarditis, arrhythmia, acute myocyte injury, thrombotic events, and cardiogenic shock. Here, we present a case of a 45-year-old African American male who tested positive for COVID-19 infection six months after receiving a heart transplant. The patient was asymptomatic initially, but two weeks later he developed dyspnea, early satiety, and abdominal bloating. The patient was admitted to the hospital for acute renal failure and subsequently diagnosed with moderate acute T cell-mediated allograft rejection (Grade 2R) by endomyocardial biopsy. Three months after testing positive for COVID-19, the patient suffered a sudden cardiac death. At autopsy, the epicardium was diffusely edematous and showed vascular congestion. The coronary arteries showed a striking concentric narrowing of lumens and diffusely thickened arterial walls of all major extramural arteries deemed consistent with a rapidly progressive form of cardiac allograft vasculopathy (CAV). SARS-CoV-2 nucleocapsid protein was localized by immunohistochemistry (IHC) in endothelial cells of venules and capillaries within the epicardium. Our localization of SARS-CoV-2 in coronary vessel endothelial cells by IHC suggests that endothelial cell infection, endotheliitis, and immune-related inflammation may be a primary mechanism of vascular injury. The present case represents an early onset rapidly progressive form of CAV. This case may be the first case of post-transplant arteriopathy occurring in such a short time that includes corresponding autopsy, surgical pathology, and IHC data.
{"title":"Early, rapidly progressive vasculopathy in a transplanted heart: A possible complication of COVID-19","authors":"Bryan G. Pearson , David H. Walker , Alfred S. Lea , Wissam Khalife , Karen K. Kislingbury , Scott D. Lick , Paul J. Boor","doi":"10.1016/j.carpath.2024.107661","DOIUrl":"10.1016/j.carpath.2024.107661","url":null,"abstract":"<div><p>The epidemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has had a significant global impact, especially on immunosuppressed populations such as heart transplant recipients. While SARS-CoV-2 initially infects the respiratory system, cardiovascular complications induced by coronavirus disease 2019 (COVID-19) include cardiac arrest, myocardial infarction, heart failure, myocarditis, arrhythmia, acute myocyte injury, thrombotic events, and cardiogenic shock. Here, we present a case of a 45-year-old African American male who tested positive for COVID-19 infection six months after receiving a heart transplant. The patient was asymptomatic initially, but two weeks later he developed dyspnea, early satiety, and abdominal bloating. The patient was admitted to the hospital for acute renal failure and subsequently diagnosed with moderate acute T cell-mediated allograft rejection (Grade 2R) by endomyocardial biopsy. Three months after testing positive for COVID-19, the patient suffered a sudden cardiac death. At autopsy, the epicardium was diffusely edematous and showed vascular congestion. The coronary arteries showed a striking concentric narrowing of lumens and diffusely thickened arterial walls of all major extramural arteries deemed consistent with a rapidly progressive form of cardiac allograft vasculopathy (CAV). SARS-CoV-2 nucleocapsid protein was localized by immunohistochemistry (IHC) in endothelial cells of venules and capillaries within the epicardium. Our localization of SARS-CoV-2 in coronary vessel endothelial cells by IHC suggests that endothelial cell infection, endotheliitis, and immune-related inflammation may be a primary mechanism of vascular injury. The present case represents an early onset rapidly progressive form of CAV. This case may be the first case of post-transplant arteriopathy occurring in such a short time that includes corresponding autopsy, surgical pathology, and IHC data.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107661"},"PeriodicalIF":3.7,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1054880724000577/pdfft?md5=4c05cd0287d9bbfade0fdd50c91b742f&pid=1-s2.0-S1054880724000577-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141157819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-21DOI: 10.1016/j.carpath.2024.107655
Kader Yılar , Buse Naz Çandır , Ceyhun Küçük , Baha Berk Arpak , Kemal Özdemir , Aysin Kale , Osman Coskun , Özcan Gayretli
Objectives
Morphometric information of the structures within the borders of the aortic root is a guide for surgical interventions. It is essential to determine the effects of aortic calcification and atheroma plaque findings on the structures of this region. This study aims to establish the normal values of aortic root structures and to investigate the impact of pathologic findings in order to guide diagnosis and treatment in the clinic.
Methods
The aortic root structures were morphometrically analyzed in fresh hearts of 110 patients (89 males, 21 females) brought to the forensic medicine institution. The distances between the bases of the aortic sinuses, their widths and heights, and the lengths of the commissures were measured to differentiate between pathologic and non-pathologic aortic classes. Parameters were compared according to gender, age, body mass index, and body surface area.
Results
The mean age was 44.71 ± 15.57 years in 21 female patients and 53.66 ± 15.67 years in 89 male patients. The results of the pathologic aorta group with calcification and atheroma plaque findings were higher than the non-pathologic aorta group in all parameters (P < .05).
Conclusions
Calcification and the presence of atheroma plaque in the aorta increase the size of the structures at the aortic root. Gender, age, body mass index, and body surface area are among the criteria that will cause changes in the structures of this region. These results will help surgeons to know the normal values of aortic root structures and to consider the effects of pathologic findings in aortic valve repair operations.
{"title":"Calcification and atheroma plaques: is there any impact on the anatomical features of the aortic root and its elements?","authors":"Kader Yılar , Buse Naz Çandır , Ceyhun Küçük , Baha Berk Arpak , Kemal Özdemir , Aysin Kale , Osman Coskun , Özcan Gayretli","doi":"10.1016/j.carpath.2024.107655","DOIUrl":"10.1016/j.carpath.2024.107655","url":null,"abstract":"<div><h3>Objectives</h3><p>Morphometric information of the structures within the borders of the aortic root is a guide for surgical interventions. It is essential to determine the effects of aortic calcification and atheroma plaque findings on the structures of this region. This study aims to establish the normal values of aortic root structures and to investigate the impact of pathologic findings in order to guide diagnosis and treatment in the clinic.</p></div><div><h3>Methods</h3><p>The aortic root structures were morphometrically analyzed in fresh hearts of 110 patients (89 males, 21 females) brought to the forensic medicine institution. The distances between the bases of the aortic sinuses, their widths and heights, and the lengths of the commissures were measured to differentiate between pathologic and non-pathologic aortic classes. Parameters were compared according to gender, age, body mass index, and body surface area.</p></div><div><h3>Results</h3><p>The mean age was 44.71 ± 15.57 years in 21 female patients and 53.66 ± 15.67 years in 89 male patients. The results of the pathologic aorta group with calcification and atheroma plaque findings were higher than the non-pathologic aorta group in all parameters (<em>P</em> < .05).</p></div><div><h3>Conclusions</h3><p>Calcification and the presence of atheroma plaque in the aorta increase the size of the structures at the aortic root. Gender, age, body mass index, and body surface area are among the criteria that will cause changes in the structures of this region. These results will help surgeons to know the normal values of aortic root structures and to consider the effects of pathologic findings in aortic valve repair operations.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107655"},"PeriodicalIF":2.3,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-14DOI: 10.1016/j.carpath.2024.107652
Kasper Favere , Manon Van Hecke , Sander Eens , Matthias Bosman , Kim Stobbelaar , An Hotterbeekx , Samir Kumar-Singh , Peter L. Delputte , Erik Fransen , Johan De Sutter , Pieter-Jan Guns , Tania Roskams , Hein Heidbuchel
<div><h3>Background and aims</h3><p>Viral infections are the leading cause of myocarditis. Besides acute cardiac complications, late-stage sequelae such as myocardial fibrosis may develop, importantly impacting the prognosis. Coxsackievirus B3 (CVB)-induced myocarditis in mice is the most commonly used translational model to study viral myocarditis and has provided the majority of our current understanding of the disease pathophysiology. Nevertheless, the late stages of disease, encompassing fibrogenesis and arrhythmogenesis, have been underappreciated in viral myocarditis research to date. The present study investigated the natural history of CVB-induced myocarditis in C57BL/6J mice, expanding the focus beyond the acute phase of disease. In addition, we studied the impact of sex and inoculation dose on the disease course.</p></div><div><h3>Methods and results</h3><p>C57BL/6J mice (12 weeks old; n=154) received a single intraperitoneal injection with CVB to induce viral myocarditis, or vehicle (PBS) as control. Male mice (n=92) were injected with 5 × 10<sup>5</sup> (regular dose) (RD) or 5 × 10<sup>6</sup> (high dose) (HD) plaque-forming units of CVB, whereas female mice received the RD only. Animals were sacrificed 1, 2, 4, 8, and 11 weeks after CVB or PBS injection. Virally inoculated mice developed viral disease with a temporary decline in general condition and weight loss, which was less pronounced in female animals (<em>P</em><.001). In male CVB mice, premature mortality occurred between days 8 and 23 after inoculation (RD: 21%, HD: 20%), whereas all female animals survived. Over the course of disease, cardiac inflammation progressively subsided, with faster resolution in female mice. There were no substantial group differences in the composition of the inflammatory cell infiltrates: predominance of cytotoxic T cells at day 7 and 14, and a switch from arginase1-reactive macrophages to iNOS-reactive macrophages from day 7 to 14 were the main findings. There was concomitant development and maturation of different patterns of myocardial fibrosis, with enhanced fibrogenesis in male mice. Virus was almost completely cleared from the heart by day 14. Serum biomarkers of cardiac damage and cardiac expression of remodeling genes were temporarily elevated during the acute phase of disease. Cardiac CTGF gene upregulation was less prolonged in female CVB animals. <em>In vivo</em> electrophysiology studies at weeks 8 and 11 demonstrated that under baseline conditions (<em>i.e.</em> in the absence of proarrhythmogenic drugs), ventricular arrhythmias could only be induced in CVB animals. The cumulative arrhythmia burden throughout the entire stimulation protocol was not significantly different between CVB and control groups.</p></div><div><h3>Conclusion</h3><p>CVB inoculation in C57BL/6J mice represents a model of acute self-limiting viral myocarditis, with progression to different patterns of myocardial fibrosis. Sex, but not inoculation dose, seems t
{"title":"The natural history of CVB3 myocarditis in C57BL/6J mice: an extended in-depth characterization","authors":"Kasper Favere , Manon Van Hecke , Sander Eens , Matthias Bosman , Kim Stobbelaar , An Hotterbeekx , Samir Kumar-Singh , Peter L. Delputte , Erik Fransen , Johan De Sutter , Pieter-Jan Guns , Tania Roskams , Hein Heidbuchel","doi":"10.1016/j.carpath.2024.107652","DOIUrl":"10.1016/j.carpath.2024.107652","url":null,"abstract":"<div><h3>Background and aims</h3><p>Viral infections are the leading cause of myocarditis. Besides acute cardiac complications, late-stage sequelae such as myocardial fibrosis may develop, importantly impacting the prognosis. Coxsackievirus B3 (CVB)-induced myocarditis in mice is the most commonly used translational model to study viral myocarditis and has provided the majority of our current understanding of the disease pathophysiology. Nevertheless, the late stages of disease, encompassing fibrogenesis and arrhythmogenesis, have been underappreciated in viral myocarditis research to date. The present study investigated the natural history of CVB-induced myocarditis in C57BL/6J mice, expanding the focus beyond the acute phase of disease. In addition, we studied the impact of sex and inoculation dose on the disease course.</p></div><div><h3>Methods and results</h3><p>C57BL/6J mice (12 weeks old; n=154) received a single intraperitoneal injection with CVB to induce viral myocarditis, or vehicle (PBS) as control. Male mice (n=92) were injected with 5 × 10<sup>5</sup> (regular dose) (RD) or 5 × 10<sup>6</sup> (high dose) (HD) plaque-forming units of CVB, whereas female mice received the RD only. Animals were sacrificed 1, 2, 4, 8, and 11 weeks after CVB or PBS injection. Virally inoculated mice developed viral disease with a temporary decline in general condition and weight loss, which was less pronounced in female animals (<em>P</em><.001). In male CVB mice, premature mortality occurred between days 8 and 23 after inoculation (RD: 21%, HD: 20%), whereas all female animals survived. Over the course of disease, cardiac inflammation progressively subsided, with faster resolution in female mice. There were no substantial group differences in the composition of the inflammatory cell infiltrates: predominance of cytotoxic T cells at day 7 and 14, and a switch from arginase1-reactive macrophages to iNOS-reactive macrophages from day 7 to 14 were the main findings. There was concomitant development and maturation of different patterns of myocardial fibrosis, with enhanced fibrogenesis in male mice. Virus was almost completely cleared from the heart by day 14. Serum biomarkers of cardiac damage and cardiac expression of remodeling genes were temporarily elevated during the acute phase of disease. Cardiac CTGF gene upregulation was less prolonged in female CVB animals. <em>In vivo</em> electrophysiology studies at weeks 8 and 11 demonstrated that under baseline conditions (<em>i.e.</em> in the absence of proarrhythmogenic drugs), ventricular arrhythmias could only be induced in CVB animals. The cumulative arrhythmia burden throughout the entire stimulation protocol was not significantly different between CVB and control groups.</p></div><div><h3>Conclusion</h3><p>CVB inoculation in C57BL/6J mice represents a model of acute self-limiting viral myocarditis, with progression to different patterns of myocardial fibrosis. Sex, but not inoculation dose, seems t","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107652"},"PeriodicalIF":2.3,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1054880724000486/pdfft?md5=9abb2fe6eb6fe235fd9c688088a30ead&pid=1-s2.0-S1054880724000486-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140944094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-11DOI: 10.1016/j.carpath.2024.107653
José Edson Caetano-da-Silva , Elda Gonçalves-Santos , Elisa L.B.C. Domingues , Ivo S. Caldas , Graziela D.A. Lima , Lívia F. Diniz , Reggiani V. Gonçalves , Rômulo D. Novaes
By uncoupling oxidative phosphorylation, 2,4-dinitrophenol (DNP) attenuates reactive oxygen species (ROS) biosynthesis, which are known to aggravate infectious myocarditis in Chagas disease. Thus, the impact of DNP-based chemotherapy on Trypanosoma cruzi-induced acute myocarditis was investigated. C56BL/6 mice uninfected and infected untreated and treated daily with 100 mg/kg benznidazole (Bz, reference drug), 5 and 10 mg/kg DNP by gavage for 11 days after confirmation of T. cruzi infection were investigated. Twenty-four hours after the last treatment, the animals were euthanized and the heart was collected for microstructural, immunological and biochemical analyses. T. cruzi inoculation induced systemic inflammation (e.g., cytokines and anti-T. cruzi IgG upregulation), cardiac infection (T. cruzi DNA), oxidative stress, inflammatory infiltrate and microstructural myocardial damage in untreated mice. DNP treatment aggravated heart infection and microstructural damage, which were markedly attenuated by Bz. DNP (10 mg/kg) was also effective in attenuating ROS (total ROS, H2O2, and O2−), nitric oxide (NO), lipid (malondialdehyde - MDA) and protein (protein carbonyl - PCn) oxidation, TNF, IFN-γ, IL-10, and MCP-1/CCL2, anti-T. cruzi IgG, cardiac troponin I levels, as well as inflammatory infiltrate and cardiac damage in T. cruzi-infected mice. Our findings indicate that DNP aggravated heart infection and microstructural cardiomyocytes damage in infected mice. These responses were related to the antioxidant and anti-inflammatory properties of DNP, which favors infection by weakening the pro-oxidant and pro-inflammatory protective mechanisms of the infected host. Conversely, Bz-induced cardioprotective effects combined effective anti-inflammatory and antiparasitic responses, which protect against heart infection, oxidative stress, and microstructural damage in Chagas disease.
2,4-二硝基苯酚(DNP)通过解偶联氧化磷酸化,可抑制活性氧(ROS)的生物合成,而众所周知,活性氧会加重南美锥虫病感染性心肌炎的病情。因此,我们研究了基于 DNP 的化疗对克鲁兹锥虫诱发的急性心肌炎的影响。研究人员对未感染和感染的 C56BL/6 小鼠进行了调查,这些小鼠在确认感染 T. cruzi 后,每天灌胃 100 毫克/千克苯并咪唑(Bz,参考药物)、5 毫克/千克和 10 毫克/千克 DNP,连续 11 天。最后一次治疗 24 小时后,动物被安乐死,收集心脏进行显微结构、免疫学和生化分析。在未经处理的小鼠中,接种 T. cruzi 会诱发全身炎症(如细胞因子和抗 T. cruzi IgG 上调)、心脏感染(T. cruzi DNA)、氧化应激、炎症浸润和心肌微结构损伤。DNP 处理会加重心脏感染和微结构损伤,而 Bz 则会明显减轻这些损伤。DNP(10 毫克/千克)还能有效减轻 ROS(总 ROS、H2O2 和 O2-)、一氧化氮(NO)、脂质(丙二醛 - MDA)和蛋白质(蛋白质羰基 - PCn)氧化、TNF、IFN-γ、IL-10 和 MCP-1/CCL2、抗 T. cruzi IgG、心肌肌钙蛋白 I 水平,以及 T. cruzi 感染小鼠的炎症浸润和心脏损伤。我们的研究结果表明,DNP 会加重感染小鼠的心脏感染和心肌细胞微结构损伤。这些反应与 DNP 的抗氧化和抗炎特性有关,DNP 会削弱感染宿主的促氧化和促炎症保护机制,从而有利于感染。相反,Bz诱导的心脏保护作用结合了有效的抗炎和抗寄生虫反应,可防止恰加斯病的心脏感染、氧化应激和微结构损伤。
{"title":"The mitochondrial uncoupler 2,4-dinitrophenol modulates inflammatory and oxidative responses in Trypanosoma cruzi-induced acute myocarditis in mice","authors":"José Edson Caetano-da-Silva , Elda Gonçalves-Santos , Elisa L.B.C. Domingues , Ivo S. Caldas , Graziela D.A. Lima , Lívia F. Diniz , Reggiani V. Gonçalves , Rômulo D. Novaes","doi":"10.1016/j.carpath.2024.107653","DOIUrl":"10.1016/j.carpath.2024.107653","url":null,"abstract":"<div><p>By uncoupling oxidative phosphorylation, 2,4-dinitrophenol (DNP) attenuates reactive oxygen species (ROS) biosynthesis, which are known to aggravate infectious myocarditis in Chagas disease. Thus, the impact of DNP-based chemotherapy on <em>Trypanosoma cruzi</em>-induced acute myocarditis was investigated. C56BL/6 mice uninfected and infected untreated and treated daily with 100 mg/kg benznidazole (Bz, reference drug), 5 and 10 mg/kg DNP by gavage for 11 days after confirmation of <em>T. cruzi</em> infection were investigated. Twenty-four hours after the last treatment, the animals were euthanized and the heart was collected for microstructural, immunological and biochemical analyses. <em>T. cruzi</em> inoculation induced systemic inflammation (e.g., cytokines and anti-<em>T. cruzi</em> IgG upregulation), cardiac infection (<em>T. cruzi</em> DNA), oxidative stress, inflammatory infiltrate and microstructural myocardial damage in untreated mice. DNP treatment aggravated heart infection and microstructural damage, which were markedly attenuated by Bz. DNP (10 mg/kg) was also effective in attenuating ROS (total ROS, H<sub>2</sub>O<sub>2</sub>, and O<sub>2</sub><sup>−</sup>), nitric oxide (NO), lipid (malondialdehyde - MDA) and protein (protein carbonyl - PCn) oxidation, TNF, IFN-γ, IL-10, and MCP-1/CCL2, anti-<em>T. cruzi</em> IgG, cardiac troponin I levels, as well as inflammatory infiltrate and cardiac damage in <em>T. cruzi-</em>infected mice. Our findings indicate that DNP aggravated heart infection and microstructural cardiomyocytes damage in infected mice. These responses were related to the antioxidant and anti-inflammatory properties of DNP, which favors infection by weakening the pro-oxidant and pro-inflammatory protective mechanisms of the infected host. Conversely, Bz-induced cardioprotective effects combined effective anti-inflammatory and antiparasitic responses, which protect against heart infection, oxidative stress, and microstructural damage in Chagas disease.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107653"},"PeriodicalIF":3.7,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140915908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-03DOI: 10.1016/j.carpath.2024.107649
Angela Pucci , Martina Rossetti , Chiara Lenzi , Maximilian L Buja
Aortic diseases require a multidisciplinary management for diagnosis, treatment and follow-up with better outcomes in referral centers using a team-based approach. The setting up of a multi-disciplinary aortic team for the discussion of complex cases has been already proposed; it is also supported by the ACC/AHA. Surgeons and radiologists, more or less other physicians such as cardiologists, geneticists, rheumatologists/internal medicine specialists and pathologists are involved into such a team. The role of the cardiovascular pathologist is to examine the aortic specimens, to diagnose and classify the aortic lesions. Herein, the role of the pathologist in the aortic team is discussed and the pathobiology of aortic diseases is reviewed for reference by pathologists. The aortic specimens are mainly obtained from emergency or elective surgical procedures on the thoracic aorta, less frequently from organ/tissue (including cardiac or heart valve) donors, post-mortem procedures or abdominal aortic surgery. In the last decade, together with the progress of medical sciences, the histological definitions and classifications of the aortic pathology are undergoing thorough revisions that are addressed to an etiopathogenetic approach because of possible clinico-pathological correlations, therapeutic and prognostic impact. Pathologists may also have an important role in research and teaching. Therefore, histological analyses of the aortic specimens require adequate sample processing and pathologist expertise because histology contributes to definite diagnosis, correct management of patients and even (in genetic diseases) families, but also to research in the challenging field of aortopathies.
{"title":"The cardiovascular pathologist in the aortic team","authors":"Angela Pucci , Martina Rossetti , Chiara Lenzi , Maximilian L Buja","doi":"10.1016/j.carpath.2024.107649","DOIUrl":"10.1016/j.carpath.2024.107649","url":null,"abstract":"<div><p>Aortic diseases require a multidisciplinary management for diagnosis, treatment and follow-up with better outcomes in referral centers using a team-based approach. The setting up of a multi-disciplinary aortic team for the discussion of complex cases has been already proposed; it is also supported by the ACC/AHA. Surgeons and radiologists, more or less other physicians such as cardiologists, geneticists, rheumatologists/internal medicine specialists and pathologists are involved into such a team. The role of the cardiovascular pathologist is to examine the aortic specimens, to diagnose and classify the aortic lesions. Herein, the role of the pathologist in the aortic team is discussed and the pathobiology of aortic diseases is reviewed for reference by pathologists. The aortic specimens are mainly obtained from emergency or elective surgical procedures on the thoracic aorta, less frequently from organ/tissue (including cardiac or heart valve) donors, <em>post-mortem</em> procedures or abdominal aortic surgery. In the last decade, together with the progress of medical sciences, the histological definitions and classifications of the aortic pathology are undergoing thorough revisions that are addressed to an etiopathogenetic approach because of possible clinico-pathological correlations, therapeutic and prognostic impact. Pathologists may also have an important role in research and teaching. Therefore, histological analyses of the aortic specimens require adequate sample processing and pathologist expertise because histology contributes to definite diagnosis, correct management of patients and even (in genetic diseases) families, but also to research in the challenging field of aortopathies.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"72 ","pages":"Article 107649"},"PeriodicalIF":3.7,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140859840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}