Cardiovascular Screening of Athletes: Implications in Reducing the Risk of Sudden Cardiac Deaths

doi:10.21203/rs.3.rs-1678568/v1

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Cardiovascular Screening of Athletes: Implications in Reducing the Risk of Sudden Cardiac Deaths

https://doi.org/10.21203/rs.3.rs-1678568/v1

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Sudden cardiac death (SCD) in sports is defined as unexpected death during exercise or shortly after physical exertion (within 24 hours of exercise cessation) in athletes who appeared perfectly healthy otherwise. To highlight the importance of cardiovascular screening in athletes for reducing incidences of SCD, we performed a prospective study and analysed 280 athletes who were recruited and followed up between 2016 to 2021 at the Agel Košice-Šaca Hospital (city and country) for cardiovascular screening using electrocardiography (ECG) and other imaging modalities such as echocardiography (ECHO). During the screening, arrhythmias were diagnosed in thirteen athletes and higher degrees of AV block and ventricular extrasystoles were diagnosed in four athletes. These athletes subsequently underwent interventional procedures. At the end of the follow up period and interventional procedures, three athletes were diagnosed with sever cardiovascular disease (CVD), which led to early termination of their sports career. Our findings suggest that endurance athletes in particular are at risk for arrhythmias and chronic myocardial remodelling and that most of the diseases that are associated with an increased risk of SCD could be identified by changes in resting ECG. We also confirmed that endurance athlete, both professional and recreational, are at higher risk of developing atrial fibrillation later in life. In addition, we emphasize on the benefit of an automated ECG module and echocardiographic examination, and suggest that SCD prevention in athletes lies in improving and expanding cardiovascular screening.

Arrhythmia

Sudden Cardiac Death

Athlete’s Heart

Cardiomyopathy

Electrocardiogram

Sudden cardiac death (SCD) in athletes is a sport-related death and is defined as sudden and unexpected death during exercise, or shortly after physical exertion (within 24 hours of exercise cessation) in healthy athletes [1]. Sudden death in athletes shows a clear sex predilection with male athletes posing considerably higher risk compared with the female counterparts (male: female > 10:1). Higher SCD risk for male athletes’ results from their greater participation in competitive sports, as well as more intense training loads compared to the female athletes. In addition, more frequent use of banned performance-enhancing substances could also contribute to higher incidences of SCD in male athletes. It has recently been published that male gender alone is also a risk factor for sudden death in athletes, most likely as a consequence of the greater prevalence and/or phenotypic expression of cardiac diseases with risk of arrhythmic cardiac arrest, such as cardiomyopathies and premature coronary artery disease in young men [2]. According to statistics, the most common cause of death is cardiovascular disease (CVD), which accounts for ~ 2%, of the total cases in sports of different age categories. The immediate cause of death is cardiac arrhythmia. It is mainly caused by congenital or hereditary structural and also functional abnormalities of the cardiovascular system. Physical activity then tends to be a precipitating factor in the sudden death of a young athlete. Many of these diseases have no warning signs and sudden death can often be their first and unfortunately last symptom [1]. The role of screening examinations is to detect pre-existing cardiovascular abnormalities in order to reduce the risk of SCD. The problem is that cardiac remodelling associated with regular physical activity results in physiological ECG changes in athletes. During exercise, after load and cardiac output increase and electrolyte changes occur, which, together with an increase in catecholamines and sympathetic nervous system activity, may subsequently induce the development of arrhythmias, syncope and SCD, especially in athletes with unrecognized congenital or acquired cardiac diseases [3].

Pathophysiological factors that may trigger cardiovascular events or increase in myocardial susceptibility during exercise include: increased myocardial oxygen consumption and simultaneous shortening of diastole and coronary perfusion time, changes in parasympathetic and sympathetic tone, release of thromboxane A2 and other coronary vasoconstrictors, increase in blood coagulation, increase in blood lactate concentration (lactic acidosis), intra- and extracellular electrolyte disturbances, increase in serum free fatty acid concentration, and excessive rise in body temperature [3].

This is a prospective monocentric study, conducted between 2016 and 2021 in the cardiology outpatient clinic and sports centre of Agel Košice-Šaca Hospital, Kosice, Slovakia. During five-years monitoring, after signing informed consent, we examined 280 athletes, in whom we recorded medical history by questionnaire method (Annex 1) focused on risk factors and the presence of CVD symptoms, and performed a physical examination, during which we recorded resting 12-lead ECG with a resting ECG (BTL 18 SDS module Drezner) and monitored resting heart rate and individual intervals in the ECG, resting blood pressure, BMI, ECHO parameters, and physical performance using VO2 max during spiroergometric examination. We also monitored the occurrence of ectopic activity during resting and stress ECG examination.

Inclusion criteria: patient selection was contingent on meeting the definition of sports activity and physical activity of at least 200 minutes per week. An athlete is considered as a competitive athlete, when he /she participate in an organised sporting activity of a team or individual nature that requires regular intensive training and competition against an opponent. [2]. Exclusion criteria were based on a history of any pre-existing cardiovascular disease, medication use, doping, and/or a positive family history of SCD before the age of 50 years. Written informed consent was obtained from all study participants prior to measurements and examinations. Information was provided both orally and in writing, in a manner appropriate to the person's education and intelligence, in the person's native language, without technical terms. The study was approved by the ethics committee at the Agel Košice-Šaca Hospital prior to initiation and all the methods were performed in accordance with the relevant guidelines and regulations.

In this study, a total of 280 athletes including 243 (86.78%) males and 37 (13.22%) females (chart-1), aged between 18 and 62 years were analysed. The average age of the athletes was 29.4 ± 9.14 years.

ECG examination – We performed 12-lead resting ECG (BTL 18– SDS module Drezner 2013) for all athletes.

ECHO (Echocardiography) - We monitored basic parameters such as cardiac compartment dimensions, valvular function, left ventricular systolic and diastolic function, but we mainly focused on the interventricular septal thickness.

Spiroergometric examination - Each athlete underwent a spiroergometric examination on a bicycle or treadmill, where we monitored VO2 max as an indicator of trainability, ECG and BP (blood pressure) during exercise.

This study provides an overview and background information on the risk of arrhythmias in athletes and is dedicated to the specific variables studied in a group of recreational and professional athletes from the Košice region, Slovakia. We divided the athletes into five groups according to the type of sports (Chart 2) In general, there are two different types of sports, the first category encompasses isotonic, or dynamic sports, such as marathon runners, football players, ice hockey players, basketball players, and the second comprises of isometric, or static sports, such as weightlifters. In our work, we have focused on tracking dynamic sports.

The largest group of athletes was those with interventricular septal thickness (IVS) between 12–13 mm and the second largest group athletes had IVS thickness between 13–14 mm. We performed 24- to 72-hour ECG Holter monitoring in all these athletes with IVS thickness above 12 mm. In these athletes, we could not demonstrate the presence of more frequent ectopic activity and complex cardiac rhythm disturbances. So, we also performed genetic testing for Fabry disease in all of them, and the results were negative. We also failed to demonstrate a statistically significant difference in the thickness of the IVS among the sports monitored. (Chart-3)

Prevalence of cardiovascular abnormalities in potentially healthy athletes in our cohort

A thorough medical history by questionnaire (Table 1) revealed the presence of cardiac symptoms and/or a positive family history of cardiovascular disease in twenty athletes.

Table 1

– Prevalence of cardiac symptoms
	Basketball	Running	Ice hockey	Other
Presyncope	1	2	2	2
Palpitations	2	1	2	2
Dyspnoe	0	0	2	0
Tachycardia	1	2	0	1

In these athletes, in addition to the resting ECG examination, echocardiographic examination and ECG stress test, we extended the diagnostic procedure to include other examinations, such as 24 to 72 hour ECG Holter monitoring, or if required by the differential diagnostic procedure, cardiac magnetic resonance imaging (CMRI), and electrophysiological study (EPS).

In twelve athletes, we found structural diseases that required more extensive diagnostic or medical procedures - Electrophysiological study (EP), Selective Coronarography (SCG), Radiofrequency Catheter Ablation (RFCA), Cardiac Magnetic Resonance Imaging (CMRI), endomyocardial biopsy. After medical intervention, nine out of twelve athletes returned to the original sport within 3 months. In three athletes, we found sever heart disease, which prevented them from returning to competetive sport. Both athletes with cardiomyopathies had IVS thickness above 13.0 mm. (Table-2). Other athletes with mild cardiovascular defects (mild aortic stenosis, mild tricuspid regurgitation, second-degree AV block Mobitz type II, intermittent junctional rhythm) are in our dispensary with more frequent check-ups while their sporting career is not interrupted. During the follow-up period, we detected arrhythmias in 13 athletes. (Table-3)

Table 2

– Prevalence of structural heart diseases
Sport type	Basketball	Running	Football	Ice hockey	Other
AVnRT	0	0	0	2	1
HCMP	0	0	0	0	1
Heart Valve D.	0	0	0	1	0
nsVT	1				1
AF	0	5	0	0	0
AVRC	0	0	0	0	1

Table 3

– Severe Cardiovascular Disease (CVD)
	Ice hockey	Other
ARVC/D	1	0
HCMP	0	1
AoR/BAV	1	0

Table 4

– Prevalence of arrhythmias in our cohort
AVnRT	3
nsVT	2
FP	5
VES	2
AV Block II	1

AVNRT (AV Nodal Reentrant Tachycardia) was diagnosed in three athletes including one professional cyclist, two professional ice hockey players). All three athletes underwent successful radiofrequency ablation of the arrhythmogenic pathway at cardiovascular disease institutes in Slovakia and returned to their original sport three months after the procedure after a follow-up 72-hour ECG HM and ergometric examination. (Table-4)

Ventricular Extrasystoles (VES) - As of now, we are monitoring two athletes (one basketball and one hockey player) for ventricular extrasystoles, with structurally normal hearts (CMRI without pathology). They do not require further intervention or therapy for the time being. (Fig-1)

Regarding VES, although polymorphic VES are often benign, it could be a sign of unrecognized CVD. Ventricular extrasystoles from Right Ventricular Outflow Tract Tachycardia (RVOT), Left Bundle Branch Block (LBBB) shape and inferior type electrical axis of the heart, are most commonly benign, but on the other hand, they are also frequently present in patients in the early phase of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D), especially if the QRS complex is above 160 ms.

However, more than 2 polymorphic VES in the resting 10-minute ECG are not common findings and occur in less than 1% of athletes, and requires further investigations in order to detect hidden CVDs. If the ECG HM is normal and there is suppression of the VES during the ECG stress test, no further examinations are necessary. Recent studies have shown that in athletes who had more than 2,000 polymorphic VES during 24-hour monitoring, up to 30% of them had CVD not detected by further examinations, whereas in athletes with less than 2,000 polymorphic VES during 24 hours, CVD was detected in only 3% and in 0% of athletes who had less than 100 polymorphic VES in 24 hours. Consequently, in athletes with more than 2,000 polymorphic VES in 24 hours, further investigations, mainly CMRI and electrophysiological examinations, are recommended

Ventricular tachycardia - VT was diagnosed in two cases including a triathlete and a professional basketball player. The first case was a continuous, spontaneously terminating VT, with arrhythmogenic right ventricular cardiomyopathy later revealed by CMRI, endomyocardial biopsy, so that the athlete had to cease active sport according to current international recommendations. Soon after that, he was subsequently implanted with an ICD (Implantable Cardioverter-Defibrillator) due to recurrent Ventricular Tachycardia/Fibrillation (VT/VF) in the secondary prevention of SCD. The second case was a finding during a 72-hour ECG HM in a basketball player who experienced repeated palpitations and had pre-collapse. The athlete with ventricular tachycardia (VT) and a structurally normal heart (CMRI) underwent successful catheter ablation. This was VT from the right ventricular outflow tract. If the VT is successfully ablated by catheter ablation and cannot be induced after the procedure, the athlete can return to sports in 2–4 weeks after the ablation according to the recommendations [4]. This was the case in this case and the basketball player returned to her original sport 3 months later.

Atrioventricular block - We observed an AV block of Mobitz II grade 2 in two athletes (ice hockey), and an intermittent junctional rhythm in one athlete. In all three athletes the changes occurred during ECG HM monitoring in sleep, without the presence of symptoms, both echocardiographic and exercise stress test were without pathological findings. These athletes remain in our dispensary, without any interruption or modification in their sports activities.

In athletes, first-degree AV block or second-degree Wenckebach block (Mobitz type I) occurs frequently within the "athlete’s heart", which was also observed in our cohort. AV block typically occurs in sleep or at rest. Rarely, Mobitz type II AV block or grade III AV block may be noted in athletes, but this requires more thorough clinical and diagnostic investigation.

Atrial fibrillation (AF) - AF occurred in five athletes (runners), with a history of palpitations, with an average age of 52 years. In all cases, it was of the paroxysmal type, detected during 72-hour ECG HM. CHADSVASC 2 score was 0, and anticoagulation therapy was not indicated in any of the cases. These findings confirmed recent studies, which have shown a three times higher prevalence of paroxysmal AF in highly trained endurance athletes. [5]. The susceptibility of athletes to the development of AF could be explained in part by an increase in vagal tone, changes in atrial repolarization, and last but not the least, remodelling and changes in atrial size as an adaptation to physical strain. It is not uncommon for endurance athletes to exceed physical activity by more than ten times the recommendations for cardiovascular protection. There is a direct correlation between the intensity of endurance exercise and left atrial dilation, which is related to the rise in venous pressure and venous return. Prolonged intense endurance sport leads to mild dilation of both atria and right ventricle and can disrupt the architecture, leading to micro-damage, sinoatrial node changes occur. This cycle of acute and chronic changes ultimately induces inflammatory changes and fibrotic remodelling, which represents an arrhythmogenic substrate. The most common trigger for paroxysmal AV is ectopic deposits around the pulmonary veins in the left atrium. As long-term monitoring has shown, especially in endurance athletes, there is mild dilatation of the cardiac sinuses, also of the left atrium, and left atrial size above 40 mm is relatively common in athletes (20%) with an upper limit of up to 45 mm in women and 50 mm in men [6]. Echocardiographic examination may reveal structural heart disease, and anticoagulation therapy for AV is indicated according to current international recommendations, but potential haemorrhagic complications in contact sports remain a concern [7]. Asymptomatic paroxysms of AV, which are common not only in athletes but also in the general population and account for approximately 1/3 of cases, remain a problem as well. Therefore, longer-term (most often 7-day) ECG monitoring is required for their diagnosis. It appears that paroxysmal type of AV is more common in athletes than a persistent and permanent type. Because of this, the detection of AF in athletes on a simple short ECG recording is very low with a high percentage of falsely negative results [8].

ARVC/D - We detected arrhythmogenic right ventricular dysplasia with persistent ventricular tachycardia in one athlete, a triathlete with a history of recurrent syncope during exercise or physical strain. After confirming this diagnosis by CMRI and endomyocardial biopsy, ECG HM, and exercise stress test, the patient underwent RFCA (radiofrequency catheter ablation) of an arrhythmogenic substrate for ventricular tachycardia and was subsequently implanted with an ICD at the National Institute for Cardiovascular Diseases. This athlete has retired from professional sports and after repeated stress ECG examinations with negative results, without arrhythmia induction, he is playing sports at a recreational level of very low workload intensity and heart rate up to 100/min. ARVC is characterized by enlargement, dysfunction and fibro-fatty infiltration of the right ventricle. Ventricular tachycardia morphology of left bundle branch block is often triggered by physical activity, as it was in the case of our athlete. Typical symptoms in these patients are pre-syncope, syncope or SCD during sports. T-wave inversion in leads V1-V3 is observed in more than 85% of patients. Epsilon waves as a distinct abnormality on ECG after QRS complex, is observed in less than 1/3 of patients with ARVC. In the athlete's heart, we can also observe inversion of T waves in leads V1-V3, but these normalize during stress testing, whereas in ARVC patients they typically remain inverted. Right ventricular dilatation has also been described in the athlete's heart, but in most cases its function is normal. MRI of the heart and endomyocardial biopsy contributes to the diagnosis of ARVC, which has a very high sensitivity and specificity [3]. (Fig-2)

HCMP - Hypertrophic cardiomyopathy was detected in one athlete, a handball player. HCMP is one of the leading causes of cardiac arrest in athletes [9]. Hypertrophy without dilatation, focal hypertrophy, bizarre ECG changes, abnormal left ventricular filling pressures, and a family history of hypertrophic cardiomyopathy often prompt further investigations in the athlete. Genetic testing is possible but is reduced because of the high percentage of false-negative results. A high suspicion for HCMP should be in athletes, whose interventricular septal thickness is above 13mm in females and above 15mm in males. If a diagnosis of HCMP is made, both the ESC (European Society of Cardiology) and BC 36 consensus recommend a ban for all competitive sports. The decision to implant an ICD is based on a positive family history for SCD, syncope, persistent ventricular tachycardia, and severe left ventricular hypertrophy [3]. The disease is progressive and can lead to sudden cardiac death due to malignant arrhythmia triggered by extreme physical strain. Hypertrophic cardiomyopathy the most common cause of sudden cardiac death in athletes. The diagnosis is based on the detection of left ventricular hypertrophy by echocardiography or magnetic resonance imaging. Echocardiographic examination and cardiac magnetic resonance imaging in our case showed eccentric thickening of the left ventricular myocardium with a maximum in the mid-ventricular IVS section- 15.5mm. (Fig-3) The posterior papillary muscle was also thickened. The myocardium showed no signs of fibrosis. The athlete had been asymptomatic thus far. On the basis of these findings, we also completed genetic testing focusing on the genes for hypertrophic cardiomyopathy. The examination showed that the patient was heterozygous for the genes for hypertrophic cardiomyopathy - variants c4472C:G in the MYH7 gene and c12-50 12-47dupACAG in the TNNI3 gene were detected in the heterozygous state inherited from the mother, variant c975C:T in the MYH7 gene and variant c649A:G in the MYBPC3 gene inherited from the father. On the basis of these findings, we ordered the termination of his career as a professional athlete and also recommended genetic testing in his brother. This case is also interesting because the patient has a positive genetic load - mutation of several genes encoding myocardial sarcomere proteins in both parents (MYH7, TNNI3, MYBPC3), with no family history of sudden cardiac death. In the repeated 24-hour ECG HM, we only detected sporadic supraventricular and ventricular monotopic extrasystoles, less than 1% of the monitored time, without the presence of complex cardiac rhythm disturbances. The patient is currently not receiving any pharmacotherapy, he remains in dispensary care, and according to current recommendations for the diagnosis and treatment of HCMP, ICD implantation has not yet been indicated. (Fig-4)

SCD in young athletes is typically the result of structural and arrhythmogenic heart disease, which is underdiagnosed in this population, also because athletes are often completely asymptomatic. Therefore, the European Society of Cardiology (ESC) has issued recommendations for the inclusion of ECG in preventive sports examinations for all athletes. Nowadays, there is a steady increase in the number of recreational athletes and practitioners do not have much experience in assessing 12-lead ECG in athletes and often use the same criteria for its evaluation as in the general population of non-sporting people [7]. In endurance sports (long distance running, cycling, swimming) it is typical that an increased cardiac output is maintained for a long time with reduced peripheral vascular resistance, resulting in a continuous volume overload for all cardiac compartments. The morphological reflection of these changes is the echocardiographic image of eccentric hypertrophy, which is characterized by increased wall thickness and left ventricular dilatation. In contrast, high-impact and strength sports (weightlifting, American football, etc.) are characterized by normal or only slightly increased cardiac output and increased peripheral vascular resistance, resulting in increased blood pressure and increased left ventricular afterload. The typical morphological consequence in this type of strain is a thickening of the left ventricular walls (which in the athletic heart is rarely above 13 mm) with its normal size or only mild dilatation. ECG shows mostly concentric hypertrophy of the left ventricle. Then there are sports where these characteristics overlap (football, basketball, hockey, etc.), and the echocardiographic image is also not so clearly defined and is distinguished by the type of physical strain, which predominates. Without physiological classification, such left ventricular eccentric and concentric hypertrophy may be misinterpreted as hypertrophic cardiomyopathy.

Anatomically, this disease is characterized by generalized or localized left ventricular hypertrophy. Available literature data suggest that the risk of SCD in genetically determined hypertrophic cardiomyopathy is 0.6% and the overall mortality rate is 1.3%. No studies published to date confirming an association between a particular mutation and a higher or, conversely, lower risk of SCD. The problem remains when these changes may also occur in the athlete's heart. Increased left ventricular wall thickness results from increased ventricular pressure, volume overload, or both mechanisms [10]. A 2–5 mm decrease in left ventricular wall thickness after a deconditioning phase lasting 3–6 weeks almost certainly rules out HCMP and supports the diagnosis of athlete's heart [11]. The extreme left ventricular remodelling that occurs in some ultra-elite athletes raises some concern as to whether such extreme morphological adaptation may have potentially adverse clinical consequences, as 10–40% of such endurance athletes have a left ventricular end-diastolic cavity diameter above 60 mm. Such extent of enlargement is actually observed in patients with dilated cardiomyopathy. In fact, severe remodelling in a certain percentage of athletes may not recede after the cessation of active activity. Left ventricular enlargement persists in about 20 percent of elite athletes even 5 years after the end of sporting activity.

Endurance athletes have increased n. vagus tone with prolongation of the PR interval and a decrease in resting heart rate as part of the heart's adaptation to regular exercise, and isolated voltage criteria for left ventricular hypertrophy are often present, which we have confirmed in our cohort of runners. Our automated ECG module has high sensitivity and specificity to detect increased risk of sudden cardiac death in the studied population of athletes and aids in the correct interpretation of ECG changes in athletes. Endurance athletes, both professional and recreational, are more likely to have chronic myocardial remodelling, complex arrhythmias, and a higher risk of developing atrial fibrillation later in life, which we have confirmed in this study. Supraventricular arrhythmias in athletes are most often benign and do not always require therapy. Occasionally, however, they can be significantly symptomatic or cause hemodynamic collapse. In such case, however, they definitely do require therapy.

This study highlights the importance of cardiovascular screening in athletes as part of their regular medical check-ups with the emphasis on reducing SCD in sport and the importance of legislation. It also emphasizes the merit of ECG and other imaging modalities such as echocardiography in cardiovascular screening in athletes, and points out the impact of education on sports check-ups in athletes and coaches of sports clubs. The paper highlights the importance of taking a thorough medical history and confirms that endurance athletes in particular are at risk of arrhythmias and chronic myocardial remodelling and that most diseases that are associated with increased risk of SCD are identifiable by changes in resting ECG. Our study has also confirmed that endurance athletes, both professional and recreational, are at higher risk of developing atrial fibrillation later in life, fibrillation is more often paroxysmal, and does not require anticoagulation therapy due to low CHADSVASC2 scores. Supraventricular arrhythmias in athletes are most often benign and do not always require therapy.

Occasionally, however, they may be significantly symptomatic or cause hemodynamic collapse. In such cases, however, they definitively do require therapy. During the follow-up monitored period, we detected arrhythmias in thirteen athletes in our cohort of athletes, most of whom subsequently underwent interventional procedures for arrhythmia, and we continue to monitor four other athletes for higher degrees of AV block and ventricular extrasystoles. As in previously published studies, we could not confirm relation between the thickness of the interventricular septum in athletes and a higher incidence of ectopic activity or complex arrhythmias; however, an IVS thickness of more than 13.0 mm in athletes always raises suspicion of cardiomyopathy or other disease. Three athletes in whom we detected cardiomyopathy and heart valve disease, which had to stop their sporting career, the interventricular septal thickness averaged 14.5 mm. We believe that the prevention of SCD in athletes lies in improving and expanding the cardiovascular screening. The risk of health deterioration through sport may be present at all ages and can only be prevented if the athlete has a comprehensive knowledge of his/her health condition and the intensity and frequency of his/her physical exertion is adapted accordingly.

ARVC/D – Arrhythmogenic Right Ventricular Cardiomyopathy/Displasia

AVNRT – AV Nodal Reentrant Tachycardia

AF – Atrial Fibrillation

BMI – body mass index

BP – blood pressure

CMRI - Cardiac Magnetic Resonance Imaging

CVD - Cardiovascular Disease

ECG – Electrocardiogram

EPS – electrophysiology study

ESC – European Society of Cardiology

ECG HM - Elektrocardiogram holter monitoring

ECHO -echocardiography

HCMP – Hypertrophic Cardiomyopathy

ICD – Implantable Cardioverter-Defibrillator

IVS -Interventricular Septum

LBBB - Left Bundle Branch Block(LBBB)

RFCA – Radiofrequency Catheter Ablation

RVOT - Right Ventricular Outflow Tract Tachycardia

SCD – Sudden Cardiac Death

SCG – selective coronarography

VES – Ventricular Extrasystoles

VT – Ventricular Tachycardia

VF – Ventricular Tachycardia

Ethical approval and consent to participate: The study was approved by the ethics committee at the Agel Košice-Šaca Hospital prior to initiation.Verbal and written informed consent was obtained from all subjects involved in the study.

Consent for publication: Not applicable

Availability of data and materials; The datasets generated and/or analysed during the current study are not publicly available due to our university policy of not putting data on web, but are available from the corresponding author on reasonable request.

Competing interest: We declare no competing Interest

Funding: We received no funding for this work

Authors' contribution: Dr. Venova conceptualized the study, Dr. Fatima helped in writting the manuscript, Dr. Zenuch helped in statistical Analysis, Dr. Fedacko read and approved the final manuscript.

Acknowledgement: We acknowledge our university for helping us in this work

Author information: Natalia Vaňovais from Clinic of Internal medicine University of Pavol Jozef Šafarik, Košice and Hospital Agel Košice Šaca, Slovakia, Lúčna 57, 04018 Košice-Šaca., Ghizal Fatima is from Department of Biotechnology, Era University, Lucknow, India. Pavol Zenuch belong to Clinic of Cardiology, Faculty of Medicine, Pavol Jozef Safarik University, Kosice, Slovakia. Jan Fedacko is fromCentre of Clinical and Preclinical Research MEDIPARK, Pavol Jozef Safarik University, Faculty of Medicine, Trieda SNP 1, 041 90 Kosice, Slovakia

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No competing interests reported.

Chart1.png
Chart 1 - Distribution of cohort by gender
Chart2.png
Chart 2 - Distribution of athletes by the type of sport
Chart3.png
Chart 3 – Distribution of IVS by thickness

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Cardiovascular Screening of Athletes: Implications in Reducing the Risk of Sudden Cardiac Deaths

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Prevalence of cardiovascular abnormalities in potentially healthy athletes in our cohort

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