We present a previously unrecognized, reversible cause for complete atrioventricular block in the sick neonate. An 18 day old 33 weeker with Tetralogy of Fallot was admitted with sinus rhythm on ECG. Soon after, the baby developed episodes of apnea during which ECG showed complete atrioventricular block. This was unresponsive to atropine and isoprenaline, and heart rate continued to deteriorate. Mechanical ventilation was initiated in view of the critical condition and in preparation for an emergency temporary pacing wire insertion. Remarkably, ventilation restored sinus rhythm. The probable mechanisms by which apnea and acute hypoxia can cause atrioventricular block include carotid chemoreceptor mediated reflex vagal stimulation, depression of atrioventricular nodal conduction, and increase in endogenous adenosine levels. It is prudent to consider this reversible mechanism in the differential diagnosis of new onset atrioventricular block in the sick neonate, as early recognition may help avoid unnecessary invasive interventions.
{"title":"Apnea mediated transient complete atrioventricular block in a pre-term neonate","authors":"Sakthi Saravanan , Navaneetha Sasikumar , Raman Krishna Kumar","doi":"10.1016/j.ppedcard.2025.101866","DOIUrl":"10.1016/j.ppedcard.2025.101866","url":null,"abstract":"<div><div>We present a previously unrecognized, reversible cause for complete atrioventricular block in the sick neonate. An 18 day old 33 weeker with Tetralogy of Fallot was admitted with sinus rhythm on ECG. Soon after, the baby developed episodes of apnea during which ECG showed complete atrioventricular block. This was unresponsive to atropine and isoprenaline, and heart rate continued to deteriorate. Mechanical ventilation was initiated in view of the critical condition and in preparation for an emergency temporary pacing wire insertion. Remarkably, ventilation restored sinus rhythm. The probable mechanisms by which apnea and acute hypoxia can cause atrioventricular block include carotid chemoreceptor mediated reflex vagal stimulation, depression of atrioventricular nodal conduction, and increase in endogenous adenosine levels. It is prudent to consider this reversible mechanism in the differential diagnosis of new onset atrioventricular block in the sick neonate, as early recognition may help avoid unnecessary invasive interventions.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"79 ","pages":"Article 101866"},"PeriodicalIF":0.8,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Childhood and adolescent obesity have emerged as significant public health concerns, contributing to an increased risk of cardiovascular disease (CVD) later in life. Over the past four decades, extensive research has examined the relationship between obesity and CVD among young populations, highlighting the need for early intervention strategies. Bibliometric analysis offers a comprehensive overview of research trends, influential studies, and key thematic areas within this field.
Aim of review
This study aims to map the scientific landscape of global research on obesity and cardiovascular disease among children and adolescents from 1984 to 2024. By employing bibliometric methods, we identify prolific authors, leading institutions, impactful publications, and emerging research themes, providing insights into the evolution of this critical area of study.
Key scientific concepts of review
The bibliometric analysis was conducted using the Scopus database, focusing on publication trends, citation networks, and keyword co-occurrence patterns. The study identifies research hotspots, including metabolic risk factors, lifestyle interventions, genetic predisposition, and public health policies targeting obesity-related CVD in young populations. Additionally, the review highlights collaborative networks among global researchers and suggests future directions for advancing knowledge and policy-making in this domain.
{"title":"Global trends in obesity and cardiovascular disease research among children and adolescents: A bibliometric analysis (1984–2024)","authors":"Deepanshi Saxena , Sudip Bhattacharya , Akanksha Singh , Alok Singh","doi":"10.1016/j.ppedcard.2025.101867","DOIUrl":"10.1016/j.ppedcard.2025.101867","url":null,"abstract":"<div><h3>Background</h3><div>Childhood and adolescent obesity have emerged as significant public health concerns, contributing to an increased risk of cardiovascular disease (CVD) later in life. Over the past four decades, extensive research has examined the relationship between obesity and CVD among young populations, highlighting the need for early intervention strategies. Bibliometric analysis offers a comprehensive overview of research trends, influential studies, and key thematic areas within this field.</div></div><div><h3>Aim of review</h3><div>This study aims to map the scientific landscape of global research on obesity and cardiovascular disease among children and adolescents from 1984 to 2024. By employing bibliometric methods, we identify prolific authors, leading institutions, impactful publications, and emerging research themes, providing insights into the evolution of this critical area of study.</div></div><div><h3>Key scientific concepts of review</h3><div>The bibliometric analysis was conducted using the Scopus database, focusing on publication trends, citation networks, and keyword co-occurrence patterns. The study identifies research hotspots, including metabolic risk factors, lifestyle interventions, genetic predisposition, and public health policies targeting obesity-related CVD in young populations. Additionally, the review highlights collaborative networks among global researchers and suggests future directions for advancing knowledge and policy-making in this domain.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"79 ","pages":"Article 101867"},"PeriodicalIF":0.8,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144988374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-09DOI: 10.1016/j.ppedcard.2025.101869
Sara I. Abo Elnour , Mahmoud I. Abo Elnour , Heba A. Borayek
Background
The fat surrounding the kidney, heart, and increased carotid intima media thickness (CIMT) have been closely related to adverse cardiovascular outcomes in children with end stage kidney disease (ESKD).
Objectives
To evaluate epicardial fat thickness (EFT), perirenal fat thickness (PFT), and CIMT in hemodialysis patients and to assess the risk factors for increasing the thickness of these parameters.
Methods
This case-control study included 60 children with ESKD on regular hemodialysis and 60 apparently healthy children. EFT was measured using two-dimensional echocardiography, whereas CIMT and PFT were measured utilizing neck Doppler and abdominal ultrasound, respectively.
Results
The case group had significantly impaired systolic function with lower ejection fraction (EF) (mean = −0.87 ± 1.3) compared to the control group (mean = 0.33 ± 0.48, p < 0.0001) and impaired diastolic function with Tei index significantly higher in cases (mean = 0.56) compared to controls (0.37). We found a significant increase in EFT, CIMT, and PFT in cases compared to controls (all p < 0.001). We observed significant positive correlations between PFT and duration of hemodialysis (r = 0.412, p = 0.024), serum urea (r = 0.370, p = 0.044), and serum creatinine (r = 0.373, p = 0.042). We found positive correlations between EFT and each of the interventricular septum (IVS) thickness (r = 0.462, p = 0.042) and left ventricular end diastolic diameter (LVEDD) (r = 0.508, p = 0.004).
Conclusion
Children with ESKD who undergo regular hemodialysis have left ventricular systolic and diastolic dysfunction. The EFT, CIMT, and PFT were higher in children with ESKD. PFT was positively associated with duration of hemodialysis, LVEDD, and Tei index. EFT was positively correlated with IVS thickness and LVEDD. Rather than using broad measures of total adiposity, assessments of PFT, CIMT, and epicardial fat are more practical techniques for assessing cardiovascular risk in children with ESKD.
研究背景：终末期肾病（ESKD）患儿肾脏、心脏周围的脂肪和颈动脉内膜中膜厚度（CIMT）的增加与不良心血管结局密切相关。目的评价血液透析患者心外膜脂肪厚度（EFT）、肾周脂肪厚度（PFT）和CIMT，并探讨其厚度升高的危险因素。方法本研究纳入60例定期血液透析的ESKD患儿和60例表面健康的患儿。使用二维超声心动图测量EFT，而使用颈部多普勒和腹部超声分别测量CIMT和PFT。结果与对照组（平均= 0.33±0.48,p < 0.0001）相比，病例组收缩功能明显受损，射血分数（EF）较低（平均= - 0.87±1.3）；舒张功能受损，Tei指数显著高于对照组（平均= 0.56）。我们发现，与对照组相比，病例中EFT、CIMT和PFT显著增加（均p <； 0.001）。我们观察到PFT与血液透析持续时间（r = 0.412, p = 0.024）、血清尿素（r = 0.370, p = 0.044）和血清肌酐（r = 0.373, p = 0.042）呈正相关。我们发现EFT与室间隔（IVS）厚度（r = 0.462, p = 0.042）和左室舒张末期内径（LVEDD） （r = 0.508, p = 0.004）呈正相关。结论ESKD患儿经定期血液透析后存在左室收缩和舒张功能障碍。ESKD患儿的EFT、CIMT和PFT较高。PFT与血液透析持续时间、LVEDD和Tei指数呈正相关。EFT与IVS厚度、LVEDD呈正相关。评估PFT、CIMT和心外膜脂肪是评估ESKD儿童心血管风险的更实用的技术，而不是使用广泛的总脂肪测量方法。
{"title":"Cardiorenal fat, and carotid intima media thickness in children with end stage kidney disease in Fayoum governorate","authors":"Sara I. Abo Elnour , Mahmoud I. Abo Elnour , Heba A. Borayek","doi":"10.1016/j.ppedcard.2025.101869","DOIUrl":"10.1016/j.ppedcard.2025.101869","url":null,"abstract":"<div><h3>Background</h3><div>The fat surrounding the kidney, heart, and increased carotid intima media thickness (CIMT) have been closely related to adverse cardiovascular outcomes in children with end stage kidney disease (ESKD).</div></div><div><h3>Objectives</h3><div>To evaluate epicardial fat thickness (EFT), perirenal fat thickness (PFT), and CIMT in hemodialysis patients and to assess the risk factors for increasing the thickness of these parameters.</div></div><div><h3>Methods</h3><div>This case-control study included 60 children with ESKD on regular hemodialysis and 60 apparently healthy children. EFT was measured using two-dimensional echocardiography, whereas CIMT and PFT were measured utilizing neck Doppler and abdominal ultrasound, respectively.</div></div><div><h3>Results</h3><div>The case group had significantly impaired systolic function with lower ejection fraction (EF) (mean = −0.87 ± 1.3) compared to the control group (mean = 0.33 ± 0.48, <em>p</em> < 0.0001) and impaired diastolic function with Tei index significantly higher in cases (mean = 0.56) compared to controls (0.37). We found a significant increase in EFT, CIMT, and PFT in cases compared to controls (all <em>p</em> < 0.001). We observed significant positive correlations between PFT and duration of hemodialysis (<em>r</em> = 0.412, <em>p</em> = 0.024), serum urea (<em>r</em> = 0.370, <em>p</em> = 0.044), and serum creatinine (<em>r</em> = 0.373, <em>p</em> = 0.042). We found positive correlations between EFT and each of the interventricular septum (IVS) thickness (<em>r</em> = 0.462, p = 0.042) and left ventricular end diastolic diameter (LVEDD) (<em>r</em> = 0.508, <em>p</em> = 0.004).</div></div><div><h3>Conclusion</h3><div>Children with ESKD who undergo regular hemodialysis have left ventricular systolic and diastolic dysfunction. The EFT, CIMT, and PFT were higher in children with ESKD. PFT was positively associated with duration of hemodialysis, LVEDD, and Tei index. EFT was positively correlated with IVS thickness and LVEDD. Rather than using broad measures of total adiposity, assessments of PFT, CIMT, and epicardial fat are more practical techniques for assessing cardiovascular risk in children with ESKD.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"79 ","pages":"Article 101869"},"PeriodicalIF":0.8,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-07DOI: 10.1016/j.ppedcard.2025.101865
Anusha Bai Kalithkar , Juanita Hunter
Fetal tachyarrhythmia, defined as a fetal heart rate exceeding 180 beats per minute, is one of the common indications for referral to fetal cardiology. Emerging data suggest an increased incidence of fetal arrhythmias in pregnancies complicated by maternal COVID-19 infection. We report a case of fetal SVT in the setting of maternal COVID-19 infection and outline the clinical approach and therapeutic strategies employed in management.
{"title":"Incessant fetal supraventricular tachycardia in a COVID-19 positive pregnancy","authors":"Anusha Bai Kalithkar , Juanita Hunter","doi":"10.1016/j.ppedcard.2025.101865","DOIUrl":"10.1016/j.ppedcard.2025.101865","url":null,"abstract":"<div><div>Fetal tachyarrhythmia, defined as a fetal heart rate exceeding 180 beats per minute, is one of the common indications for referral to fetal cardiology. Emerging data suggest an increased incidence of fetal arrhythmias in pregnancies complicated by maternal COVID-19 infection. We report a case of fetal SVT in the setting of maternal COVID-19 infection and outline the clinical approach and therapeutic strategies employed in management.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"79 ","pages":"Article 101865"},"PeriodicalIF":0.8,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-17DOI: 10.1016/j.ppedcard.2025.101861
Ahmed Abdulgawad , Ahmed Mansour , Mohammed Bin Joubah , Yasser Balubaid , Gaser Abdelmohsen
Background
Lactic acidosis is a critical metabolic derangement frequently observed following pediatric cardiac surgery, often attributed to low cardiac output and resultant tissue hypoperfusion. However, thiamine deficiency can disrupt aerobic metabolism, leading to excessive lactate accumulation. Infants undergoing complex surgical interventions risk developing thiamine deficiency in the postoperative period, especially if prolonged parenteral nutrition is administered without adequate supplementation.
Case description
A full-term female neonate diagnosed with transposition of the great arteries underwent an arterial switch operation on day 11 of life. Her postoperative course was complicated by feeding intolerance, suspected necrotizing enterocolitis (NEC), and prolonged parenteral nutrition (TPN). Despite the resolution of sepsis and NEC being ruled out, persistent lactic acidosis and feeding intolerance continued. On postoperative day 57, thiamine deficiency was suspected and treated with intravenous supplementation. After thiamin therapy, there was a rapid decline in lactate levels (from 14 mmol/L to <2 mmol/L within 24 h) and resolution of clinical symptoms.
Conclusion
This case illustrates how thiamine deficiency may contribute to persistent lactic acidosis and feeding intolerance in neonates receiving prolonged TPN following complex cardiac surgery, underscoring the value of considering nutritional deficiencies in the differential diagnosis. Early recognition and timely supplementation can significantly improve outcomes, emphasizing the need for clinical awareness and routine thiamine supplementation in high-risk postoperative care.
{"title":"Prolonged lactic acidosis following congenital cardiac surgery: A case report highlighting the potential role of thiamine deficiency","authors":"Ahmed Abdulgawad , Ahmed Mansour , Mohammed Bin Joubah , Yasser Balubaid , Gaser Abdelmohsen","doi":"10.1016/j.ppedcard.2025.101861","DOIUrl":"10.1016/j.ppedcard.2025.101861","url":null,"abstract":"<div><h3>Background</h3><div>Lactic acidosis is a critical metabolic derangement frequently observed following pediatric cardiac surgery, often attributed to low cardiac output and resultant tissue hypoperfusion. However, thiamine deficiency can disrupt aerobic metabolism, leading to excessive lactate accumulation. Infants undergoing complex surgical interventions risk developing thiamine deficiency in the postoperative period, especially if prolonged parenteral nutrition is administered without adequate supplementation.</div></div><div><h3>Case description</h3><div>A full-term female neonate diagnosed with transposition of the great arteries underwent an arterial switch operation on day 11 of life. Her postoperative course was complicated by feeding intolerance, suspected necrotizing enterocolitis (NEC), and prolonged parenteral nutrition (TPN). Despite the resolution of sepsis and NEC being ruled out, persistent lactic acidosis and feeding intolerance continued. On postoperative day 57, thiamine deficiency was suspected and treated with intravenous supplementation. After thiamin therapy, there was a rapid decline in lactate levels (from 14 mmol/L to <2 mmol/L within 24 h) and resolution of clinical symptoms.</div></div><div><h3>Conclusion</h3><div>This case illustrates how thiamine deficiency may contribute to persistent lactic acidosis and feeding intolerance in neonates receiving prolonged TPN following complex cardiac surgery, underscoring the value of considering nutritional deficiencies in the differential diagnosis. Early recognition and timely supplementation can significantly improve outcomes, emphasizing the need for clinical awareness and routine thiamine supplementation in high-risk postoperative care.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"78 ","pages":"Article 101861"},"PeriodicalIF":0.6,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144685455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-14DOI: 10.1016/j.ppedcard.2025.101860
E. McGovern , L. Bezold , D. Winlaw , N.J. Ollberding , M.M. Hossain , S. Shahanavaz
Background
From 2006 to 2015, Kentucky had the highest rate of infant mortality attributable to congenital heart disease (CHD) in the USA. Across the country, mortality was associated with male sex, prematurity, non-Hispanic black race, lower maternal education, higher % of poverty, and increasing distance from a top 50 cardiac center.
Objectives
We sought to update these observations during a more contemporary era, with specific emphasis on Kentucky's performance.
Methods
The National Center for Health Statistics linked birth and infant death period data sets from 2016 to 2020 were used to calculate the incidence of CHD infant mortality. Chi-square tests were conducted to test for differences in deaths according to factors of interest for the entire USA and Kentucky. We also examined the mortality rate in Kentucky, which differed from 2016 to 2017 vs. 2018–2020, which coincided with the creation of a joint program between one of Kentucky's pediatric cardiac centers and a top 50 center in Ohio.
Results
There was a national trend for improvement in CHD infant mortality. The national mortality rate in 2016–2020 was 0.3 deaths per 1000 live births compared to 0.34 in 2006–2015 (p < 0.001). Kentucky was no longer among the worst in the USA. In the USA, male sex, prematurity, non-Hispanic black race, lower level of maternal education, and healthcare payment not by private insurance were associated with a higher incidence of mortality (p < 0.001). For Kentucky, prematurity, non-Hispanic black race, poverty, and healthcare payment other than private insurance increased CHD infant mortality. Mortality rates in Kentucky for 2016–2017 and 2018–2020 were similar.
Conclusion
CHD infant mortality improved in the more contemporary era, and Kentucky was no longer the worst performing state. Male sex, prematurity, non-Hispanic black race, lower level of maternal education, and poverty continue to be associated with a higher incidence of CHD infant mortality.
{"title":"CHD infant mortality disparities in the USA: Positive changes in the previously worst performing state","authors":"E. McGovern , L. Bezold , D. Winlaw , N.J. Ollberding , M.M. Hossain , S. Shahanavaz","doi":"10.1016/j.ppedcard.2025.101860","DOIUrl":"10.1016/j.ppedcard.2025.101860","url":null,"abstract":"<div><h3>Background</h3><div>From 2006 to 2015, Kentucky had the highest rate of infant mortality attributable to congenital heart disease (CHD) in the USA. Across the country, mortality was associated with male sex, prematurity, non-Hispanic black race, lower maternal education, higher % of poverty, and increasing distance from a top 50 cardiac center.</div></div><div><h3>Objectives</h3><div>We sought to update these observations during a more contemporary era, with specific emphasis on Kentucky's performance.</div></div><div><h3>Methods</h3><div>The National Center for Health Statistics linked birth and infant death period data sets from 2016 to 2020 were used to calculate the incidence of CHD infant mortality. Chi-square tests were conducted to test for differences in deaths according to factors of interest for the entire USA and Kentucky. We also examined the mortality rate in Kentucky, which differed from 2016 to 2017 vs. 2018–2020, which coincided with the creation of a joint program between one of Kentucky's pediatric cardiac centers and a top 50 center in Ohio.</div></div><div><h3>Results</h3><div>There was a national trend for improvement in CHD infant mortality. The national mortality rate in 2016–2020 was 0.3 deaths per 1000 live births compared to 0.34 in 2006–2015 (<em>p</em> < 0.001). Kentucky was no longer among the worst in the USA. In the USA, male sex, prematurity, non-Hispanic black race, lower level of maternal education, and healthcare payment not by private insurance were associated with a higher incidence of mortality (<em>p</em> < 0.001). For Kentucky, prematurity, non-Hispanic black race, poverty, and healthcare payment other than private insurance increased CHD infant mortality. Mortality rates in Kentucky for 2016–2017 and 2018–2020 were similar.</div></div><div><h3>Conclusion</h3><div>CHD infant mortality improved in the more contemporary era, and Kentucky was no longer the worst performing state. Male sex, prematurity, non-Hispanic black race, lower level of maternal education, and poverty continue to be associated with a higher incidence of CHD infant mortality.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"78 ","pages":"Article 101860"},"PeriodicalIF":0.8,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144721315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-10DOI: 10.1016/j.ppedcard.2025.101859
Peter Rippey , Jada Ashford , Zachariah El-fallah , Korey Shively , Jorge Sucar , Christian Cooper , Emily Ribeiro , Samantha Glenn Etheredge , Cade C. Smelley , Lynn A. Batten
Background
Sudden cardiac arrest occurs in 1 per 50,000 to 80,000 people per year. Preparticipation screening may identify athletes who may be at risk for developing sudden cardiac arrest.
Aim of review
The purpose of this article is to review the etiologies of sudden cardiac arrest, preparticipation screening, and use of electrocardiograms in screening athletes for cardiac problems.
Key scientific concepts of review
Sudden cardiac arrest may occur in young athletes who have hypertrophic cardiomyopathy, anomalous origin of a coronary artery, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, aortic dissection, myocarditis, Wolff-Parkinson-White syndrome, long QT syndrome, Brugada syndrome, commotio cordis, aortic valve stenosis, coarctation of the aorta, congenital heart block, short QT syndrome, or coronary artery disease. Preparticipation screening may include history, physical examination, and an electrocardiogram. Several guidelines for screening are available. The American Heart Association 14-element screening protocol includes seven questions about personal history, three questions about family history, and four physical examination findings. The electrocardiogram may identify cardiac conditions such as cardiomyopathy, Wolff-Parkinson-White syndrome, and long QT syndrome that may not manifest on physical examination. Widespread use of an electrocardiogram in screening may be limited by cost and practitioner training. Successful implementation of the use of an electrocardiogram in screening may depend on specific training for practitioners in interpreting the electrocardiogram in young athletes. It is important to identify specialists who may help with further evaluation of any findings consistent with critical cardiovascular disease.
{"title":"Preparticipation screening and electrocardiograms in athletes","authors":"Peter Rippey , Jada Ashford , Zachariah El-fallah , Korey Shively , Jorge Sucar , Christian Cooper , Emily Ribeiro , Samantha Glenn Etheredge , Cade C. Smelley , Lynn A. Batten","doi":"10.1016/j.ppedcard.2025.101859","DOIUrl":"10.1016/j.ppedcard.2025.101859","url":null,"abstract":"<div><h3>Background</h3><div>Sudden cardiac arrest occurs in 1 per 50,000 to 80,000 people per year. Preparticipation screening may identify athletes who may be at risk for developing sudden cardiac arrest.</div></div><div><h3>Aim of review</h3><div>The purpose of this article is to review the etiologies of sudden cardiac arrest, preparticipation screening, and use of electrocardiograms in screening athletes for cardiac problems.</div></div><div><h3>Key scientific concepts of review</h3><div>Sudden cardiac arrest may occur in young athletes who have hypertrophic cardiomyopathy, anomalous origin of a coronary artery, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, aortic dissection, myocarditis, Wolff-Parkinson-White syndrome, long QT syndrome, Brugada syndrome, commotio cordis, aortic valve stenosis, coarctation of the aorta, congenital heart block, short QT syndrome, or coronary artery disease. Preparticipation screening may include history, physical examination, and an electrocardiogram. Several guidelines for screening are available. The American Heart Association 14-element screening protocol includes seven questions about personal history, three questions about family history, and four physical examination findings. The electrocardiogram may identify cardiac conditions such as cardiomyopathy, Wolff-Parkinson-White syndrome, and long QT syndrome that may not manifest on physical examination. Widespread use of an electrocardiogram in screening may be limited by cost and practitioner training. Successful implementation of the use of an electrocardiogram in screening may depend on specific training for practitioners in interpreting the electrocardiogram in young athletes. It is important to identify specialists who may help with further evaluation of any findings consistent with critical cardiovascular disease.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"78 ","pages":"Article 101859"},"PeriodicalIF":0.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144711870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-03DOI: 10.1016/j.ppedcard.2025.101853
Sharadhi Thalner , Reem Youssef , James Wood , Jeremy L. Herrmann , J.P. Lavik , Erin Rudzinski , Umesh Dyamenahalli , Mark Ayers
Introduction
Infective endocarditis (IE) following transcatheter pulmonary valve placement is a significant concern. Fungal endocarditis, though rare, poses significant diagnostic and therapeutic challenges, particularly when caused by Histoplasma capsulatum.
Case report
We present a 24-year-old female with tetralogy of Fallot (ToF) and a history of transcatheter prosthetic pulmonary valve replacement, who developed IE secondary to active histoplasmosis. Initial symptoms included worsening fatigue and jaundice, leading to hospitalization. Echocardiography revealed new stenosis of the pulmonary valve, prompting further investigation. Despite negative blood cultures, serological and molecular tests for histoplasmosis were positive, confirming the diagnosis. Treatment commenced with amphotericin B, followed by surgical valve replacement two weeks later, revealing hyphal elements indicative of H. capsulatum. The patient subsequently received prolonged antifungal therapy with itraconazole with near complete resolution of symptoms and a mild residual gradient.
Conclusion
This case emphasizes the necessity for heightened awareness of fungal pathogens in patients with prosthetic devices, particularly in the context of culture-negative endocarditis. Early diagnosis and intervention, including surgical resection and appropriate antifungal treatment, are critical for improving patient outcomes.
{"title":"Histoplasma endocarditis in a prosthetic pulmonary valve: A case report","authors":"Sharadhi Thalner , Reem Youssef , James Wood , Jeremy L. Herrmann , J.P. Lavik , Erin Rudzinski , Umesh Dyamenahalli , Mark Ayers","doi":"10.1016/j.ppedcard.2025.101853","DOIUrl":"10.1016/j.ppedcard.2025.101853","url":null,"abstract":"<div><h3>Introduction</h3><div>Infective endocarditis (IE) following transcatheter pulmonary valve placement is a significant concern. Fungal endocarditis, though rare, poses significant diagnostic and therapeutic challenges, particularly when caused by <em>Histoplasma capsulatum</em>.</div></div><div><h3>Case report</h3><div>We present a 24-year-old female with tetralogy of Fallot (ToF) and a history of transcatheter prosthetic pulmonary valve replacement, who developed IE secondary to active histoplasmosis. Initial symptoms included worsening fatigue and jaundice, leading to hospitalization. Echocardiography revealed new stenosis of the pulmonary valve, prompting further investigation. Despite negative blood cultures, serological and molecular tests for histoplasmosis were positive, confirming the diagnosis. Treatment commenced with amphotericin B, followed by surgical valve replacement two weeks later, revealing hyphal elements indicative of <em>H. capsulatum</em>. The patient subsequently received prolonged antifungal therapy with itraconazole with near complete resolution of symptoms and a mild residual gradient.</div></div><div><h3>Conclusion</h3><div>This case emphasizes the necessity for heightened awareness of fungal pathogens in patients with prosthetic devices, particularly in the context of culture-negative endocarditis. Early diagnosis and intervention, including surgical resection and appropriate antifungal treatment, are critical for improving patient outcomes.</div></div>","PeriodicalId":46028,"journal":{"name":"PROGRESS IN PEDIATRIC CARDIOLOGY","volume":"78 ","pages":"Article 101853"},"PeriodicalIF":0.6,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144696942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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