Cardiovascular Pathology最新文献

{"title":"Mast cells and arteriogenesis: A systematic review","authors":"Alice Nassar ,&nbsp;Elizabeth Wagura ,&nbsp;Marios Loukas","doi":"10.1016/j.carpath.2025.107716","DOIUrl":"10.1016/j.carpath.2025.107716","url":null,"abstract":"<div><div>Vascular occlusive diseases remain a major health burden worldwide, necessitating a deeper understanding of the adaptive responses that mitigate their impact. Arteriogenesis, the growth and remodeling of collateral vessels in response to arterial occlusion, is a vital defense mechanism that counteracts fluid shear stress-induced vascular stenosis or occlusion. While physical factors driving arteriogenesis have been extensively studied, the specific cellular mediators involved are poorly understood. Notably, the role of innate and adaptive immune cells, particularly mast cells, in arteriogenesis has received limited attention. This systematic review bridges this knowledge gap by investigating the contribution of mast cells to vascular cell proliferation and leukocyte recruitment in arteriogenesis. A comprehensive search of major databases using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines reveals the critical connection between mast cells, inflammatory cells, innate immune cells, and growth factors in arteriogenesis. Our findings highlight the molecular mechanisms of mast cell activation, sheer stress exertion, and pro-arteriogenic growth factor recruitment. Furthermore, we explore the endogenous and exogenous factors, including nitrite, dipyridamole, thrombin, and cobra venom, triggering mast cell-mediated release of pro-arteriogenic factors. Additionally, we examine the impact of recombinant parathyroid hormone (rPTH) therapy on mast cell numbers and arteriogenesis in bone defect and allograft healing. Our review provides compelling evidence for the pro-arteriogenic role of mast cells, particularly during the early inflammatory phase of vessel occlusion, suggesting that targeting mast cell activation may be a promising therapeutic strategy for enhancing arteriogenesis and treating ischemia-related diseases.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107716"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945104","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(25)00006-7","DOIUrl":"10.1016/S1054-8807(25)00006-7","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107720"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143180498","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(25)00007-9","DOIUrl":"10.1016/S1054-8807(25)00007-9","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107721"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143180499","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":"Takayasu arteritis with medio-medial intussusception?","authors":"Pradeep Vaideeswar ,&nbsp;Pranav Bhatia ,&nbsp;Bharati Malankar","doi":"10.1016/j.carpath.2024.107709","DOIUrl":"10.1016/j.carpath.2024.107709","url":null,"abstract":"<div><div>We present an autopsy case of a child with Takayasu arteritis who succumbed due to cerebrovascular accident with an interesting finding in the inflamed aorta. On account of necro-inflammatory changes in the media of the distal descending thoracic aorta coupled with the shear stress of accelerated hypertension, there was a medial detachment, which migrated and lay between the intima and media of the abdominal aorta. This displacement was visualized on gross and histopathological examination as a ‘laminated’ appearance of coils of discontinuous inflamed tunica media, reminiscent of a hydatid cyst, which has been designated as medio-medial intussusceptions.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107709"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766272","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":"An autopsy case of TFE3-rearranged PEComa-like neoplasm with systematic embolization involving the heart","authors":"Ikoi Omatsu ,&nbsp;Hiroki Mukai ,&nbsp;Toshifumi Doi ,&nbsp;Takeshi Ishikawa ,&nbsp;Yoshito Itoh ,&nbsp;Eiichi Konishi ,&nbsp;Yukiko Shishido-Hara","doi":"10.1016/j.carpath.2025.107715","DOIUrl":"10.1016/j.carpath.2025.107715","url":null,"abstract":"<div><div>A rare autopsy case of malignant <em>transcription factor E3</em> (<em>TFE3</em>)-rearranged perivascular epithelioid cell tumor (PEComa)-like neoplasm is presented. An 84-year-old woman manifested multiple cerebral infarctions and repetitive embolic events in the supra mesenchymal artery (SMA), and the presence of a mobile mass in the heart's left ventricle was also revealed. Tumoral lesions were also found in a pelvic space and a right pleural cavity, and a biopsy was performed from one of the disseminated tumor masses in the right pleura. Pathological diagnosis of <em>TFE3</em>-rearranged PEComa-like neoplasm was defined based on the evidence of partial expression of Melan A, and strong nuclear expression of TFE3 and by detection of the Xp11.2 locus split signal with FISH. A post-mortem analysis via autopsy revealed the widespread intravascular tumors in the heart's left ventricle, supra mesenchymal vein (SMV), and partial vein. The left intraventricular tumoral mass was associated with thrombus and fibrine, and thrombotic emboli were also found in SMA, SMV, and left pulmonary arteries. Interestingly, organ-based tumor invasion accompanying desmoplastic reactions was hardly seen. The small intestine was perforated, likely due to ischemia, which resulted in suppurative peritonitis and sepsis. This was thought of as the direct cause of death.</div><div>This is the first report of a precise autopsy investigation of <em>TFE3</em>-rearranged PEComa-like neoplasm. Tumoral localization was mostly intravascular or disseminative in the pleural cavity. Given the limited understanding of this tumoral pathophysiology, this case offers valuable insights for prompt diagnosis and effective treatment strategies.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107715"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963758","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":"Sudden death in a case of triple-vessel, non-atherosclerotic, diffuse ectasia and aneurysmal dilatations of the coronary arteries: An autopsy report","authors":"Shatishraj Jothee ,&nbsp;Zhao Peng Koo ,&nbsp;Mary N. Sheppard ,&nbsp;Tuan Minanoriah binti Tuan Muda","doi":"10.1016/j.carpath.2024.107714","DOIUrl":"10.1016/j.carpath.2024.107714","url":null,"abstract":"<div><div>Aneurysmal Coronary Artery Disease (ACAD) can occur as localized dilations of a segment of one or more coronary arteries or diffuse ectasia-type dilatations of one or more coronaries. Atherosclerosis remains the most common cause of these aneurysms, with Kawasaki Disease being implicated in the Asian population. We present a case of a 62-year-old Asian woman who dies suddenly with no prior symptoms. and underwent an autopsy. Her heart showed diffuse aneurysmal dilatations of the epicardial coronary arteries, with a giant saccular aneurysm of the left main coronary artery. Histopathology revealed medial degeneration of the aneurysmal wall with no evidence of atheroma or vasculitis. Following a review of the pathological causes of coronary aneurysms, it is likely that the cause of such diffuse dilatations of the coronaries could be previous vasculitis such as Kawasaki disease.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107714"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926595","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":"Relationship between myocardial fibrosis and left bundle branch block. Does it exist?","authors":"Elena Rimskaya ,&nbsp;Olga Aparina ,&nbsp;Olga Stukalova ,&nbsp;Semen Kormilitsyn ,&nbsp;Nataliia Mironova ,&nbsp;Petr Chumachenko ,&nbsp;Sergey Ternovoy ,&nbsp;Sergey Golitsyn","doi":"10.1016/j.carpath.2024.107713","DOIUrl":"10.1016/j.carpath.2024.107713","url":null,"abstract":"<div><h3>Aim</h3><div>to assess the relation of focal and diffuse left ventricular (LV) fibrosis to left bundle branch block (LBBB).</div></div><div><h3>Materials and methods</h3><div>60 patients with dilated cardiomyopathy and LBBB (DCM-LBBB), 50 DCM-nonLBBB patients, 15 patients with LBBB and structurally normal heart (idiopathic LBBB) and 10 healthy volunteers (HV) underwent cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE). LGE LV images were post-proceeded for core scar (CS) and gray zone (GZ) calculation. Diffuse LV fibrosis was estimated on LGE-CMR images with the diffuse intensity ratio (DIR). Endomyocardial biopsy (EMB) was performed in 15(24.6 %) DCM-LBBB and 16 (32 %) non-LBBB DCM patients and allowed the quantification of collagen volume fraction (CVF).</div></div><div><h3>Results</h3><div>The percentage of CVF correlated with the DIR value in the same segment (<em>r</em> = 0.66, <em>p</em> &lt; 0.001). The value of CVF in EMB and frequency of LGE in both DCM groups was comparable (<em>p</em> = 0.8). In DCM-nonLBBB patients the percentage of CS was significantly higher (4.0[1.6; 11.7]% versus 1.4[0.1;8.5]% in DCM-LBBB patients, <em>p</em> = 0.047), whereas percentage of GZ and total fibrosis in both DCM groups was comparable. DIR value was higher in patients with idiopathic LBBB than in HV (0.54±0.09 versus 0.34±0.1, р&lt;0,001).</div></div><div><h3>Conclusion</h3><div>Neither focal nor interstitial fibrosis is associated with LBBB in DCM patients. Diffuse inflammation in DCM-LBBB patients may contribute to the progression of systolic dysfunction but is not a cause of LBBB. The increased value of interstitial fibrosis in patients with idiopathic LBBB may reflect latent diffuse process in myocardium inexorably leading to DCM development.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107713"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920800","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":"Corrigendum to “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 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.2024.107710","DOIUrl":"10.1016/j.carpath.2024.107710","url":null,"abstract":"","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107710"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853068","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":"Unlocking vascular vitality: Exploring the impact of LIMA harvesting technique on endothelial health","authors":"Serkan Mola ,&nbsp;Alp Yıldırım ,&nbsp;Nilüfer Onak Kandemir ,&nbsp;Gökay Deniz ,&nbsp;Enis Burak Gül ,&nbsp;Ertekin Utku Ünal","doi":"10.1016/j.carpath.2024.107699","DOIUrl":"10.1016/j.carpath.2024.107699","url":null,"abstract":"<div><h3>Background</h3><div>This study investigates the impact of different harvesting techniques on the morphology and endothelial function of the left internal mammary artery (LIMA) grafts in coronary artery bypass grafting (CABG).</div></div><div><h3>Methods</h3><div>Fifty-three patients undergoing elective CABG were randomly assigned to two groups based on the harvesting technique: traditional clipping and nonclipping. Histological analyses revealed that arteries in the nonclipped group exhibited greater dilation and preserved endothelial integrity compared to the control group.</div></div><div><h3>Results</h3><div>The nonclipped group exhibited greater arterial dilation and preserved endothelial integrity compared to the clipped group. Immunostaining for endothelial nitric oxide synthase (eNOS) showed significantly higher expression in the nonclipped group, conversly COX-2 staining showed fewer expression in the nonclipped group indicating better endothelial function preservation.</div></div><div><h3>Conclusion</h3><div>These findings suggest that maintaining perfusion during LIMA harvesting may improve endothelial function and potentially enhance graft patency in the long term. Further research is warranted to validate these results and optimize harvesting techniques for CABG procedures.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107699"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364510","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":"Serotonin transporter deficiency in mice results in an increased susceptibility to HTR2B-dependent pro-fibrotic mechanisms in the cardiac valves and left ventricular myocardium","authors":"Estibaliz Castillero ,&nbsp;Chiara Camillo ,&nbsp;Dov Levine ,&nbsp;Alex M. D'Angelo ,&nbsp;Yaagnik Kosuri ,&nbsp;Juan B. Grau ,&nbsp;Robert J. Levy ,&nbsp;Giovanni Ferrari","doi":"10.1016/j.carpath.2024.107689","DOIUrl":"10.1016/j.carpath.2024.107689","url":null,"abstract":"<div><div>Increased serotonin (5HT) concentration and signaling, can lead to pathological remodeling of the cardiac valves. We previously showed that a reduction of the 5HT transporter (SERT) expression in the mitral valve (MV) contributes to the progression of degenerative MV regurgitation (MR). We sought to investigate the myocardial and valvular phenotype of SERT^-/- mice in order to identify remodeling mechanisms specific to the MV and left ventricular (LV) remodeling. Using 8- and 16-week-old WT and SERT^-/- mice we show that male and female animals deficient of SERT have pathological remodeling of the cardiac valves, myocardial fibrosis, diminished ejection fraction and altered left ventricular dimensions. In the MV and intervalvular area of the aortic valve (AV)-MV, gene expression, including Col1a1 mRNA, was progressively altered with age up until 16 weeks of age. In contrast, in the AV and myocardium, most gene expression changes occurred earlier and plateaued by 8 weeks. To explore basal differences in susceptibility to remodeling stimuli among cardiac valves, valve interstitial cells (VIC) were isolated from AV, MV, tricuspid valve (TV), pulmonary valve (PV) and fibroblasts (Fb) from the myocardial apex from 16 weeks old wild type (WT) mice. After 24h stimulation with 10 µM of 5HT, the gene expression of Col1a1 and Acta2 were upregulated in MVIC to a higher degree than in VIC from other valves and Fb. Treatment with TGFβ1 similarly upregulated Cola1 and Acta2 in MVIC and AVIC, while the increase was milder in right heart VIC and Fb. Experiments were also carried out with human VIC. In comparison to mice, human left heart VIC were more sensitive to 5HT and TGFβ1, upregulating COL1A1 and ACTA2; TGFβ1 upregulated HTR2B expression in all VIC. Our results support the hypothesis that a deleterious cardiac effect of SERT downregulation may be mediated by increased susceptibility to HTR2B-dependent pro-fibrotic mechanisms, which are distinct among VIC populations and cardiac fibroblasts, regardless of SERT activity. Given that HTR2B mechanisms involved in VIC and myocardial remodeling response are due to both 5HT and also to downstream related TGFβ1 and TNFα activity, targeting HTR2B could be a therapeutic strategy for dual treatment of MR and LV remodeling.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"74 ","pages":"Article 107689"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153174","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}