Cardiovascular Pathology最新文献

{"title":"Standardized Diagnosis of Lymphocytic Myocarditis at Autopsy: Application of the Seaport Criteria.","authors":"Graziano Domenico Luigi Crudele, Stefania Rizzo, Elisa Carturan, Cristina Basso, Monica De Gaspari","doi":"10.1016/j.carpath.2026.107869","DOIUrl":"https://doi.org/10.1016/j.carpath.2026.107869","url":null,"abstract":"<p><strong>Background: </strong>The histological diagnosis of lymphocytic myocarditis at autopsy is challenged by limited reproducibility and the lack of standardized criteria applicable to non-biopsy specimens. This study aimed to assess the feasibility and diagnostic performance of the new Seaport criteria for autopsy in a heterogeneous cohort of clinical autopsies.</p><p><strong>Methods: </strong>An autopsy cohort of 50 consecutive cases was retrospectively revaluated, including 10 sudden death cases originally diagnosed as lymphocytic myocarditis and 40 controls (ischemic heart disease, brain diseases, liver diseases, and metastatic neoplasms). Each case was reclassified according to Seaport criteria as myocarditis (focal, multifocal, or diffuse), lymphocytic infiltrate of uncertain significance (LIUS), or no inflammation. Immunohistochemistry (CD3, CD68, C4d) and molecular testing for viral genome were carried out in myocarditis/LIUS cases.</p><p><strong>Results: </strong>By applying the Seaport criteria for autopsy, active lymphocytic myocarditis was confirmed in 9 of 10 originally diagnosed cases, either focal (33%) or multifocal (67%) and never diffuse; one case was reclassified as LIUS. Three additional cases among controls showed LIUS, yielding an overall LIUS prevalence of 8% in the entire series. A subepicardial confluent topography was observed in four myocarditis cases. Temporal assessment revealed subacute forms in 55.6% and acute in 44.4%. Immunohistochemistry confirmed the lymphocytic type, and viral genome was identified in 3/9 myocarditis cases.</p><p><strong>Conclusions: </strong>The Seaport criteria are a useful tool in the autopsy setting, supporting a standardized approach to the diagnosis of lymphocytic myocarditis. Refinement of these criteria including topographic distribution of inflammation is warranted. The clinical significance of LIUS remains to be assessed in larger series with clinicopathological correlations.</p>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":" ","pages":"107869"},"PeriodicalIF":2.0,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223380","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":"Bicuspid Aortic Valve with Giant Non-Coronary Sinus Aneurysm Compressing the Sinoatrial Node Causing Arrhythmia and Coarctation of the Aorta: A Case on Clinical Decision-Making and Surgical Challenges.","authors":"Sida Liu, Zhaoyu Zhang, Kai Yang, Weiqiang Chen, Wenfeng Cao, Lixing Wang, Shuqiang Dong, Yu Zhang","doi":"10.1016/j.carpath.2026.107866","DOIUrl":"https://doi.org/10.1016/j.carpath.2026.107866","url":null,"abstract":"<p><strong>Background: </strong>Bicuspid aortic valve, the most common congenital valvular disease, frequently coexists with aortic pathologies. Symptomatic arrhythmias from unruptured giant aortic sinus aneurysm compressing the sinoatrial node are exceedingly rare. The coexistence of bicuspid aortic valve, arrhythmogenic sinus aneurysm, coarctation of the aorta, and right coronary artery occlusion represents an extraordinarily complex malformation with scarce documentation and controversial management strategies.</p><p><strong>Case presentation: </strong>A 67-year-old male patient presented with chest tightness and palpitations. Echocardiography and computed tomography angiography revealed Type 0 bicuspid aortic valve (two-sinus type) with giant unruptured non-coronary sinus aneurysm (52 mm × 48 mm), descending coarctation of the aorta (14 mm), post-stenotic aneurysm (42 mm), and right coronary artery occlusion. Imaging confirmed direct sinoatrial node compression. First-stage surgery comprised biological aortic valve replacement, sinus repair, and coronary artery bypass grafting. The coarctation of the aorta was managed conservatively based on borderline transcoarctation gradient and favorable clinical status.</p><p><strong>Conclusion: </strong>Direct mechanical sinoatrial node compression combined with compromised nodal arterial supply constituted the pathophysiological basis for arrhythmia. For bicuspid aortic valve with multisegmental aortic disease, individualized strategy based on anatomical characteristics, hemodynamic parameters (such as transcoarctation gradient, aortic isthmus ratio, and extremity blood pressure difference), and systemic condition is essential. Staged repair prioritizing hemodynamically threatening lesions reduces surgical trauma and spinal ischemia risk, providing clinical guidance for managing such rare complex aortic pathologies.</p>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":" ","pages":"107866"},"PeriodicalIF":2.0,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206619","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":"Atrial Cardiomyopathy Through the Pathologist's Lens: From Tissue Remodeling to Clinical Expression.","authors":"Domenico Corradi","doi":"10.1016/j.carpath.2026.107868","DOIUrl":"https://doi.org/10.1016/j.carpath.2026.107868","url":null,"abstract":"<p><p>Atrial cardiomyopathy (ACM) provides a useful framework for understanding structural, architectural, contractile, and electrophysiological disease of the atria. ACM and atrial fibrillation (AF) are closely linked but are not interchangeable: ACM favors arrhythmogenesis, whereas sustained AF can accelerate atrial injury. This review considers ACM from the pathologist's perspective, encompassing primary atrial disease and secondary remodeling associated with valvular disease and classical cardiomyopathies. The histologic spectrum includes cardiomyocyte hypertrophy and myocytolysis, interstitial and replacement fibrosis, endocardial fibroelastosis, adipose and inflammatory infiltration, vascular injury, and amyloid deposition. Structural remodeling is regionally heterogeneous, and appendage specimens may underrepresent abnormalities elsewhere in the atrium. Histologic interpretation requires attention to intrinsic regional architecture, associated lesions, previous interventions, and methods of quantification. At the molecular and cellular level, genetic susceptibility and acquired stressors converge on cardiomyocyte dysfunction, inflammation, fibroblast activation, and extracellular-matrix remodeling. Correlating these tissue changes with mapping, imaging, biomarkers, and clinical outcomes will be necessary to validate noninvasive phenotypes and identify clinically meaningful disease subsets. At present, ACM should prompt etiologic investigation and risk assessment but does not by itself constitute an indication for specific therapy.</p>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":" ","pages":"107868"},"PeriodicalIF":2.0,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206616","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":"Audit of temporal artery biopsy reporting in South Australia.","authors":"Carlee Ruediger, Kathryn Dyer, Suellen Lyne, Jem Ninan, Susan Lester, Jannatul Tuli, Aashka Mishra, David Moffat, Jessica Stanhope, Catherine L Hill","doi":"10.1016/j.carpath.2026.107856","DOIUrl":"10.1016/j.carpath.2026.107856","url":null,"abstract":"<p><strong>Background: </strong>Despite histopathology playing a central role in the diagnosis of giant cell arteritis (GCA), until recently, there was no guideline for reporting on temporal artery biopsies (TAB). The Society for Cardiovascular Pathology established such consensus guidelines in 2023. The aim of this audit was to assess the extent to which South Australian TAB reports aligned with the reporting guidelines, and whether reporting practices changed across time.</p><p><strong>Methods: </strong>All SA Pathology TAB reports from 2010, 2017 and 2024 were assessed against the reporting guidelines, which contain four main areas of reporting (diagnosis, comment, gross descriptions, and microscopic descriptions (with 7 sub-points)). If all areas and microscopic descriptions were reported, the report was classified as 'complete'. Trends were examined over time, where possible using multi-level mixed-effects models to account for the reporting pathologist, with a 5% level of significance.</p><p><strong>Results: </strong>There were 76 TAB reports in 2010, 92 in 2017 and 126 in 2024. No reports were complete in reporting with no statistically significant change over time. The only statistically significant changes over time observed were the decreased reporting of a final diagnosis (p = 0.001), and final diagnosis comment (p = 0.004).</p><p><strong>Conclusion: </strong>In South Australia, no TAB reports fully aligned with the Society for Cardiovascular Pathology reporting statement. Reporting did not improve over time, including after guideline publication. Targeted strategies are needed to standardise reporting and support better diagnostic quality and patient care.</p>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":" ","pages":"107856"},"PeriodicalIF":2.0,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825341","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":"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":"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}