Death In Athletes Research Articles

Is Brugada Syndrome a Risk for Sudden Cardiac Death in Athletes? A Review of the Current Literature

Is Brugada Syndrome a Risk for Sudden Cardiac Death in Athletes? A Review of the Current Literature

Focused echocardiographic screening of the aortic valve and aorta in elite rugby players

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Grant from the charitable organisation Cardiac Risk in the Young. Background Pre-participation cardiac screening (PPS) of professional rugby players in the United Kingdom consists of an ECG-based evaluation. However, structural abnormalities that would not manifest on an ECG, such as aortic dilatation might be underdiagnosed and aortic dissection has previously been identified as a cause of sudden cardiac death in athletes (1). Purpose To trial focused transthoracic echocardiography (FTTE) screening for aortopathy as part of PPS and to determine normative aortic root measurements in rugby players, comparing dimensions with sedentary controls. Methods Professional male rugby players undergoing PPS were consented to have an FTTE performed as part of their cardiac evaluation. The aortic valve was visualised in the parasternal long and short axis views to delineate valve morphology. Aortic root measurements were taken at the sinus of Valsalva (SOV), sinotubular junction (STJ) and ascending aorta (AA) at end-diastole, from inner edge to inner edge. All measurements were indexed to the individuals height (in metres). Dilatation was defined as a dimension of >40mm at any aortic level. The findings were compared with a control population of sedentary age, and height-matched volunteers (defined as <2 hours physical activity per week) recruited from a national screening programme offered by the charitable organisation Cardiac Risk in the Young (CRY). Results 131 rugby players were screened, mean age 20.5years and on average engaged in 16 hours of mixed aerobic and strength-based training per week. 187 age-and-height-matched sedentary controls were included. Overall, rugby players had a significantly larger aortic root at all levels measured, compared with controls (Table 1). The only exception was the indexed ascending aorta dimensions. 2 rugby players had aortic dimensions >40mm at the SOV compared with no controls. A bicuspid aortic valve (BAV) was identified in 1 in one rugby player and 2 controls. These were excluded from the comparison of aortic dimensions due to the likelihood of them having an associated aortopathy. Conclusion Incorporating FTTE as part of existing PPS algorithms is an inexpensive way of screening for aortopathy and BAV. Identifying abnormalities may enable individuals to be suitably followed-up. Elite rugby players have a larger aortic root than sedentary controls. The significance of this requires corroboration in larger-scale, longitudinal studies.

Exercise in Hypertrophic Cardiomyopathy: Recent Conceptual Changes and Recommendations for Pre-Exercise Tests.

Traditionally, individuals with hypertrophic cardiomyopathy (HCM) have been advised not to participate in more than low-intensity exercises. HCM was originally described in the context of sudden death, and early literature from the registry showed that HCM was the most common cause of sudden cardiac death in young athletes. Therefore, there has long been a concern that exercise could trigger ventricular arrhythmia and sudden cardiac death. Although a few patients with HCM may progress along deteriorating disease pathways, many have no clinically significant symptoms or adverse events, no need for major treatment, and a normal life expectancy. Therefore, the routine restriction of any exercise intensity in this large group deprives them of the multiple benefits of exercise and may have detrimental effects on long-term clinical outcomes. However, it has been reported that light to moderate exercise is acceptable for many patients with HCM, and recent evidence suggests that vigorous exercise does not increase the risk of sudden death in this population. Thus, we reviewed previous literature regarding the effects of exercise in patients with HCM and provided cutting-edge information on the safety and concerns of exercise. In addition, based on our experience and previous research, we reviewed the conditions that should be met before starting exercise and the tests required to confirm them.

Sudden Cardiac Death in Athletes: Consensuses and Controversies.

Exercise is widely considered beneficial for cardiovascular health. However, on rare occasions, athletes experience sudden cardiac death without any preceding symptoms. The devastating nature of these events necessitates us to understand the underlying causes. In younger athletes (age <35), the underlying causes are usually hereditary/genetic, whereasin older athletes (age >35), coronary artery disease is prevalent. Sudden cardiac death in athletes can occur regardless of the presence of any structural abnormality in the heart. Despite divergence between guidelines, the majority of cardiology societies recommend at least taking a comprehensive history and performing physical examinations for initial screening for all athletes.This article reviews the consensuses and controversies regarding the incidence, causes, and prevention of sudden cardiac death in athletes.

Integrating Bioinformatics and Network Pharmacology to Explore the Therapeutic Target and Molecular Mechanisms of Schisandrin on Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease and is currently the leading cause of sudden death in adolescent athletes. Schisandrin is a quality marker of the traditional Chinese medicine Schisandra chinensis, which has an excellent therapeutic effect on HCM, but its pharmacological mechanism remains unclear. This study aimed to explore the potential and provide scientific evidence for schisandrin as a lead compound against hypertrophic cardiomyopathy. The drug-like properties of schisandrin were predicted using the SwissADME website. Then, the PharmMapper database was used to predict potential drug targets and match gene names in the Uniprot database. HCM targets were collected from NCBI, OMIM, and Genecards databases and intersected with drug targets. The intersection targets were imported into the STRING database for PPI analysis, and core targets were identified. KEGG and GO enrichment analysis was performed on the core targets through the DAVID database, and all network maps were imported into Cytoscape software for visualization optimization. HCM-related datasets were downloaded from the GEO database to analyze core targets and screen differentially expressed target genes for molecular docking. After the PPI network analysis of the intersection targets of drugs and diseases, 12 core targets were screened out. The KEGG analysis results showed that they were mainly involved in Rap1, TNF, FoxO, PI3K-Akt, and other signaling pathways. After differential analysis, PPARG, EGFR, and MMP3 targets were also screened. The molecular docking results showed that schisandrin was well bound to the protein backbone of each target. This study used network pharmacology combined with differential expression and molecular docking to predict that schisandrin may treat HCM by acting on PPARG, EGFR, and MMP3 targets, and the regulatory process may involve signaling pathways, such as Rap1, TNF, FoxO, and PI3K-Akt, which may provide a valuable reference for subsequent studies.

Comparison of four electrocardiographic criteria for the detection of cardiac abnormalities in Singapore athletes.

Sudden cardiac death in athletes is a rare occurrence, the most common cause being hypertrophic cardiomyopathy, which increases the risk of sustained ventricular tachycardia or ventricular fibrillation. Most of these young athletes are asymptomatic prior to the cardiac arrest. Several electrocardiogram criteria such as the European Society of Cardiology group 2 Criteria changes, Seattle Criteria, Refined Criteria, and most recently the 2017 International Criteria, have sought to improve the accuracy of identifying these at-risk athletes during pre-participation screening while minimising unnecessary investigations for the majority of athletes at low risk.We aimed to compare the above four criteria in our Singapore athlete population to identify which criterion performed the best in detecting cardiac abnormalities on echocardiography. Out of 1,515 athletes included in Changi General Hospital, Singapore registry between June 2007 and June 2014, the electrocardiograms of 270 athletes with further cardiac investigations were analysed. We compared the above four electrocardiographic criteria to evaluate which performed best for detecting cardiac abnormalities on echocardiography in our Southeast Asian athlete population. The European Society of Cardiology, Seattle, Refined and 2017 International Criteria had a sensitivity of 20%, 0%, 20% and 5%, respectively; a specificity of 64%, 93%, 84% and 97%, respectively; a positive predictive value of 4%, 0%, 9% and 11%, respectively; and a negative predictive value of 91%, 92%, 93% and 93%, respectively for detecting abnormalities on echocardiography. The latest 2017 International Criteria performed the best as it had the highest specificity and positive predictive value, joint highest negative predictive value, and lowest false positive rate.

Prevalence and diagnostic significance of de-novo 12-lead electrocardiogram patterns following covid-19 infection in elite soccer players

Abstract Funding Acknowledgements Type of funding sources: None. Background Considering that myocarditis is implicated in 5-15% of all exercise related sudden cardiac deaths in athletes, following a novel viral pandemic, the identification and risk-stratification of affected athletes remains an important priority. Given its widespread availability, the inclusion of a 12-lead electrocardiogram (ECG) is common to all consensus-based protocols from North America and Europe. However, a single cross-sectional ECG is problematic because several physiological repolarisation changes are also common manifestations in individuals with myopericarditis. Purpose The aim of our study was to report on the prevalence and diagnostic significance of de-novo ECG patterns following COVID-19 infection in a well-defined cohort of elite soccer players in the English, Dutch and Brazilian leagues. Methods In this multicentre observational study, between March 2020–May 2022, we evaluated consecutive athletes with COVID-19 infection. ECGs were reported in accordance with the International recommendations for ECG interpretation in athletes. The following patterns were also considered abnormal if they were not detected on the pre-COVID-19 infection ECG: PR-segment depression, new J-point and ST segment elevation, low QRS voltages, QRS fragmentation, new ST-segment depression, new T-wave inversion, biphasic T-waves and a reduction in the T-wave amplitude by 50% or T-wave flattening. Athletes exhibiting de-novo ECG changes underwent cardiovascular magnetic resonance (CMR) scans. One club mandated CMR scans for all players (n=30) following COVID-19 infection, despite the absence of cardiac symptoms or de-novo ECG changes. Results 511 soccer players (median age 21-years, IQR:18-26-years) were included, of which 88% were male and 58% white. 17 (3%) athletes demonstrated de-novo ECG changes, which included, a reduction in T-wave amplitude in the inferior and lateral leads (n=5), inferior leads (n=4) and lateral leads (n=4); inferior T-wave inversion (n=7), and ST-segment depression (n=2). 15 (88%) athletes with de-novo ECG changes revealed CMR evidence of inflammatory cardiac sequalae. All athletes who underwent a mandatory CMR irrespective of illness severity or ECG findings, had normal findings. Athletes revealing de-novo ECG changes, had a higher prevalence of cardiac symptoms (71% v 12%; p&amp;lt;0.0001) and longer median symptom duration (5-days, IQR:3-10) compared with athletes without de-novo ECG changes (2-days, IQR:1-3; p&amp;lt;0.001). Among athletes without cardiac symptoms, the additional yield of de-novo ECG changes to detect cardiac inflammation was 17%. Conclusions 3% of athletes demonstrated de-novo ECG changes post COVID-19 infection, of which 88% were diagnosed with inflammatory cardiac sequalae. Most affected athletes exhibited cardiac symptoms; however de-novo ECG changes contributed to a diagnosis of cardiac inflammation in 17% of athletes without cardiac symptoms.

Sudden cardiac arrest and role of sport preparticipation screening in children

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Competitive sports activity may increase the risk of life-threatening ventricular arrhythmias and sudden cardiac death (SCD) in athletes with underlying cardiovascular diseases (CVD). Preparticipation screening (PPS) offers the potential to early identify CVD and reduce this risk, but the optimal age of sport PPS start is not known. Purpose The aim of this study is to assess the burden of sudden cardiac arrest (SCA) and the diagnostic yield of PPS for CVD at risk of SCA in two different age groups: 8-11 year-old and 12-15 year-old. Methods Data on the incidence and causes of SCA from 2011 to 2020 were retrieved from the sudden death registry of our region, hospital records and local press. During the same period, we assessed 25,251 young competitive athletes aged 8-15 years who underwent 58,185 annual PPS (mean 2.3/athlete) including history, physical examination, ECG and exercise testing. Further tests were required in case of abnormalities at first-line screening. Results Over 10 years, 21 sudden deaths and 5 resuscitated SCA occurred: 6 in athletes (incidence 0.7/100.000/year) versus 20 in non-athletes (0.7/100.000/year). 67% athletes versus 5% non-athletes who suffered SCA were successfully resuscitated (aborted sudden cardiac death=aSCD), (results according to the age-group in Figure 1). Idiopathic ventricular fibrillation was the most common diagnosis accounting for 14/26 (54%) cases. The incidence of SCA was 0.2/100.000/year in the age group 8-11 year-old versus 1.3/100.000/year in the age group 12-15 year-old. By PPS, 26 (0.1%) athletes received a diagnosis of at-risk CVD, significantly more often in children ≥12 year-old (0.06%/evaluation) than &amp;lt;12 year-old (0.02%/evaluation, p=0.02), (Figure 2). During follow-up, 2 screened athletes suffered SCA due to idiopathic ventricular fibrillation, both ≥12 year-old at the time of PPS. Conclusions The incidence of SCA was 6 times higher in the age group 12-15 years compared with the 8-11 years group. Similarly, the diagnostic yield of PPS for at-risk CVD was significantly higher after 12 years of age. This suggests that systematic PPS may not be justified before 12 year-old.

Echocardiography in the pre-participation screening: an old topic revisited

Abstract Funding Acknowledgements Type of funding sources: None. Background Preparticipation screenings (PPs) have been conceived for the potential to prevent sudden cardiac death (SCD) in young athletes by early identification of hidden cardiac diseases. Commonly used protocols include family history collection, physical examination and resting electrocardiogram (ECG). Transthoracic echocardiography has been hypothesized to have a primary role in the PPs. The aim of the present study was to evaluate the additional role of echocardiogram in identifying cardiovascular (CV) abnormalities that might be undetected by commonly used PPS. Methods We retrospectively reviewed Ferrari Formula Benessere, a corporate wellness program - database and analyzed data recorded from 2017 to 2022 to compare two medical models: a "standard" PPS including medical history, physical examination, ECG and exercise stress testing (EST) versus an "advanced" PPS comprising history, physical examination, ECG, EST and echocardiography. Results From an initial sample size of 7500 subjects, we included 500 subjects (420 male, 33.69 ± 7.9 mean aged) enrolled for the first time in the corporate wellness program between 2017 and 2022. 339 (67.8%) subjects had no abnormal findings at "standard" PPS and, even if would have not required further evaluation, performed an echocardiography anyway ("advanced" PPS): 31 (9.1%) showed some abnormal CV findings at echocardiography, such as patent foramen ovalis or bicuspid aortic valve. Conclusions Screening echocardiogram showed an additional value in detect subjects with CV abnormalities, otherwise undiagnosed with "standard" PPS protocol.

Early-life physical performance predicts the aging and death of elite athletes.

Athleticism and the mortality rates begin a lifelong trajectory of decline during early adulthood. Because of the substantial follow-up time required, however, observing any longitudinal link between early-life physical declines and late-life mortality and aging remains largely inaccessible. Here, we use longitudinal data on elite athletes to reveal how early-life athletic performance predicts late-life mortality and aging in healthy male populations. Using data on over 10,000 baseball and basketball players, we calculate age at peak athleticism and rates of decline in athletic performance to predict late-life mortality patterns. Predictive capacity of these variables persists for decades after retirement, displays large effect sizes, and is independent of birth month, cohort, body mass index, and height. Furthermore, a nonparametric cohort-matching approach suggests that these mortality rate differences are associated with differential aging rates, not just extrinsic mortality. These results highlight the capacity of athletic data to predict late-life mortality, even across periods of substantial social and medical change.

Long &lt;i&gt;QT&lt;/i&gt; Syndrome in Young Athletes

Long QT syndrome is a disease associated with a high risk of sudden cardiac (arrhythmic) death. The frequency of sudden cardiac death is approximately 1: 100,000 young athletes, while autopsies often do not detect changes, which indicates a primary arrhythmogenic death. The article describes two clinical cases of young athletes with prolongation of the QT interval. The possible causes of the long QT syndrome and the difficulties of diagnosing this syndrome in children and adolescents involved in sports are discussed. Regardless of the reasons leading to the prolongation of the QT interval, there is a risk of arrhythmic events. Timely diagnosis of long QT syndrome is the way to the primary prevention of sudden cardiac death in young athletes.

Arrhythmic Risk Stratification among Patients with Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a cardiac muscle disorder characterized by generally asymmetric abnormal hypertrophy of the left ventricle without abnormal loading conditions (such as hypertension or valvular heart disease) accounting for the left ventricular wall thickness or mass. The incidence of sudden cardiac death (SCD) in HCM patients is about 1% yearly in adults, but it is far higher in adolescence. HCM is the most frequent cause of death in athletes in the Unites States of America. HCM is an autosomal-dominant genetic cardiomyopathy, and mutations in the genes encoding sarcomeric proteins are identified in 30-60% of cases. The presence of this genetic mutation carries more than 2-fold increased risk for all outcomes, including ventricular arrhythmias. Genetic and myocardial substrate, including fibrosis and intraventricular dispersion of conduction, ventricular hypertrophy and microvascular ischemia, increased myofilament calcium sensitivity and abnormal calcium handling, all play a role as arrhythmogenic determinants. Cardiac imaging studies provide important information for risk stratification. Transthoracic echocardiography can be helpful to evaluate left ventricular (LV) wall thickness, LV outflow-tract gradient and left atrial size. Additionally, cardiac magnetic resonance can evaluate the prevalence of late gadolinium enhancement, which when higher than 15% of LV mass is a prognostic maker of SCD. Age, family history of SCD, syncope and non-sustained ventricular tachycardia at Holter ECG have also been validated as independent prognostic markers of SCD. Arrhythmic risk stratification in HCM requires careful evaluation of several clinical aspects. Symptoms combined with electrocardiogram, cardiac imaging tools and genetic counselling are the modern cornerstone for proper risk stratification.

Athletic Trainers Knowledge and Practices for Sudden Cardiac Death

Sudden cardiac death (SCD) is one of the leading causes of death in athletics, despite athletic trainers working as first responders for athletic events. The purpose of this study was to assess athletic trainers’ knowledge of SCD, and to analyze perceptions regarding evidence-based practice. This study aimed to answer how the NATA position statement has impacted athletic trainers practice, and to identify potential limitations in implementing best practice.

Mitral Valve Prolapse and Sudden Cardiac Death in Athletes at High Risk.

Mitral valve prolapse (MVP) is the most frequent valvulopathy in the general population, with usually a favourable prognosis. Although it can be associated with some complications, ventricular arrhythmias (VA) and sudden cardiac death (SCD) are the most worrying. The estimated risk of SCD in MVP is between 0.2% to 1.9% per year, including MVP patients with and without severe mitral regurgitation (MR). The association between SCD and MVP is expressed by a phenotype called "malignant MVP" characterized by transthoracic echocardiography (TTE) findings such as bileaflet myxomatous prolapse and mitral annulus disjunction (MAD), ECG findings such as repolarization abnormalities, complex ventricular arrhythmias (c-VAs) and LV fibrosis of papillary muscles (PMs) and inferobasal wall visualized by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR). Therefore, attention is raised for patients with "arrhythmic MVP" characterized from an ECG point of view by frequent premature ventricular contractions (PVCs) arising from one or both PMs as well as by T-wave inversion in the inferolateral leads. In athletes, SCD is the most frequent medical cause of death and in young subjects (< 35 years) usually is due to electrical mechanism affecting who has a silent cardiovascular disease and are not considered per se a cause of increased mortality. In MVP, SCD was reported to happen during sports activity or immediately after and valve prolapse was the only pathological aspect detected. The aim of the present paper is to explore the association between SCD and MVP in athletes, focusing attention on ECG, TTE in particular, and CMR findings that could help to identify subjects at high risk for complex arrhythmias and eventually SCD. In addition, it is also examined if sports activity might predispose patients with MVP to develop major arrhythmias.

The safety of sports in children with inherited arrhythmia substrates.

Sudden cardiac death (SCD) is a rare and devastating event in children and remains a leading cause of death in young athletes. Channelopathies and cardiomyopathies, in particular long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), hypertrophic cardiomyopathy (HCM), and arrhythmogenic cardiomyopathy (ACM) are associated with exercise-related SCD. Implantable cardioverter-defibrillators (ICDs) are often placed for secondary prevention for athletes with cardiomyopathy or channelopathy. There remains concern regarding the safety of return to participation with an ICD in place. Guidelines have historically recommended that patients with inherited heart rhythm disorders be restricted from competitive sports participation. Increasing evidence suggests a lower risk of exercise-related cardiac events in young athletes with inherited heart rhythm disorders. In this review, we highlight current knowledge, evolving guidelines, and present a multidisciplinary approach involving shared decision-making and appropriate planning for safe sports participation of children with inherited heart rhythm disorders.

Prevention of Sudden Cardiac Death in Non-Competitive Athletes: ECG Screening by Telecardiology Is Useful and Cost-Effective

<i>Background: </i>Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport. There are several hereditary, structural, or electrical heart diseases associated with SCD, most of them can be identified or suggested by abnormalities on a resting 12-lead electrocardiogram (ECG). <i>Objective: </i>To evaluate usefulness and cost-effectiveness of ECG screening, using a telecardiology system, in order to detect cardiovascular diseases that might cause SCD in a cohort of non-competitive athletes (NCA). <i>Methods: </i>ECGs received at the Telecardiology Center (Telemedico Srl, Genoa) for non-competitive sports, in a 3-month period were analyzed. According to the age we distinguished: NCA < 35 years (group A) and NCA > 35 years (group B). <i>Results: </i>A total of 6345 NCA (4078 males, 64.2%) were evaluated between the ages of 5 and 50 years (mean ± SD: 28.4 ± 12.6). Group A (age < 35 years) consisted of 3453 (54.4%) NCA and group B (age > 35 years) of 2892 (45.6%) respectively. An ECG pattern at risk of SCD has been identified in 295 (4.6%) subjects. Prevalence of ECG abnormalities was higher for group B (154/2892; 5.3%) than group A (141/3453; 4.1%); the difference was significant (p= 0.016). The average cost per ECG was € 12. The cost of ECG screening to identify a risk situation of SCD was € 258. <i>Conclusion: </i>ECG screening through telecardiology of NCA results to be feasible, useful and cost-effective.

Echocardiography in the preparticipation screening: an old topic revisited.

Preparticipation screenings have been conceived for the potential to prevent sudden cardiac death in young athletes by early identification of hidden cardiac diseases. Commonly used protocols include family history collection, physical examination, and resting electrocardiogram. Transthoracic echocardiography has been hypothesized to have a primary role in the preparticipation screening. The present study aimed to evaluate the additional role of echocardiogram in identifying cardiovascular abnormalities that might be undetected by commonly used preparticipation screening. We retrospectively reviewed Ferrari Formula Benessere, a corporate wellness program database, and analyzed data recorded from 2017 to 2022 to compare two medical models: a 'standard' preparticipation screening including medical history, physical examination, electrocardiogram and exercise stress testing versus an 'advanced' preparticipation screening comprising history, physical examination, electrocardiogram, exercise stress testing and echocardiography. From an initial sample size of 7500 patients, we included 500 patients (420 male, 33.69 ± 7.9 mean age) enrolled for the first time in the corporate wellness program between 2017 and 2022. Three hundred and thirty-nine (67.8%) patients had no abnormal findings at 'standard' preparticipation screening and, even if they would have not required further evaluation, we performed echocardiography anyway ('advanced' preparticipation screening): 31 (9.1%) showed some abnormal cardiovascular findings at echocardiography, such as patent foramen ovalis, bicuspid aortic valve, aortic root ectasia or mitral valve prolapse. Screening echocardiogram showed an additional value (about 10% more) in detecting patients with cardiovascular abnormalities, otherwise undiagnosed with the 'standard' preparticipation screening protocol.

Pediatric Myocarditis.

Myocarditis is a condition caused by acute or chronic inflammation of the cardiac myocytes, resulting in associated myocardial edema and myocardial injury or necrosis. The exact incidence is unknown, but is likely underestimated, with more mild cases going unreported. Diagnosis and appropriate management are paramount in pediatric myocarditis, as it remains a recognized cause of sudden cardiac death in children and athletes. Myocarditis in children is most often caused by a viral or infectious etiology. In addition, there are now two highly recognized etiologies related toCoronavirus disease of 2019 (COVID-19) infection and the COVID-19 mRNA vaccine. The clinic presentation of children with myocarditis can range from asymptomatic to critically ill. Related to severe acute respiratory syndrome-Coronavirus 2 (SARs-CoV-2), children are at greater risk of developing myocarditis secondary to COVID-19 compared to the mRNA COVID-19 vaccine. Diagnosis of myocarditis typically includes laboratory testing, electrocardiography (ECG), chest X-ray, and additional non-invasive imaging studies with echocardiogram typically being the first-line imaging modality. While the reference standard for diagnosing myocarditis was previously endomyocardial biopsy, with the new revised Lake Louise Criteria, cardiac magnetic resonance (CMR) has emerged as an integral non-invasive imaging tool to assist in the diagnosis. CMR remains critical, as it allows for assessment of ventricular function and tissue characterization, with newer techniques, such as myocardial strain, to help guide management both acutely and long term.

Sudden cardiac death in athletes – can we prevent it?

Introduction and purpose: Sudden cardiac death (SCD) is a rare condition, however it is the leading medical cause of death in population of athletes. This study reviews the epidemiology and common causes of SCD in this group. The literature on the role of pre-participation screening and of the other preventive measures was also reviewed. Review methods: A review of the available literature on sudden cardiac death in athletes was conducted using PubMed and Google Scholar databases. Description of the state of knowledge: SCD is the leading cause of death in athletes. However, the incidence is difficult to estimate and varies in different populations. The etiology is age-dependent, in young individuals the most common cause of sudden cardiac death are hypertrophic cardiomyopathy and congenital coronary artery anomalies. In the older athlete population (over 35 years old) atherosclerotic coronary artery disease is the main cause. Screening process varies between countries and besides taking the medical history and physical examination can involve electrocardiogram, echocardiography and other examinations. Conclusions: A review of the following studies has shown, that pre-participation screening of athletes may help to reduce the incidence of sudden death. Equal focus should be put on the availability of medical facilities during sports events, including experienced medical team and access to automated external defibrillation.

Reversible Apical Hypertrophy in a Young Competitive Athlete with Familiar Hypertrophic Cardiomyopathy.

BACKGROUND Differential diagnosis between athlete's heart and hypertrophic cardiomyopathy is sometimes challenging in sport cardiology since endurance training can cause a distinct pattern of functional and structural changes of the cardiovascular system. It is of crucial importance to accurately diagnose it and stratify the arrhythmic risk since hypertrophic cardiomyopathy is one of the leading causes of sudden cardiac death in young athletes. Apical hypertrophic cardiomyopathy is a relatively rare form of hypertrophic cardiomyopathy that predominantly affects the apex of the left ventricle and usually has a nonobstructive physiology. Few data and studies are available on influence of aerobic training (and detraining) on morphological changes in athletes with apical hypertrophic cardiomyopathy. CASE REPORT We present the case of a 19-year-old male soccer athlete with family history for obstructive hypertrophic cardiomyopathy, with electrocardiographic and morphological left ventricular remodeling in association with sports activity. Intensive aerobic training led to marked T-wave inversion on 12-lead ECG and left ventricular hypertrophy compatible with apical hypertrophic cardiomyopathy. Genetic testing confirmed the presence of familial variant c853C>T, p.(Arg 285Cys) on TNNT2 gene. After 18 months detraining, we observed a complete regression of ECG abnormalities and a reverse remodeling of the left ventricular hypertrophy. No pharmacological therapy was indicated; periodic cardiological evaluations were advised. Monitoring devices or implantable cardioverter defibrillator were not recommended. CONCLUSIONS This case suggests that intensive aerobic training can affect the pathological hypertrophic cardiomyopathy substrate, facilitating the development of left ventricular hypertrophy and, more interesting, regression of structural changes after detraining.