Cardiovascular Pathology最新文献

{"title":"Digital curation of formalin-preserved heart specimens via 3D photometric scanning: A report on recent archiving techniques and optimizations","authors":"Chrystalle Katte Carreon ,&nbsp;Danielle McClary ,&nbsp;Kyle M. McClary ,&nbsp;Stephen P. Sanders","doi":"10.1016/j.carpath.2025.107803","DOIUrl":"10.1016/j.carpath.2025.107803","url":null,"abstract":"<div><h3>Background</h3><div>Archived cardiac specimens are invaluable for understanding congenital heart defects (CHDs) and acquired heart disease. However, physical deterioration and declining autopsy rates limit ongoing acquisition and use. While micro-CT scanning has been used to digitally archive wax-infiltrated specimens, most cardiac specimens in our collection are wet formalin-preserved hearts, for which micro-CT is suboptimal.</div></div><div><h3>Objectives</h3><div>This study evaluates photogrammetry as a practical, high-fidelity digital archiving technique for wet cardiac specimens.</div></div><div><h3>Methods</h3><div>Eighty-four wet cardiac specimens representing a broad spectrum of CHD and other cardiac diseases were digitized using a handheld Artec Space Spider 3D scanner. Specimens were suspended via a custom apparatus to optimize surface coverage. Scan data were processed with Artec Studio and refined in Blender to generate anatomically accurate, textured 3D models. Two experienced cardiac morphologists validated the digital reconstructions against the physical specimens.</div></div><div><h3>Results</h3><div>Photogrammetry produced high-resolution, color-accurate 3D models closely replicating anatomical details, including complex internal structures. The custom suspension device enhanced visualization, particularly of internal chambers. Challenges included scanning smaller, darker hearts and delicate valve structures, which required manual post-processing. The digital models are accessible via a cloud-based platform for research and education.</div></div><div><h3>Conclusions</h3><div>Photogrammetry is a practical and effective method for digitally archiving wet cardiac specimens, preserving valuable anatomical data, and mitigating loss due to specimen degradation. This technique facilitates broader accessibility and enhances educational and clinical applications in the study of CHDs and other cardiac diseases.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"82 ","pages":"Article 107803"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145666407","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}

{"title":"Cardiac granular cell tumor at autopsy: a case report.","authors":"Pavitra Attanayake, Stephen Cohle, Ping Zhang","doi":"10.1016/j.carpath.2026.107827","DOIUrl":"10.1016/j.carpath.2026.107827","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":" ","pages":"107827"},"PeriodicalIF":1.9,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621444","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}

{"title":"Meta-analysis of differential gene expression in idiopathic pulmonary arterial hypertension","authors":"Andy P. Huang ,&nbsp;Sarah Voskamp ,&nbsp;Ameneh A. Ebadi ,&nbsp;Jennifer L. Liedel ,&nbsp;Jennifer S. Nelson ,&nbsp;Joseph Kuruvilla","doi":"10.1016/j.carpath.2025.107805","DOIUrl":"10.1016/j.carpath.2025.107805","url":null,"abstract":"<div><h3>Background</h3><div>Idiopathic pulmonary arterial hypertension (IPAH) is a subtype of pulmonary arterial hypertension and impacts both children and adults. IPAH has overall poor survival, highlighting the importance of understanding pathogenesis. We aimed to identify differentially expressed genes in the lungs of patients with IPAH to shed light on its complex genetic background.</div></div><div><h3>Methods</h3><div>Search Tag Analyze Resource for NCBI’s Gene Expression Omnibus (STARGEO) was utilized to identify samples. Human lung samples from patients with IPAH and healthy controls were included. Meta-analysis was conducted on genes demonstrating differential expression (p&lt;0.05, experimental log ratio &gt; |0.05|). Ingenuity pathway analysis (IPA) was utilized to conduct pathway analysis.</div></div><div><h3>Results</h3><div>Top upregulated genes include HBD, HBB, ZBED1, PPFIBP1, PTPRD, and IPCEF1, which contribute to oxygen transport and utilization, cell growth, and smooth muscle migration. Top downregulated genes include BPIFB1, PROK2, NLRP12, and CAV2, which largely regulate bone morphogenic protein signaling, control cell growth and apoptosis, and regulate inflammation. Cardiac hypertrophy signaling represented the top canonical pathways associated with IPAH. Top activated upstream regulators were lipopolysaccharide and ESR1.</div></div><div><h3>Conclusion</h3><div>Changes in genes associated with cell growth, smooth muscle migration, and oxidative stress response may relate to the pathogenesis of IPAH, possibly through allowing uncontrolled cell growth and proliferation or dysregulated inflammation. Future studies should validate these findings. Identifying genes and pathways demonstrating altered expression is a preliminary step to developing targeted therapeutics.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107805"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696122","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}

{"title":"COVER 3: Editorial Board","authors":"","doi":"10.1016/S1054-8807(26)00004-9","DOIUrl":"10.1016/S1054-8807(26)00004-9","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107813"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145921112","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}

{"title":"Descriptive study of the clinical and myocardial status of a population with anatomopathological aortic valve amyloidosis","authors":"Karoline Gomes Amorim,&nbsp;Jamile Gomes Pereira de Barros,&nbsp;Guilherme de Sá Ramos Calado,&nbsp;Edenilson de Souza Teixeira,&nbsp;Hideki Zimermann Kamitani,&nbsp;Vanessa Ellen Silva Carmo,&nbsp;Pedro Pereira Tenório","doi":"10.1016/j.carpath.2025.107807","DOIUrl":"10.1016/j.carpath.2025.107807","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107807"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145741151","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}

{"title":"Transforming growth factor-beta (TGF-β) in the pathogenesis of hereditary thoracic aneurysm disorders","authors":"Wendy A. Espinoza Camejo ,&nbsp;Emily E. Bramel ,&nbsp;Elena Gallo MacFarlane","doi":"10.1016/j.carpath.2025.107790","DOIUrl":"10.1016/j.carpath.2025.107790","url":null,"abstract":"<div><div>The transforming growth factor-beta (TGF-β) signaling pathway regulates biological processes critical to embryonic development and tissue homeostasis, including cell proliferation, differentiation, adhesion and migration. Perturbations in TGF-β signaling are linked to a wide range of human diseases, including those affecting the cardiovascular system. This review summarizes decades-long evidence documenting the importance of this pathway to hereditary forms of aortic disease and presents current perspectives on its role in pathogenesis. We discuss the dual role of TGF-β signaling in aneurysm progression, and its protective and maladaptive effects on vascular smooth muscle cells (VSMCs) phenotype, extracellular matrix (ECM) composition, and other disease-relevant signaling pathways.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107790"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530565","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}

{"title":"Regional and temporal changes in early structural remodeling following myocardial infarction via semi-automatic image analysis","authors":"Catherine C. Eberman ,&nbsp;Yuming Liu ,&nbsp;Kevin W. Eliceiri ,&nbsp;Colleen M. Witzenburg","doi":"10.1016/j.carpath.2025.107801","DOIUrl":"10.1016/j.carpath.2025.107801","url":null,"abstract":"<div><div>Reperfusion therapy, the restoration of blood flow following myocardial infarction, is one of the most effective treatment strategies. Unlike early reperfusion, late reperfusion therapy (LRT) has not been linked to differences in infarct size or collagen density. To evaluate the spatial-temporal effects of LRT, we conducted multimodal imaging of histologic sections of rat myocardium following permanent coronary artery occlusion or three hours of occlusion. Semi-automatic partitioning identified the infarct core, border, and peripheral regions from label-free liquid crystal based polarized light microscopy (PolScope) images taken over 5 days of healing. Brightfield and standard polarized light microscopy images of hematoxylin-eosin or Picrosirius Red stained sections were used to determine cellular and collagen fiber densities, respectively. Even when we consider multiple definitions for the vulnerable infarct border, its size decreased faster in LRT samples. Temporal patterns in collagen density also indicated LRT led to a more rapid progression through the necrotic phase of healing (when the infarct is vulnerable to rupture) and earlier progression to the fibrotic phase of healing (when the infarct stabilizes). Notably, we also observed a broader region of provisional non-collagenous matrix in LRT samples during the necrotic phase of healing. Together these findings suggest LRT accelerates healing and potentially changes the spatial pattern of provisional matrix deposition during the period the heart is most susceptible to rupture events.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107801"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145595425","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}

{"title":"Comparative investigation of Cx3cr1-Expressing Cardiac Macrophages in Atrioventricular Nodes of Wild-Type and Catecholaminergic Polymorphic Ventricular Tachycardia Mouse Model","authors":"Arzuhan Koc Buyuker ,&nbsp;Sumeyye Ozyaman ,&nbsp;Behnaz Karadogan ,&nbsp;Aylin Nebol ,&nbsp;Ilknur Keskin ,&nbsp;Esra Cagavi","doi":"10.1016/j.carpath.2025.107799","DOIUrl":"10.1016/j.carpath.2025.107799","url":null,"abstract":"<div><div>Cardiac macrophages were recently discovered to regulate cardiomyocyte function at the atrioventricular (AV) nodes of healthy murine and human hearts. Macrophages and immune mediators have been implicated in ischemia-induced cardiac damage and arrhythmia; however, the relevance of macrophages in congenital arrhythmia pathogenesis remains unclear. Here, the wild-type (WT) mice and <em>Calsequestrin2</em> gene null mutant (<em>Casq2^-/-</em>) transgenic model of catecholaminergic polymorphic ventricular tachycardia (CPVT) were comparatively evaluated for cardiac macrophage population at the histological level. The localization and density of the chemokine receptor, Cx3cr1-expressing cardiac macrophages were investigated <em>ex vivo</em> in heart sections from WT and <em>Casq2</em>^<em>-/-</em> mice at the AV node region using immunofluorescence, Masson’s Trichrome, and Hematoxylin-Eosin staining. Cx3cr1⁺ cardiac macrophages were localized in all cardiac layers and chambers of the heart, as well as septum and valve roots. Cx3cr1⁺ macrophages were coimmunostained and confirmed for expression of CD68 as a pan-macrophage marker. Macrophages were detected in close proximity to the cTnT⁺ cardiomyocytes in the myocardium of both WT and <em>Casq2</em>^<em>-/-</em> transgenic mice. Macrophage clusters were abundantly observed in the Hcn4 immunoreactive AV node region in healthy murine hearts. Subsequent quantification of signal intensities of Cx3cr1⁺ cardiac macrophages in the AV nodes in the <em>Casq2</em>^<em>-/-</em> transgenic mice was significantly lower than in WT mice. These results demonstrated a decline in Cx3cr1⁺ cardiac macrophages in AV node regions of CPVT mouse hearts, which could imply a potential contribution to arrhythmia. Our findings could serve as a valuable source for future functional investigations of macrophages in the pathogenesis of congenital arrhythmia.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107799"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562838","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}

{"title":"Characterization of the clinical, histopathologic, and immunohistochemical features of large papillary fibroelastomas and their S100-expressing spindle cell component and its potential relationship to cardiac valvular interstitial cells","authors":"Faye Victoria C. Casimero ,&nbsp;James R. Stone","doi":"10.1016/j.carpath.2025.107800","DOIUrl":"10.1016/j.carpath.2025.107800","url":null,"abstract":"<div><div>Papillary fibroelastomas (PFEs) are uncommon, benign cardiac tumors most commonly measuring less than 1 cm and arising on cardiac valves. Large PFEs (≥1 cm), though clinically significant due to embolic potential, remain less well characterized. This study aimed to define the clinical, histopathologic, and immunohistochemical features of large PFEs, with a focus on the spindle cell component. A retrospective analysis was performed on 24 large PFEs resected between 2011 and 2024. Histologic analysis included hematoxylin and eosin staining, elastic staining, and immunohistochemistry for S100, calretinin, and CD31. The presence of a spindle cell component was defined as the presence of ≥10 non-surface spindle cells in a single 400x high-power field (HPF). S100⁺ spindle cells were quantified across 10 HPFs. Myxomatous mitral valves were also evaluated for comparison. Large PFEs were located in both cardiac chambers (n = 13) and on valves (n = 11). The median patient age was 69 years, and in all cases the tumor had been identified on imaging. Embolic events occurred in three (13%) of the cases, all from left-sided lesions. Seventeen (71%) of the large PFEs contained a spindle cell component, with significantly higher S100⁺ spindle cell density in valvular PFEs compared to chamber PFEs (median 14 vs. 1 per HPF; <em>P</em> = 0.045). In the large PFEs, CD31 was diffusely positive in surface endothelium, with variable endothelial S100 co-expression. There was only rare calretinin staining. The valvular interstitial cells in valves with myxomatous degeneration were also diffusely positive for S100. The presence of S100⁺ spindle cells in large PFEs suggests that a process similar to valvular interstitial cell activation and/or endothelial-to-mesenchymal transition may be important in PFE tumor pathogenesis.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107800"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562832","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}

{"title":"Genetic mutations, pathology, and single-nucleus transcriptomic landscape in LVHT patients reveal differential progression to heart transplantation","authors":"Yifan Wang ,&nbsp;Weiteng Wang ,&nbsp;Han Mo,&nbsp;Xiumeng Hua,&nbsp;Hao Cui,&nbsp;Xiao Chen,&nbsp;Yue Zhang,&nbsp;Shun Liu,&nbsp;Yiqi Zhao,&nbsp;Jiangping Song","doi":"10.1016/j.carpath.2025.107808","DOIUrl":"10.1016/j.carpath.2025.107808","url":null,"abstract":"<div><h3>Background</h3><div>Left ventricular hypertrabeculation/non-compaction (LVHT/LVNC) is characterized by a thinned myocardial wall, prominent trabeculations, and deep intertrabecular recesses. It presents with unique cardiac morphology and hemodynamic features but displays considerable clinical heterogeneity. The factors influencing disease progression to heart transplantation remain unclear. No studies have investigated the relationship between transcriptomic or pathological features of LVHT and progression to transplantation.</div></div><div><h3>Methods</h3><div>We enrolled 74 patients diagnosed with LVHT, among whom 63 underwent whole-exome sequencing to assess genetic variants. Explanted heart tissue was obtained from 24 patients who received heart transplantation, and single-nucleus RNA sequencing was performed on the compacted and non-compacted layers of the left ventricle in 3 LVHT patients, compared with 3 normal controls. In addition, myocardial composition, fibrosis, fat content, and the extent of non-compaction were evaluated histopathologically.</div></div><div><h3>Results</h3><div>Genetic variants were detected in 46 % of patients but were not associated with progression to heart transplantation. The compacted and non-compacted layers of LVHT hearts exhibited highly similar transcriptional profiles. Notch signaling was enriched in LVHT-related cardiomyocyte clusters. <em>MAML3</em>, a Notch coactivator, was significantly upregulated in LVHT compared with other cardiomyopathies and normal myocardium, and was associated with faster progression to transplantation. Histopathological analysis further demonstrated that both myocardial fibrosis and the anatomical distribution of non-compaction were linked to cardiac function and transplant outcomes.</div></div><div><h3>Conclusion</h3><div>LVHT is associated with distinct transcriptomic and pathological features that influence the rate of progression to heart transplantation. The Notch pathway–related molecule <em>MAML3</em> may serve as a potential marker of disease progression in LVHT.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"81 ","pages":"Article 107808"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755469","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}