Pub Date : 2025-05-10DOI: 10.1016/j.carpath.2025.107742
Jing Wang , Yahui Zhang , Caixing Cao , Jiale Hua , Li Xing , Changxin Wu
Regulating the differentiation of monocytes into M2 macrophages can promote the regression of Atherosclerosis (AS) plaque. However, the key molecules regulating the differentiation of monocytes to M2 are unknown. In this study, we reported that adenosine-activated protein kinase α1 (AMPKα1) plays an anti-AS role by polarizing monocytes to an M2 phenotype via promoting fatty acid oxidation (FAO). AMPKα1 enhances the decomposition of cholesterol esters by increasing lysosomal acid lipase expression to provide fatty acids for FAO. Furthermore, AMPKα1 can induce lysosomal biogenesis and enhance lipolysis by promoting the transcription factor EB (TFEB) expression and facilitating TFEB nuclear translocation. In conclusion, AMPKα1 enhances the decomposition of cholesterol esters by increasing lysosomal acid lipase expression to produce fatty acids, which may represent a mechanism to promote FAO and inflammatory monocytes differentiation towards M2 phenotype.
{"title":"The anti-atherosclerosis effect and molecular mechanism of AMPKα1 by polarizing monocytes to an M2 phenotype via cell-intrinsic lysosomal lipolysis","authors":"Jing Wang , Yahui Zhang , Caixing Cao , Jiale Hua , Li Xing , Changxin Wu","doi":"10.1016/j.carpath.2025.107742","DOIUrl":"10.1016/j.carpath.2025.107742","url":null,"abstract":"<div><div>Regulating the differentiation of monocytes into M2 macrophages can promote the regression of Atherosclerosis (AS) plaque. However, the key molecules regulating the differentiation of monocytes to M2 are unknown. In this study, we reported that adenosine-activated protein kinase α1 (AMPKα1) plays an anti-AS role by polarizing monocytes to an M2 phenotype via promoting fatty acid oxidation (FAO). AMPKα1 enhances the decomposition of cholesterol esters by increasing lysosomal acid lipase expression to provide fatty acids for FAO. Furthermore, AMPKα1 can induce lysosomal biogenesis and enhance lipolysis by promoting the transcription factor EB (TFEB) expression and facilitating TFEB nuclear translocation. In conclusion, AMPKα1 enhances the decomposition of cholesterol esters by increasing lysosomal acid lipase expression to produce fatty acids, which may represent a mechanism to promote FAO and inflammatory monocytes differentiation towards M2 phenotype.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"78 ","pages":"Article 107742"},"PeriodicalIF":2.3,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976867","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}
The likelihood of a plaque to cause an acute coronary syndrome (ACS) depends on several factors, both lesion- and patient-related. One of the most investigated and established contributing factors is the presence of high-risk or “vulnerable plaque” characteristics, which have been correlated with increased incidence of major adverse cardiovascular events (MACE). The recognition, however, that a significant percentage of vulnerable plaques do not result in causing clinical events has led the scientific community towards the more multifaceted concept of “vulnerable patients”. Incorporating the morphological features of an atherosclerotic plaque into its hemodynamic surroundings can better predict the chance of its disruption, as altered fluid dynamics play a significant role in plaque destabilization. The advances in coronary imaging and the field of computational fluid dynamics (CFD) can contribute to develop more accurate lesion- and patient-related ACS prediction models that take into account both the morphology of a plaque and the forces applied upon it. The aim of this review is to provide the latest data regarding the aforementioned predictive factors as well as relevant preventive measures.
{"title":"Defining “Vulnerable” in coronary artery disease: predisposing factors and preventive measures","authors":"Eleni Adamopoulou, Kyriakos Dimitriadis, Konstantinos Kyriakoulis, Nikolaos Pyrpyris, Eirini Beneki, Christos Fragkoulis, Dimitris Konstantinidis, Konstantinos Aznaouridis, Konstantinos Tsioufis","doi":"10.1016/j.carpath.2025.107736","DOIUrl":"10.1016/j.carpath.2025.107736","url":null,"abstract":"<div><div>The likelihood of a plaque to cause an acute coronary syndrome (ACS) depends on several factors, both lesion- and patient-related. One of the most investigated and established contributing factors is the presence of high-risk or “vulnerable plaque” characteristics, which have been correlated with increased incidence of major adverse cardiovascular events (MACE). The recognition, however, that a significant percentage of vulnerable plaques do not result in causing clinical events has led the scientific community towards the more multifaceted concept of “vulnerable patients”. Incorporating the morphological features of an atherosclerotic plaque into its hemodynamic surroundings can better predict the chance of its disruption, as altered fluid dynamics play a significant role in plaque destabilization. The advances in coronary imaging and the field of computational fluid dynamics (CFD) can contribute to develop more accurate lesion- and patient-related ACS prediction models that take into account both the morphology of a plaque and the forces applied upon it. The aim of this review is to provide the latest data regarding the aforementioned predictive factors as well as relevant preventive measures.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"77 ","pages":"Article 107736"},"PeriodicalIF":2.3,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847364","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 : 2025-03-26DOI: 10.1016/j.carpath.2025.107735
Faizan Ahmed , Tehmasp Rehman Mirza , Sherif Eltawansy , Zoha Khan , Yusra Mashkoor , Najam Gohar , Hira Zahid , Kainat Aman , Zaima Afzaal , Mushood Ahmed , Hritvik Jain , Aman Ullah , Nisar Asmi , Farman Ali , Adnan Bhat , Paweł Łajczak , Ogechukwu Obi , Muhammad Owais , Naveen Baskaran
Background
Heart failure (HF) carries varying mortality based on demographic distribution. Moreover, the interaction of HF with chronic obstructive pulmonary disease (COPD) raises this mortality. In this study, implementing national databases over a long time could assist in understanding mortality rates in patients suffering from two significant chronic diseases, HF and COPD.
Methods
This analysis utilized the CDC WONDER (Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research) system to assess the mortality trends between HF and COPD-associated HF in US adults aged 25–85+ from 1999 to 2020.
Results
This investigation detected a total of 6,755,700 deaths occurred in patients with HF in ages above 25. Fatalities of 1,141,819 (16.9 %) were associated with HF and comorbid COPD. Age-adjusted mortality Rates (AAMR) of HF-related deaths decreased from 162.7 to 154.4. (Average Annual Percentage Changes (AAPC): -0.49, 95 % CI: -0.63 to -0.34, p < 000001, while the overall AAMR for HF with COPD among adults increased from 24.5 in 1999 to 28.2 in 2020. Men had significantly higher HF-related AAMRs and HF with comorbid COPD-related mortality than women. HF-related AAMRs were highest among NH Black or African Americans, followed by NH Whites. At the same time, on the other side, HF and COPD had the highest mortality in non-Hispanic (NH) White individuals, followed by NH Black individuals, then Hispanic individuals. Mortality in HF with COPD was the highest in the Northeast, then the Midwest, South, and least in the West states.
Conclusion
Implementation of a CDC database provided guidance over two decades about the US population mortality attributed to HF with and without the presence of COPD, which contributed to a better understanding of national trends in prevailing diseases with remarkable chronicity.
{"title":"Temporal and demographic disparities in mortality trends for heart failure and COPD-associated heart failure in U.S. Adults: A 1999–2020 analysis of CDC WONDER data","authors":"Faizan Ahmed , Tehmasp Rehman Mirza , Sherif Eltawansy , Zoha Khan , Yusra Mashkoor , Najam Gohar , Hira Zahid , Kainat Aman , Zaima Afzaal , Mushood Ahmed , Hritvik Jain , Aman Ullah , Nisar Asmi , Farman Ali , Adnan Bhat , Paweł Łajczak , Ogechukwu Obi , Muhammad Owais , Naveen Baskaran","doi":"10.1016/j.carpath.2025.107735","DOIUrl":"10.1016/j.carpath.2025.107735","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure (HF) carries varying mortality based on demographic distribution. Moreover, the interaction of HF with chronic obstructive pulmonary disease (COPD) raises this mortality. In this study, implementing national databases over a long time could assist in understanding mortality rates in patients suffering from two significant chronic diseases, HF and COPD.</div></div><div><h3>Methods</h3><div>This analysis utilized the CDC WONDER (Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research) system to assess the mortality trends between HF and COPD-associated HF in US adults aged 25–85+ from 1999 to 2020.</div></div><div><h3>Results</h3><div>This investigation detected a total of 6,755,700 deaths occurred in patients with HF in ages above 25. Fatalities of 1,141,819 (16.9 %) were associated with HF and comorbid COPD. Age-adjusted mortality Rates (AAMR) of HF-related deaths decreased from 162.7 to 154.4. (Average Annual Percentage Changes (AAPC): -0.49, 95 % CI: -0.63 to -0.34, <em>p</em> < 000001, while the overall AAMR for HF with COPD among adults increased from 24.5 in 1999 to 28.2 in 2020. Men had significantly higher HF-related AAMRs and HF with comorbid COPD-related mortality than women. HF-related AAMRs were highest among NH Black or African Americans, followed by NH Whites. At the same time, on the other side, HF and COPD had the highest mortality in non-Hispanic (NH) White individuals, followed by NH Black individuals, then Hispanic individuals. Mortality in HF with COPD was the highest in the Northeast, then the Midwest, South, and least in the West states.</div></div><div><h3>Conclusion</h3><div>Implementation of a CDC database provided guidance over two decades about the US population mortality attributed to HF with and without the presence of COPD, which contributed to a better understanding of national trends in prevailing diseases with remarkable chronicity.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"77 ","pages":"Article 107735"},"PeriodicalIF":2.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742523","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 : 2025-03-13DOI: 10.1016/j.carpath.2025.107733
Marc K. Halushka , Giulia d'Amati , Melanie C. Bois , Monica De Gaspari , Carla Giordano , Karin Klingel , Charles Leduc , Keiko Ohta-Ogo , Ilke Ozcan , Stefania Rizzo , Celeste Santos-Martins , Atsuko Seki , Cristina Basso
Lymphocytic myocarditis is a serious disease with significant morbidity and mortality. Cardiovascular pathology has an important role in its diagnosis, a diagnosis historically made using the presence of a lymphocytic infiltrate and myocyte injury (Dallas Criteria). The European Society of Cardiology (ESC) criteria, additionally, use a threshold of immune cells, determined by CD3 immunohistochemical stains to render the diagnosis of myocarditis on endomyocardial biopsy. However, the frequency of immune cells in non-myocarditis endomyocardial biopsy cases is unclear and dependent on different evaluation methods. Therefore, an international consortium of 6 centers assessed endomyocardial biopsies on patient populations for the count of CD3+ lymphocytes in the one busiest high-powered field (hpf) per case. In total, 359 biopsies, performed for reasons other than a clinical suspicion of myocarditis, were evaluated. The clinical decision to biopsy was mainly for the differential diagnosis of hypertrophic cardiomyopathy (n = 133, 37 %); amyloidosis (n = 103, 29 %); hypertensive heart disease (n = 96, 27 %) or other non-inflammatory diseases. The average number of CD3+ lymphocytes in the busiest hpf was 3.1 (median 2). Over 96 % of cases had fewer than 10 lymphocytes in the busiest hpf. There were no significant differences by sex or age, but institutional differences in the count of CD3+ lymphocytes were significant. These findings will help classify the abundance of lymphocytes on non-myocarditis endomyocardial biopsies for use in myocarditis criteria classifications.
{"title":"The frequency of CD3+ lymphocytes in non-myocarditis endomyocardial biopsies","authors":"Marc K. Halushka , Giulia d'Amati , Melanie C. Bois , Monica De Gaspari , Carla Giordano , Karin Klingel , Charles Leduc , Keiko Ohta-Ogo , Ilke Ozcan , Stefania Rizzo , Celeste Santos-Martins , Atsuko Seki , Cristina Basso","doi":"10.1016/j.carpath.2025.107733","DOIUrl":"10.1016/j.carpath.2025.107733","url":null,"abstract":"<div><div>Lymphocytic myocarditis is a serious disease with significant morbidity and mortality. Cardiovascular pathology has an important role in its diagnosis, a diagnosis historically made using the presence of a lymphocytic infiltrate and myocyte injury (Dallas Criteria). The European Society of Cardiology (ESC) criteria, additionally, use a threshold of immune cells, determined by CD3 immunohistochemical stains to render the diagnosis of myocarditis on endomyocardial biopsy. However, the frequency of immune cells in non-myocarditis endomyocardial biopsy cases is unclear and dependent on different evaluation methods. Therefore, an international consortium of 6 centers assessed endomyocardial biopsies on patient populations for the count of CD3+ lymphocytes in the one busiest high-powered field (hpf) per case. In total, 359 biopsies, performed for reasons other than a clinical suspicion of myocarditis, were evaluated. The clinical decision to biopsy was mainly for the differential diagnosis of hypertrophic cardiomyopathy (<em>n</em> = 133, 37 %); amyloidosis (<em>n</em> = 103, 29 %); hypertensive heart disease (<em>n</em> = 96, 27 %) or other non-inflammatory diseases. The average number of CD3+ lymphocytes in the busiest hpf was 3.1 (median 2). Over 96 % of cases had fewer than 10 lymphocytes in the busiest hpf. There were no significant differences by sex or age, but institutional differences in the count of CD3+ lymphocytes were significant. These findings will help classify the abundance of lymphocytes on non-myocarditis endomyocardial biopsies for use in myocarditis criteria classifications.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"77 ","pages":"Article 107733"},"PeriodicalIF":2.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633346","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 : 2025-03-11DOI: 10.1016/j.carpath.2025.107734
Manon Van Hecke , Kasper Favere , Sander Eens , Matthias Bosman , Peter L. Delputte , Pieter-Jan Guns , Tania Roskams , Hein Heidbuchel
<div><h3>Background and aims</h3><div>Myocarditis is a group of inflammatory diseases of the myocardium, with viral infections being the leading cause. Previous murine studies have demonstrated a detrimental effect of extensive exercise on the acute course of viral myocarditis. Recently, we were the first to report that continuation of moderate exercise during murine viral myocarditis modulates myocardial inflammation and fibrosis at the late stage of disease, yet we did not evaluate early time points. In this study, we aimed to evaluate the impact of moderate intensity training on the acute course of disease, and compare it to the effects of a high intensity protocol.</div></div><div><h3>Methods and results</h3><div>Two separate experiments were performed. For the moderate intensity (Mod) endurance exercise experiment, 50 male C57BL/6J mice (11 weeks old) were randomised to 3 weeks of treadmill running (ModEEX, 18 cm/sec, daily) or not (ModSED). Two weeks into the experiment, animals received a single intraperitoneal injection with either coxsackievirus B3 (CVB) to induce viral myocarditis, or phosphate-buffered saline (PBS) vehicle. For the high intensity (Hi) endurance exercise experiment, another 20 male C57BL/6J mice (17 weeks old) were randomised to 3 weeks of treadmill running (HiEEX) or not (HiSED). After two weeks of training, all animals of the Hi experiment were injected with CVB, and the training protocol was intensified with increasing running speeds until exhaustion in the final week of training. All animals were sacrificed 6-7 days after virus or vehicle administration. All groups demonstrated complete survival except for 1 animal of the HiSED group, and showed comparable clinical signs and body weight evolution. Nor moderate, neither high intensity exercise had any significant impact on plasma troponin levels, semiquantitative scores of cardiomyocyte loss, and digital areas of necrosis. Morphologically however, HiEEX mice showed markedly less inflammatory cells in the necrotic areas of the myocardial lesions compared to HiSED mice, as was confirmed by digital quantification (x10<sup>3</sup> inflammatory cells per mm<sup>2</sup> HiEEX: 6.24±0.32SEM vs HiSED: 8.02 ±0.36SEM, P=0.002). The same digital quantification did not show significant differences between ModEEX and ModSED lesions. Using an extensive panel of immunohistochemical inflammatory cell markers, a different composition of inflammatory cell subtypes was observed in the myocardial lesions of HiEEX compared to ModEEX mice, with a shift towards a pro-inflammatory milieu in HiEEX mice (ratio iNOS/Arg1 HiEEX: 0.49 vs ModEEX: 0.22, P=0.041 and ratio Tbet/GATA3 HiEEX: 4.75 vs ModEEX: 0.82, P=0.005). The cardiac viral load varied considerably, but no impact of exercise was observed, nor did cardiac expression of remodelling genes (Serpina3n, CTGF, and TGF-β) show an exercise effect.</div></div><div><h3>Conclusion</h3><div>In the acute phase of murine viral myocarditis, lesions
{"title":"The impact of moderate and high intensity endurance exercise on acute murine coxsackievirus B3 myocarditis","authors":"Manon Van Hecke , Kasper Favere , Sander Eens , Matthias Bosman , Peter L. Delputte , Pieter-Jan Guns , Tania Roskams , Hein Heidbuchel","doi":"10.1016/j.carpath.2025.107734","DOIUrl":"10.1016/j.carpath.2025.107734","url":null,"abstract":"<div><h3>Background and aims</h3><div>Myocarditis is a group of inflammatory diseases of the myocardium, with viral infections being the leading cause. Previous murine studies have demonstrated a detrimental effect of extensive exercise on the acute course of viral myocarditis. Recently, we were the first to report that continuation of moderate exercise during murine viral myocarditis modulates myocardial inflammation and fibrosis at the late stage of disease, yet we did not evaluate early time points. In this study, we aimed to evaluate the impact of moderate intensity training on the acute course of disease, and compare it to the effects of a high intensity protocol.</div></div><div><h3>Methods and results</h3><div>Two separate experiments were performed. For the moderate intensity (Mod) endurance exercise experiment, 50 male C57BL/6J mice (11 weeks old) were randomised to 3 weeks of treadmill running (ModEEX, 18 cm/sec, daily) or not (ModSED). Two weeks into the experiment, animals received a single intraperitoneal injection with either coxsackievirus B3 (CVB) to induce viral myocarditis, or phosphate-buffered saline (PBS) vehicle. For the high intensity (Hi) endurance exercise experiment, another 20 male C57BL/6J mice (17 weeks old) were randomised to 3 weeks of treadmill running (HiEEX) or not (HiSED). After two weeks of training, all animals of the Hi experiment were injected with CVB, and the training protocol was intensified with increasing running speeds until exhaustion in the final week of training. All animals were sacrificed 6-7 days after virus or vehicle administration. All groups demonstrated complete survival except for 1 animal of the HiSED group, and showed comparable clinical signs and body weight evolution. Nor moderate, neither high intensity exercise had any significant impact on plasma troponin levels, semiquantitative scores of cardiomyocyte loss, and digital areas of necrosis. Morphologically however, HiEEX mice showed markedly less inflammatory cells in the necrotic areas of the myocardial lesions compared to HiSED mice, as was confirmed by digital quantification (x10<sup>3</sup> inflammatory cells per mm<sup>2</sup> HiEEX: 6.24±0.32SEM vs HiSED: 8.02 ±0.36SEM, P=0.002). The same digital quantification did not show significant differences between ModEEX and ModSED lesions. Using an extensive panel of immunohistochemical inflammatory cell markers, a different composition of inflammatory cell subtypes was observed in the myocardial lesions of HiEEX compared to ModEEX mice, with a shift towards a pro-inflammatory milieu in HiEEX mice (ratio iNOS/Arg1 HiEEX: 0.49 vs ModEEX: 0.22, P=0.041 and ratio Tbet/GATA3 HiEEX: 4.75 vs ModEEX: 0.82, P=0.005). The cardiac viral load varied considerably, but no impact of exercise was observed, nor did cardiac expression of remodelling genes (Serpina3n, CTGF, and TGF-β) show an exercise effect.</div></div><div><h3>Conclusion</h3><div>In the acute phase of murine viral myocarditis, lesions ","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"77 ","pages":"Article 107734"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623753","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 : 2025-02-26DOI: 10.1016/j.carpath.2025.107728
L. Mwizerwa , V.L. Cousin , T. Sologashvili , J.P. Vallée , F. Gumy-Pause , J. Wacker , A.L. Rougemont
Primary pediatric heart tumors are rare, and the vast majority are benign. Primary malignant cardiac tumors are exceedingly uncommon in this age group. Due to their rarity and overlapping imaging features with the more common benign tumors, the diagnosis of primary malignant cardiac tumors is particularly challenging. We report a case of a 12-year-old male with a 7-year history of a left ventricular mass that progressively increased in size, eventually requiring surgical resection. The histological diagnosis was a myoepithelial carcinoma with an EWSR1::KLF15 fusion. Consistent with previously reported tumors harboring this fusion, a poorly differentiated small cell component was observed. Adjuvant chemotherapy comprising four cycles of ICpE and one cycle of IVE. At 11 months after completion of chemotherapy, there is no evidence of recurrent or metastatic disease.
{"title":"Intracardiac myoepithelial carcinoma with EWSR1::KLF15 fusion: A rare case of pediatric primary cardiac malignancy","authors":"L. Mwizerwa , V.L. Cousin , T. Sologashvili , J.P. Vallée , F. Gumy-Pause , J. Wacker , A.L. Rougemont","doi":"10.1016/j.carpath.2025.107728","DOIUrl":"10.1016/j.carpath.2025.107728","url":null,"abstract":"<div><div>Primary pediatric heart tumors are rare, and the vast majority are benign. Primary malignant cardiac tumors are exceedingly uncommon in this age group. Due to their rarity and overlapping imaging features with the more common benign tumors, the diagnosis of primary malignant cardiac tumors is particularly challenging. We report a case of a 12-year-old male with a 7-year history of a left ventricular mass that progressively increased in size, eventually requiring surgical resection. The histological diagnosis was a myoepithelial carcinoma with an <em>EWSR1::KLF15</em> fusion. Consistent with previously reported tumors harboring this fusion, a poorly differentiated small cell component was observed. Adjuvant chemotherapy comprising four cycles of ICpE and one cycle of IVE. At 11 months after completion of chemotherapy, there is no evidence of recurrent or metastatic disease.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"77 ","pages":"Article 107728"},"PeriodicalIF":2.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531287","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 : 2025-02-17DOI: 10.1016/j.carpath.2025.107726
L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth
Context
Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to document the historical basis for our contemporary understanding of atherosclerosis-based disease and to provide a rationale for continued support for autopsy-based research to make further progress in reducing the morbidity and mortality from atherosclerosis-related disease.
Objectives
To analyze the contributions of the autopsy-initiated pathological studies to complement and validate other lines of investigation in determining the pathology and pathogenesis of the leading worldwide cause of morbidity and mortality, namely, atherosclerosis and its major complications of coronary atherosclerosis, ischemic heart disease, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.
Data sources
Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction, and sudden cardiac death
Conclusions
Extensive published reports have confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for major diseases. This specifically has been shown by the analysis of atherosclerosis and its major manifestation of ischemic heart disease, as presented in this (Part I) and its companion (Part II) review. Autopsy-initiated pathological studies have documented the prevalence and natural history of atherosclerosis in different human populations in relationship to the prevalence of risk factors and established that the clinically silent phase of the disease begins in the first decades of life. Insights from these studies have been essential in developing and evaluating strategies for continued progress in preventing and controlling the disability and death associated with atherosclerotic heart disease.
{"title":"Insights from autopsy-initiated pathological studies of the pathogenesis and clinical manifestations of atherosclerosis and ischemic heart disease: Part I. Atherosclerosis","authors":"L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth","doi":"10.1016/j.carpath.2025.107726","DOIUrl":"10.1016/j.carpath.2025.107726","url":null,"abstract":"<div><h3>Context</h3><div>Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to document the historical basis for our contemporary understanding of atherosclerosis-based disease and to provide a rationale for continued support for autopsy-based research to make further progress in reducing the morbidity and mortality from atherosclerosis-related disease.</div></div><div><h3>Objectives</h3><div>To analyze the contributions of the autopsy-initiated pathological studies to complement and validate other lines of investigation in determining the pathology and pathogenesis of the leading worldwide cause of morbidity and mortality, namely, atherosclerosis and its major complications of coronary atherosclerosis, ischemic heart disease, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.</div></div><div><h3>Data sources</h3><div>Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction, and sudden cardiac death</div></div><div><h3>Conclusions</h3><div>Extensive published reports have confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for major diseases. This specifically has been shown by the analysis of atherosclerosis and its major manifestation of ischemic heart disease, as presented in this (Part I) and its companion (Part II) review. Autopsy-initiated pathological studies have documented the prevalence and natural history of atherosclerosis in different human populations in relationship to the prevalence of risk factors and established that the clinically silent phase of the disease begins in the first decades of life. Insights from these studies have been essential in developing and evaluating strategies for continued progress in preventing and controlling the disability and death associated with atherosclerotic heart disease.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"76 ","pages":"Article 107726"},"PeriodicalIF":2.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456995","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 : 2025-02-15DOI: 10.1016/j.carpath.2025.107727
L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth
Context
Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to retrospectively analyze the lines of research that generated the evidence for our contemporary understanding of atherosclerosis-based coronary artery disease and to provide a rationale for continued support for autopsy-based research in order to make further progress in reduction of the morbidity and mortaility from IHD.
Objectives
To analyze the contributions of the autopsy to complement and validate other lines of investigation in determining the complex interactions between coronary artery alterations linked to the major manifestations of coronary atherosclerosis, namely, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.
Data Sources
Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction and sudden cardiac death.
Conclusions
An extensive search of the published literature has confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for the treatment of atherosclerosis and its major manifestation, ischemic heart disease. This has been described in the Part I companion of the present review. Autopsy-initiated studies have documented the prevalence and clinicopathological significance of atherosclerosis in different human populations and its relationship to risk factors. It has been shown that the clinically silent phase of ischemic heart disease (IHD) begins in the first decades of life. Pathological studies have clarified the complex relationship between coronary atherosclerosis, coronary thrombosis, and myocardial ischemic events. These studies also have elucidated the pathological basis of sudden cardiac death. Insights from these studies also have been important in developing and evaluating strategies for continued progress in reducing the morbidity and mortality attributed to atherosclerosis and IHD.
{"title":"Insights from autopsy-initiated pathological studies of the pathogenesis and clinical manifestations of atherosclerosis and ischemic heart disease: Part II. Ischemic heart disease","authors":"L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth","doi":"10.1016/j.carpath.2025.107727","DOIUrl":"10.1016/j.carpath.2025.107727","url":null,"abstract":"<div><h3>Context</h3><div>Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to retrospectively analyze the lines of research that generated the evidence for our contemporary understanding of atherosclerosis-based coronary artery disease and to provide a rationale for continued support for autopsy-based research in order to make further progress in reduction of the morbidity and mortaility from IHD.</div></div><div><h3>Objectives</h3><div>To analyze the contributions of the autopsy to complement and validate other lines of investigation in determining the complex interactions between coronary artery alterations linked to the major manifestations of coronary atherosclerosis, namely, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.</div></div><div><h3>Data Sources</h3><div>Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction and sudden cardiac death.</div></div><div><h3>Conclusions</h3><div>An extensive search of the published literature has confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for the treatment of atherosclerosis and its major manifestation, ischemic heart disease. This has been described in the Part I companion of the present review. Autopsy-initiated studies have documented the prevalence and clinicopathological significance of atherosclerosis in different human populations and its relationship to risk factors. It has been shown that the clinically silent phase of ischemic heart disease (IHD) begins in the first decades of life. Pathological studies have clarified the complex relationship between coronary atherosclerosis, coronary thrombosis, and myocardial ischemic events. These studies also have elucidated the pathological basis of sudden cardiac death. Insights from these studies also have been important in developing and evaluating strategies for continued progress in reducing the morbidity and mortality attributed to atherosclerosis and IHD.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"76 ","pages":"Article 107727"},"PeriodicalIF":2.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432313","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}
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