Cardiovascular Pathology最新文献

{"title":"Decreased smooth muscle cells and fibrous thickening of the tunica media in peripheral pulmonary artery stenosis in Alagille syndrome","authors":"Yosuke Ogawa ,&nbsp;Amane Yamamoto ,&nbsp;Sho Yamazawa ,&nbsp;Masako Ikemura ,&nbsp;Yasutaka Hirata ,&nbsp;Ryo Inuzuka","doi":"10.1016/j.carpath.2024.107677","DOIUrl":"10.1016/j.carpath.2024.107677","url":null,"abstract":"<div><p>Alagille syndrome is caused by mutations in genes involved in NOTCH signaling, specifically <em>JAG1</em> and <em>NOTCH2</em>, and is associated with a high rate of peripheral pulmonary artery stenosis. In this study, we report the case of an infant with Alagille syndrome caused by a <em>JAG1</em> mutation, who succumbed to acute exacerbation of right heart failure due to severe peripheral pulmonary artery stenosis. The autopsy revealed that the peripheral pulmonary arteries were significantly stenosed, exhibiting hypoplasia and thickened vessel walls. Histological examination of the pulmonary artery walls showed a decrease in smooth muscle cells in the tunica media and an increase in collagen and elastic fibers, although the intrapulmonary arteries were intact. These findings are important for understanding the pathogenesis of Alagille syndrome and developing treatment strategies for peripheral pulmonary artery stenosis.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107677"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1054880724000735/pdfft?md5=6579b1f1ca3fc6fcdababe0d7ce5ab6c&pid=1-s2.0-S1054880724000735-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787267","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}

{"title":"Giant cell aortitis combined with arteritis and coarctation of the aorta in 3.5-month child: A case report and literature review","authors":"Yuliia Kuzyk,&nbsp;Dmytro Zerbino,&nbsp;Olga Kovalyk","doi":"10.1016/j.carpath.2024.107703","DOIUrl":"10.1016/j.carpath.2024.107703","url":null,"abstract":"<div><div>A present case showing giant cell aortitis (GGA) with coarctation of the aorta can be considered unique, even after reviewing the literature. The case of a 3.5-month-old girl who suffered an acute viral infection with an increase in body temperature (up to 39.5°C), difficulty breathing, and diarrhea is described. The girl was diagnosed with nasopharyngitis, enterocolitis, meningoencephalitis; she died 20 hours after being hospitalized from multiple organ failure. Clinical and laboratory data were collected, and a pathological examination was performed. Histological examination of the aorta and its main branches, such as the brachiocephalic trunk, left common carotid artery, left subclavian artery, as well as internal organs, was performed using hematoxylin-eosin, Hart's resorcin-fuchsin, Weigert's picrofuchsin, and Masson's trichrome. Pathological examination revealed giant cell aortitis and arteritis with coarctation of the aorta. GCA, in our case, had pathomorphological signs. First, many plaques that protruded into the lumen of the aorta and main branches, such as the brachiocephalic trunk, left common carotid artery and left subclavian artery, had a conical end that resembled the appearance of a rash. Second, granulomatous inflammation was localized in the intima of the aorta and all layers of the above-mentioned arteries.</div><div>Our case of GCA in a 3.5-month-old girl is the youngest patient among those described. We first describe GCA in relation to other severe aortic diseases. Coarctation, in combination with an aneurysm of the ascending aorta and aortitis, is a pathology that has not yet been described.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107703"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602989","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 4: Table of Contents/Barcode PMS 200","authors":"","doi":"10.1016/S1054-8807(24)00104-2","DOIUrl":"10.1016/S1054-8807(24)00104-2","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107708"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142702002","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":"High-resolution three-dimensional atlas of congenital heart defects based on micro-CT images of human postmortem wax-infiltrated heart specimens","authors":"Shuhei Toba ,&nbsp;Stephen P. Sanders ,&nbsp;Takato Yamasaki ,&nbsp;Keito Mori ,&nbsp;Kentaro Umezu ,&nbsp;Motoshi Takao ,&nbsp;Chrystalle Katte Carreon","doi":"10.1016/j.carpath.2024.107690","DOIUrl":"10.1016/j.carpath.2024.107690","url":null,"abstract":"<div><h3>Introduction</h3><div>Postmortem heart specimens are essential for education and research on the anatomy, morphology, and pathology of congenital heart defects. However, such specimens are rarely obtained these days, and the specimens stored in formalin are inexorably deteriorating. This study aimed to develop methods to archive three-dimensional data of rare human heart specimens and to publish the data.</div></div><div><h3>Methods</h3><div>All wax-infiltrated human postmortem heart specimens stored in the Cardiac Registry, Boston Children's Hospital were scanned using microfocus computed tomography (X-Tek HMXST225, Nikon Metrology, Inc.), and reproduced using a three-dimensional printer (Form 3B, Formlabs Inc.). The digital models were published as an interactive three-dimensional online atlas. The resolution of the three-dimensional data was evaluated.</div></div><div><h3>Results</h3><div>The primary diagnoses in the 88 specimens included in the study include normal cardiac anatomy (11 cases), transposition of the great arteries {S,D,D} (11 cases), ventricular septal defect (10 cases), double-outlet right ventricle (9 cases), hypoplastic left heart syndrome (9 cases), and common atrioventricular canal (7 cases). Twenty-five cases (28%) underwent previous surgical or percutaneous interventions to the heart, including Mustard procedure (1 case), Senning procedure (2 cases, one was performed on a postmortem heart specimen). The median voxel size of the three-dimensional data was 40.5 um (IQR, 32.8–64.2). All intracardiac structures were precisely reproduced as digital and physical three-dimensional models.</div></div><div><h3>Conclusions</h3><div>The methods and resultant models were considered useful for archiving and furthering the utilization of these invaluable specimens. The atlas is available at <span><span>https://www.sketchfab.com/heartmodels/collections</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107690"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1054880724000863/pdfft?md5=eb102195ecc285f6e909d438401479f0&pid=1-s2.0-S1054880724000863-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104645","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}

{"title":"Comparative evaluation of local and downstream responses in two commercially available paclitaxel-coated balloons in healthy peripheral arteries of a swine model","authors":"María Gracia de Garnica García ,&nbsp;Laura Mola Solà ,&nbsp;Claudia Pérez-Martínez ,&nbsp;Luis Duocastella Codina ,&nbsp;María Molina Crisol ,&nbsp;Alex Gómez Castel ,&nbsp;Armando Pérez de Prado","doi":"10.1016/j.carpath.2024.107688","DOIUrl":"10.1016/j.carpath.2024.107688","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the local, downstream, and systemic effects of 2 different paclitaxel-coated balloons.</p></div><div><h3>Design</h3><p>Preclinical study in healthy peripheral arteries of a swine model, with randomized allocation of the distribution of the devices: the test paclitaxel-coated balloon (PCB) (Luminor^Ⓡ), a control PCB (IN.PACT^Ⓡ), and a plain angioplasty balloon (Oceanus^Ⓡ), considering single (1×) and overlapping (3×) doses with simple blind histologic analysis.</p></div><div><h3>Methods</h3><p>Twenty animals underwent balloon angioplasty at 1× or 3× doses in the external and internal branches of both femoral arteries and were followed-up for 28 days. Postprocedural and follow-up angiography were carried out. Comprehensive necropsy and histology were used to evaluate the local, downstream and systemic effects.</p></div><div><h3>Results</h3><p>Angioplasty was successfully carried out in all animals. Significant protocol deviations appeared in 3 arteries (treated with Oceanus®) without clinical relevance. Those samples were excluded from the analysis. All the animals survived the follow-up period without major clinical issues. Local signs of drug toxicity were less marked with Luminor® than IN.PACT® at 1× dose, including endothelial loss (<em>P</em> = .0828), intima/media inflammation (<em>P = .</em>0004), transmural medial smooth muscle cell (SMC) loss (<em>P = .</em>0016), wall thickness loss (<em>P = .</em>0141), presence of fibrin in the vascular wall (<em>P = .</em>0054), and adventitial inflammation (<em>P = .</em>0080). A similar pattern was observed at the 3× dose for endothelial loss (<em>P = .</em>0011), intima/media inflammation (<em>P</em> &lt; .0001), circumferential SMC loss (<em>P = .</em>0004), medial SMC replacement with proteoglycans (<em>P = .</em>0014), fibrin (<em>P</em> = .0034), and collagen content (<em>P = .</em>0205). Downstream vascular histologic changes were mild although more prevalent in the IN.PACT® 3× group (<em>P</em> = .006). No systemic effects of toxicity were detected in any of the samples analyzed.</p></div><div><h3>Conclusion</h3><p>Luminor® showed better healing pattern (lower inflammation, and endothelial and muscular loss) than IN.PACT® balloon. The effect was evident at single and triple doses. The prevalence of downstream lesions, albeit low, was higher with the triple dose of IN.PACT® compared with Luminor®.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107688"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S105488072400084X/pdfft?md5=5cc18fef6fc22cd638ff97f9b9e647a6&pid=1-s2.0-S105488072400084X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142046409","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}

{"title":"Cause of death for heart transplant patients, an autopsy study","authors":"Justin Burk,&nbsp;Cory T. Bernadt,&nbsp;Jon Ritter,&nbsp;Chieh-Yu Lin","doi":"10.1016/j.carpath.2024.107701","DOIUrl":"10.1016/j.carpath.2024.107701","url":null,"abstract":"<div><h3>Introduction</h3><div>Heart transplantations are lifesaving for patients with end-stage heart failure. It is pertinent for the multidisciplinary care team to understand how heart transplant patients succumbed to death and the complications that occurred. In this study, we performed a comprehensive retrospective review of all the autopsies performed in our institute for heart transplant patients and report the trend of demographic data, cause of death, and autopsy findings.</div></div><div><h3>Materials and methods</h3><div>Reports, photos, and slides of autopsies performed at our institute from 1990 to 2023 for heart transplant patients were reviewed. Pertinent demographic data (age, gender, pretransplant diagnosis), clinical data (clinical history of rejection, complication, time interval from transplant to death, clinical cause of death) and pathological findings (allograft pathology, infectious etiology, other findings related to cause of death) were reviewed, documented, and analyzed.</div></div><div><h3>Results</h3><div>We identified 88 cases, consisting of 53 male and 35 female patients. The median age at transplant was 26 years, while 28.5 years was the median age at death. The median interval from transplant to death was 10 months. The cases were classified in three categories based on length of survival post-transplant: Superacute (&lt;1 month, 21%), Early (1 month-12 months, 30%), and Late (&gt; 12 months, 49%). Slides were unavailable for review in 15 cases, which were excluded from cause of death (COD) evaluation. We categorized 41.1% of cases as allograft-related COD and 58.9% as non-allograft-related COD. Six of the CODs were not perceived premortem. These unexpected CODs included moderate/severe acute cellular rejection in a patient with a recently negative biopsy, dehiscent suture caused by a fungal abscess, an aorto-bronchial fistula, CMV myocarditis, acute abdominal bleeding, and ruptured atherosclerotic plaques with acute myocardial infarction.</div></div><div><h3>Conclusion</h3><div>We systematically reviewed 33 years of heart transplant autopsies. We found that 41.1% of deaths were allograft related, with infection being the most frequent COD. While the rate of unexpected findings was low, the findings demonstrate the continued utility of autopsy in patient evaluation.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107701"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458690","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}

{"title":"BAG3 in cardiovascular diseases","authors":"Nicola De Maio ,&nbsp;Margot De Marco","doi":"10.1016/j.carpath.2024.107687","DOIUrl":"10.1016/j.carpath.2024.107687","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107687"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035332","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":"Interplay of atherosclerosis and medial degeneration in human ascending aorta","authors":"Aaron Huhta ,&nbsp;Timo Paavonen ,&nbsp;Ari Mennander ,&nbsp;Ivana Kholová","doi":"10.1016/j.carpath.2024.107702","DOIUrl":"10.1016/j.carpath.2024.107702","url":null,"abstract":"<div><div>The previous understanding has been that atherosclerosis tends to increase distally from the ascending aorta, but recent studies and practical experience have indicated that atherosclerosis occurs in the ascending aorta more than previously thought. Medial degeneration is linked to aortic aneurysms, dissection and dilatation and has been related to increased mortality. There is a lack of data on the coexistence of atherosclerosis and medial degeneration in the ascending aorta and its outcome to clinical morbidity and mortality. Earlier studies have shown coexisting atherosclerosis and medial degeneration as significant risk indicators for coronary and cerebrovascular events. We aimed to analyze aortic specimens classified according to the consensus documents of the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology particularly the comparison of variable morphological features with the atherosclerotic grade to gain more data about the coexistence of atherosclerosis and medial degeneration. We evaluated 217 specimens of human ascending aorta resected at Tampere University Heart Hospital because of aortic aneurysm, dissection or dilatation. None of the samples contained normal aortic morphology; atherosclerosis was found in a total of 75.8 % of the samples and medial degeneration in all the samples. The present study is mostly in agreement with earlier research regarding the prevalence of different histological findings, even though a higher prevalence of atherosclerosis was found compared with most studies. There was no statistically significant association between atherosclerosis and medial degeneration, but a higher atherosclerotic grade was significantly associated with the presence of smooth muscle cell nuclei loss, smooth muscle cell disorganisation, elastic fibre thinning and medial fibrosis. Our study reinforces the perception that atherosclerotic lesions significantly occur in the ascending aorta and coexist with individual components of the medial degeneration.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107702"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399492","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}

{"title":"Autophagy in myocardial ischemia and ischemia/reperfusion","authors":"Aleksandra Aljakna Khan ,&nbsp;Sara Sabatasso","doi":"10.1016/j.carpath.2024.107691","DOIUrl":"10.1016/j.carpath.2024.107691","url":null,"abstract":"<div><p>Myocardial infarction (MI) is a life-threatening condition that leads to loss of viable heart tissue. The best way to treat acute MI and limit the infarct size is to re-open the occluded coronary artery and restore the supply of oxygenated and nutrient-rich blood, but reperfusion can cause additional damage. Autophagy is an intracellular process that recycles damaged cytoplasmic components (molecules and organelles) by loading them into autophagosomes and degrading them in autolysosomes. Autophagy is increased in <em>in vivo</em> animal models of permanent ischemia and ischemia/reperfusion but by different molecular mechanisms. While autophagy is protective during permanent ischemia, it is detrimental during ischemia/reperfusion. Its modulation is being investigated as a potential target to reduce reperfusion injury. This review provides a synopsis of the current knowledge about autophagy, summarizes findings specifically in permanent ischemia and ischemia/reperfusion, and briefly discusses the potential implication of experimental findings.</p></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107691"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104644","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(24)00103-0","DOIUrl":"10.1016/S1054-8807(24)00103-0","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107707"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142702003","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}