{"title":"Long term cardiovascular effects on COVID-19 infection in children. The need for monitoring","authors":"Dareilena Karaviti , Marietta Charakida , Dimitra Dimopoulou , Antonios Marmarinos , Maria Papadaki , Despoina Maritsi , Nikos Spyridis , Margaritis Avgeris , Dimitrios Gourgiotis , Aggeliki Syggelou , Maria Tsolia","doi":"10.1016/j.ijcard.2026.134188","DOIUrl":"10.1016/j.ijcard.2026.134188","url":null,"abstract":"<div><h3>Background</h3><div>Although SARS-CoV-2 infection has been associated with mild illness in children, concerns have emerged regarding potential long-term cardiovascular and systemic effects, even in previously healthy pediatric populations.</div></div><div><h3>Objective</h3><div>The aim of this study is to assess cardiac function and long-term symptoms in children up to one year after COVID-19 infection, and to compare these findings with healthy controls without prior SARS-CoV-2 exposure.</div></div><div><h3>Methods</h3><div>In this prospective case-control study, children aged 4–17 years were divided into two groups: those with a confirmed history of COVID-19 (Group 1) and healthy controls (Group 2). Participants underwent echocardiographic evaluation—including global longitudinal strain (GLS) analysis and biochemical testing, including lipid profile and intracellular adhesion molecule −1 (ICAM-1) measurements. A structured symptom survey was used to assess cardiovascular and systemic long-COVID manifestations.</div></div><div><h3>Results</h3><div>Conventional echocardiographic indices did not differ significantly between groups. However, Group 1 showed a persistent reduction in left ventricular GLS, indicating subclinical myocardial dysfunction (<em>p</em> < 0.05). Long-COVID symptoms were reported in 23.6% of children in Group 1, with fatigue being the most common (16.6%), followed by palpitations (2.0%). Lipid profiles were similar between groups, although children with moderate to severe infections exhibited significantly elevated serum intracellular adhesion molecule-1 (sICAM-1) levels, suggestive of endothelial activation.</div></div><div><h3>Conclusion</h3><div>Even in the absence of overt cardiovascular disease, children with prior SARS-CoV-2 infection experience persistent subclinical cardiac changes and symptoms consistent with Long-COVID. These findings highlight the need for ongoing surveillance and comprehensive cardiovascular assessments in pediatric populations following COVID-19 infection.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134188"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qi Lou , Rui Bai , Luyifei Li , Bingqing Lu , Xiaoming Ai , Guangzhong Liu
{"title":"Targeting ADAMTS4 aggravates myocardial ischemia-reperfusion injury by impairing endothelial integrity and accelerating leukocyte infiltration","authors":"Qi Lou , Rui Bai , Luyifei Li , Bingqing Lu , Xiaoming Ai , Guangzhong Liu","doi":"10.1016/j.ijcard.2026.134195","DOIUrl":"10.1016/j.ijcard.2026.134195","url":null,"abstract":"<div><h3>Background</h3><div>Myocardial ischemia-reperfusion injury (MIRI) is an inevitable consequence of reperfusion therapy and a major determinant of patient prognosis. ADAM Metallopeptidase with Thrombospondin Type 1 Motif 4 (ADAMTS4) is a metalloproteinase that has been implicated in endothelial damage and inflammatory cascades, yet its role in MIRI remains undefined.</div></div><div><h3>Methods</h3><div>MIRI was modeled in mice by left coronary artery ligation and subsequently subjected to mRNA sequencing. The role of ADAMTS4 was then dissected in vivo in these MIRI mice and in vitro in cardiac endothelial cells (ECs) exposed to oxygen-glucose deprivation/reoxygenation (OGD/R), using both primary murine cardiac ECs and human cardiac microvascular ECs (hCMECs).</div></div><div><h3>Results</h3><div>ADAMTS4 was markedly up-regulated in MIRI mouse myocardium and in both primary murine cardiac ECs and hCMECs subjected to OGD/R. ADAMTS4 inhibition preserved cardiac function, shrank infarct size, and attenuated cardiomyocyte damage. At the microvascular level, ADAMTS4 silencing restored CD31 and VE-Cadherin expression, curbed leukocyte adhesion molecules, and lowered tissue myeloperoxidase activity together with pro-inflammatory cytokines. Consequently, endothelial barrier dysfunction and leukocyte transmigration provoked by OGD/R were largely reversed. Mechanistic studies suggested that ADAMTS4 may be transcriptionally regulated by FosB and JunB. Upregulation of FosB or JunB significantly enhanced the transcriptional activity of ADAMTS4. Moreover, overexpression of ADAMTS4 abrogated the protection afforded by FosB/JunB knockdown, establishing ADAMTS4 as the critical downstream executor of activating protein-1 mediated injury in MIRI.</div></div><div><h3>Conclusion</h3><div>Overall, we established that FosB and JunB transcriptionally upregulate ADAMTS4, which in turn dismantles the cardiac endothelial barrier and fuels leukocyte infiltration to exacerbate MIRI.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134195"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146062805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advancing risk stratification in normotensive pulmonary embolism — The contribution of TELOS-plus","authors":"Kotaro Nochioka","doi":"10.1016/j.ijcard.2026.134186","DOIUrl":"10.1016/j.ijcard.2026.134186","url":null,"abstract":"","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134186"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhiyu Zhang , Zeye Liu , Ke Li , Haiyang Xie , Hailu Wang , Qi Li , Fajar Prasetya , Xi Chen , Yifan Chen , Yiyin Zhang
{"title":"Deciphering the role of circulating inflammatory proteins in myocarditis: Novel strategies for targeted therapy","authors":"Zhiyu Zhang , Zeye Liu , Ke Li , Haiyang Xie , Hailu Wang , Qi Li , Fajar Prasetya , Xi Chen , Yifan Chen , Yiyin Zhang","doi":"10.1016/j.ijcard.2026.134198","DOIUrl":"10.1016/j.ijcard.2026.134198","url":null,"abstract":"<div><h3>Aims</h3><div>Myocarditis is closely linked to immune dysregulation, yet the causal roles of circulating inflammatory proteins in its development remain incompletely understood. This study aimed to explore whether specific inflammatory proteins are causally associated with myocarditis and to assess their potential translational relevance.</div></div><div><h3>Methods</h3><div>We applied a two-sample Mendelian randomization (MR) using genome-wide association studies (GWAS) summary statistics for 91 circulating inflammatory proteins and myocarditis to identify causal associations. Candidate targets were refined through differential gene expression analysis of GEO datasets, followed by enrichment and protein–protein interaction (PPI) analyses. Cell-type–specific expression was confirmed using single-cell RNA sequencing (scRNA-seq) of myocarditis tissue. Drug prediction and molecular docking analyses were performed for the key target.</div></div><div><h3>Results</h3><div>MR identified interleukin-10 receptor subunit beta (IL10RB) and leukemia inhibitory factor (LIF) as potential causal proteins for myocarditis. LIF was prioritized as a key candidate target via transcriptomics, enrichment, and PPI analysis. scRNA-seq showed high LIF expression in dendritic cells, mural cells, and fibroblasts. Drug prediction and docking evaluated its therapeutic potential.</div></div><div><h3>Conclusions</h3><div>Elevated circulating LIF levels may be causally linked to increased myocarditis risk, supporting its potential as both a predictive biomarker and a therapeutic target. These results provide a rationale for further experimental studies to clarify the context-dependent roles of LIF in myocardial inflammation and to evaluate LIF-directed interventions.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134198"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dafni Korela , Emmanouil Foukarakis , Ioannis Zaganas , Minas Drakos , Anthοula Plevritaki , Spyros Maragkoudakis , Alexandros Patrianakos , Nikolaos Kapsoritakis , Sophia Koukouraki , Olga Bourogianni , Charalampos Pontikoglou , Maria Psillaki , Helen A. Padadaki , Dimitris Samonakis , Efstathios Detorakis , Ioannis Petrakis , Kostas Stylianou , Gregory Chlouverakis , Emmanouil Giannakoudakis , Aneta Aleksova , Maria Marketou
{"title":"Cardiac remodeling and arterial stiffness progression in wild-type vs hereditary transthyretin amyloidosis in Crete","authors":"Dafni Korela , Emmanouil Foukarakis , Ioannis Zaganas , Minas Drakos , Anthοula Plevritaki , Spyros Maragkoudakis , Alexandros Patrianakos , Nikolaos Kapsoritakis , Sophia Koukouraki , Olga Bourogianni , Charalampos Pontikoglou , Maria Psillaki , Helen A. Padadaki , Dimitris Samonakis , Efstathios Detorakis , Ioannis Petrakis , Kostas Stylianou , Gregory Chlouverakis , Emmanouil Giannakoudakis , Aneta Aleksova , Maria Marketou","doi":"10.1016/j.ijcard.2025.134145","DOIUrl":"10.1016/j.ijcard.2025.134145","url":null,"abstract":"<div><h3>Background</h3><div>Hereditary transthyretin amyloidosis (hATTR) and wild-type transthyretin amyloidosis (ATTRwt) are two distinct forms of cardiac amyloidosis (CA) differing in genetics, clinical progression, and cardiac remodeling patterns. Understanding these differences is critical for accurate diagnosis and personalized management. This study compared cardiac remodeling progression and arterial stiffness in patients with wild-type and hereditary transthyretin CA in a well-characterized Cretan cohort.</div></div><div><h3>Methods</h3><div>We prospectively enrolled 39 CA patients who underwent TTR genotyping and comprehensive clinical, echocardiographic, and vascular assessments, including pulse wave velocity (PWV). Functional capacity and quality of life were evaluated at baseline and six months after tafamidis initiation.</div></div><div><h3>Results</h3><div>Pathogenic TTR variants were identified in 56 %, mainly pVal114Ala (38.5 %) and pVal50Met (18 %). Mutation carriers were younger (60.8 versus 79.1 years, <em>p</em> < 0.001) and had better functional capacity (6-min walk test, 439 ± 121 m vs. 351 ± 103 m, <em>p</em> = 0.021) and superior myocardial strain (global longitudinal strain) than ATTRwt-CA patients. hATTR-CA showed less left ventricular hypertrophy and atrial dilation. Arterial stiffness (carotid-radial PWV) was higher in hATTR both at baseline and follow-up (<em>p</em> < 0.05), with a trend toward improvement post-treatment. Quality of life favored hATTR after six months. ATTRwt patients showed a trend toward left ventricular hypertrophy regression absent in hATTR.</div></div><div><h3>Conclusions</h3><div>TTR genotype influences cardiac remodeling, vascular involvement, and function in CA. hATTR patients with pVal50Met and pVal114Ala variants are younger with better myocardial function but increased arterial stiffness compared to ATTRwt. Our findings indicate the need for genotype-specific assessment and management.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134145"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145959210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rita Barbosa Sousa , Maria Rita Lima , Pedro M. Lopes , Pedro Freitas , Francisco Gama , Cláudia Silva , Sara Guerreiro , João Abecasis , Ana Coutinho Santos , Carla Saraiva , Pedro Adragão , António M. Ferreira
{"title":"Impact of using the 2024 ESC guideline-recommended method to estimate the likelihood of obstructive coronary disease - a cardiac CT study","authors":"Rita Barbosa Sousa , Maria Rita Lima , Pedro M. Lopes , Pedro Freitas , Francisco Gama , Cláudia Silva , Sara Guerreiro , João Abecasis , Ana Coutinho Santos , Carla Saraiva , Pedro Adragão , António M. Ferreira","doi":"10.1016/j.ijcard.2026.134209","DOIUrl":"10.1016/j.ijcard.2026.134209","url":null,"abstract":"<div><h3>Introduction</h3><div>The 2024 ESC guidelines on chronic coronary syndromes integrated cardiovascular risk factors to estimate the pre-test probability (PTP) of obstructive coronary artery disease (CAD). Additionally, coronary artery calcium score (CACS) was proposed to reclassify patients with low PTP. We aimed to assess the impact of these new recommendations.</div></div><div><h3>Methods</h3><div>Single-center cross-sectional study including 1595 patients undergoing coronary computed tomography angiography (CCTA) for suspected CAD. Obstructive CAD was defined as ≥50% stenosis on CCTA, with reclassification based on downstream invasive or non-invasive test results when available. Discrimination, calibration, and reclassification were evaluated.</div></div><div><h3>Results</h3><div>Obstructive CAD prevalence was 14.0% (<em>n</em> = 223). Compared to the 2019 ESC-PTP, 2024 ESC-PTP showed improved discrimination [C-statistics of 0.76 (95%CI: 0.74–0.78) vs 0.74 (95%CI: 0.72–0.77), <em>p</em> = 0.042]. Regarding calibration, the 2019 ESC-PTP overestimated the likelihood of CAD (intercept −0.23, 95%CI: −0.38 to −0.09), while the 2024 ESC-PTP underestimated it (intercept 0.26, 95%CI: 0.11 to 0.41). The 2024 ESC-PTP reclassified 47.3% (<em>n</em> = 755) of patients, with 97.2% (<em>n</em> = 734) moving to a lower PTP category. Using CACS in patients with low PTP by the 2024 ESC-PTP (<em>n</em> = 617) would reclassify 41.3% (<em>n</em> = 255) to very low PTP. Of these, 1.6% (<em>n</em> = 4) had obstructive CAD.</div></div><div><h3>Conclusions</h3><div>The 2024 ESC-PTP model, calibrated to obstructive CAD defined by invasive coronary angiography, demonstrates slightly improved discrimination, but appears to underestimate the likelihood of CAD when evaluated against CCTA-defined disease. These guideline recommendations could obviate further testing in approximately half of the population, at the cost of 2% missed diagnoses.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134209"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Assessment of left ventricular mechanical synchrony and intraventricular blood flow energy in ischemic heart disease using a hybrid positron emission tomography-magnetic resonance system","authors":"Ayano Ikeda , Kenji Fukushima , Sachika Ishii , Keiichiro Endo , Masataka Katahira , Naoyuki Ukon , Ryo Yamakuni , Takatoyo Kiko , Takeshi Shimizu , Shiro Ishii , Masayoshi Oikawa , Hiroshi Ito , Yasuchika Takeishi","doi":"10.1016/j.ijcard.2026.134200","DOIUrl":"10.1016/j.ijcard.2026.134200","url":null,"abstract":"<div><h3>Backgrounds</h3><div>We aimed to simultaneously investigate the relationship between left ventricular (LV) mechanical synchrony and intra-LV blood flow energy in patients with ischemic heart disease (IHD) using hybrid PET/MR.</div></div><div><h3>Methods</h3><div>Sixty-six patients (mean age 67 years, male 54) who underwent rest-pharmacological stress <sup>13</sup>N ammonia PET and 4D flow MR were included. Left ventricular ejection fraction (LVEF), phase analysis (PA) parameters including histogram bandwidth (BW), phase standard deviation (PSD), and entropy were obtained from gated PET. Perfusion defect was assessed as summed defect score from static PET images. Intra-LV 4D flow MR acquisition was simultaneously performed for rest and stress. Intra-LV blood flow kinetic energy (KE mJ) was obtained from dynamic flow curve, and indexed with end-diastolic volume (KEi mJ/mL).</div></div><div><h3>Results</h3><div>A significant positive correlation was observed between LVEF and KEi at rest and stress (<em>r</em> = 0.30, <em>p</em> = 0.014; <em>r</em> = 0.42, <em>p</em> < 0.0001 for rest and stress, respectively). In contrast, summed defect score did not show a significant correlation to KEi. All PA parameters demonstrated a weak inverse correlation with KEi at rest (BW: <em>r</em> = −0.26, <em>p</em> = 0.019; PSD <em>r</em> = −0.27, <em>p</em> = 0.026; entropy r = −0.27, <em>p</em> = 0.031) and stress (BW: <em>r</em> = −0.29, <em>p</em> = 0.016; PSD <em>r</em> = −0.37, <em>p</em> = 0.0021; entropy <em>r</em> = −0.33, <em>p</em> = 0.0062).</div></div><div><h3>Conclusion</h3><div>PET derived PA was associated with intra-LV blood flow energy, suggesting impaired LV mechanical synchrony is linked to intra-LV blood flow insufficiency. These findings highlight the novel assessment of PA in clinical practice for IHD.</div></div>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":"449 ","pages":"Article 134200"},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}