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[Prevalence of Abnormal Electrocardiographic Patterns in Icelandic Soccer Players and Relationship with Echocardiographic Findings.]
Abstract
An abnormal electrocardiogram (ECG) is common among young athletes but the underlying cause is unclear. Therefore it is hard to predict how accurate ECG is when screening for sudden cardiac death (SCD) in elite athletes.
OBJECTIVE
1) to determine the prevalence of abnormal ECG patterns, among soccer players, especially in relation to age and 2) to link ECG patterns with echocardiographic findings in order to find out whether the ECG can predict disease and/or physiological changes.
MATERIALS AND METHODS
A total of 159 male soccer players (16-45 years, mean age 25.5 years) that participated in the UEFA cup competition 2008-2010 were studied. They underwent both an ECG and echocardiography along with routine history and cardiologic examination, according to UEFA protocol. RESULTS were classified and grouped according to standards set by The European Society of Cardiology and The American Society of Echocardiography.
RESULTS
84 (53%) had abnormal ECG patterns. The prevalence of abnormal ECG patterns decreased with age. Echocardiographic findings showed that left ventricular wall thickness, mass and diameter increased with age, along with left atrial diameter. Left ventricular wall thickness, diameter and mass were similar among those with an abnormal ECG and those with a normal ECG.
CONCLUSION
The prevalence of abnormal ECG´s is high in Icelandic soccer players, a finding that usually does not indicate underlying heart disease. There was no relationship between ECG changes and echocardiographic findings. High prevalance of abnormal ECG patterns in young athletes reduces the usefulness of ECG in screening for SCD.
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OBJECTIVE To assess physiological cardiac adaptation in adolescent professional soccer players. SUBJECTS AND DESIGN Over a 32 month period 172 teenage soccer players were screened by echocardiography and ECG at a tertiary referral cardiothoracic centre. They were from six professional soccer teams in the north west of England, competing in the English Football League. One was excluded because of an atrial septal defect. The median age of the 171 players assessed was 16.7 years (5th to 95th centile range: 14–19) and median body surface area 1.68 m2 (1.39–2.06 m2). MAIN OUTCOME MEASURES Standard echocardiographic measurements were compared with predicted mean, lower, and upper limits in a cohort of normal controls after matching for age and surface area. Univariate regression analysis was used to assess the correlation between echocardiographic variables and the age and surface area of the soccer player cohort. ECG findings were also assessed. RESULTS All mean echocardiographic variables were greater than predicted for age and surface area matched controls (p < 0.001). All variables except left ventricular septal and posterior wall thickness showed a modest linear correlation with surface area (r = 0.2 to 0.4, p < 0.001); however, left ventricular mass was the only variable that was significantly correlated with age (r = 0.2, p < 0.01). Only six players (3.5%) had structural anomalies, none of which required further evaluation. All had normal left ventricular systolic function. Sinus bradycardia was found in 65 (39%). The Solokow–Lyon voltage criteria for left ventricular hypertrophy were present in 85 (50%) and the Romhilt–Estes points score (five or more) in 29 (17%). Repolarisation changes were present in 19 (11%), mainly in the inferior leads. CONCLUSIONS Chamber dimensions, left ventricular wall thickness and mass, and aortic root size were all greater than predicted for controls after matching for age and surface area. Sinus bradycardia and the ECG criteria for left ventricular hypertrophy were common but there was poor correlation with echocardiographic left ventricular hypertrophy. The type of hypertrophy found reflected the combined endurance and strength based training undertaken.
neuropeptide S (NPS) and its receptor NPSR1 act along the hypothalamic-pituitary-adrenal axis to modulate anxiety, fear responses, nociception and inflammation. The importance of the NPS-NPSR1 signaling pathway is highlighted by the observation that, in humans, NPSR1 polymorphism associates with asthma, inflammatory bowel disease, rheumatoid arthritis, panic disorders, and intermediate phenotypes of functional gastrointestinal disorders. Because of the genetic complexity at the NPSR1 locus, however, true causative variations remain to be identified, together with their specific effects on receptor expression or function. To gain insight into the mechanisms leading to NPSR1 disease-predisposing effects, we performed a thorough functional characterization of all NPSR1 promoter and coding SNPs commonly occurring in Caucasians (minor allele frequency >0.02).
we identified one promoter SNP (rs2530547 [-103]) that significantly affects luciferase expression in gene reporter assays and NPSR1 mRNA levels in human leukocytes. We also detected quantitative differences in NPS-induced genome-wide transcriptional profiles and CRE-dependent luciferase activities associated with three NPSR1 non-synonymous SNPs (rs324981 [Ile107Asn], rs34705969 [Cys197Phe], rs727162 [Arg241Ser]), with a coding variant exhibiting a loss-of-function phenotype (197Phe). Potential mechanistic explanations were sought with molecular modelling and bioinformatics, and a pilot study of 2230 IBD cases and controls provided initial support to the hypothesis that different cis-combinations of these functional SNPs variably affect disease risk.
these findings represent a first step to decipher NPSR1 locus complexity and its impact on several human conditions NPS antagonists have been recently described, and our results are of potential pharmacogenetic relevance.
Cardiovascular remodelling in the conditioned athlete is frequently associated with physiological ECG changes. Abnormalities, however, may be detected which represent expression of an underlying heart disease that puts the athlete at risk of arrhythmic cardiac arrest during sports. It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential cardiac pathology. The present article represents the consensus statement of an international panel of cardiologists and sports medical physicians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and management of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. The aim of the present position paper is to provide a framework for this distinction. For every ECG abnormality, the document focuses on the ensuing clinical work-up required for differential diagnosis and clinical assessment. When appropriate the referral options for risk stratification and cardiovascular management of the athlete are briefly addressed.
Participation in regular intensive exercise is associated with a modest increase in left ventricular wall thickness (LVWT) and cavity size. The magnitude of these physiological changes is predominantly determined by a variety of demographic factors which include age, gender, size, ethnicity, and sporting discipline. A small minority of male athletes participating in sporting disciplines involving intensive isotonic and isometric exercise may exhibit substantial increases in cardiac size that overlap with the phenotypic manifestation of the cardiomyopathies. The most challenging clinical dilemma incorporates the differentiation between physiological left ventricular hypertrophy (LVH) (athlete's heart) and hypertrophic cardiomyopathy (HCM), which is recognized as the commonest cause of non-traumatic exercise related sudden cardiac death in young (<35 years old) athletes. This review aims to highlight the distribution and physiological upper limits of LVWT in athletes, determinants of LVH in athletes, and echocardiographic methods of differentiating athlete's heart from HCM.
In 1982 a nationwide program of pre-participation screening including 12-lead electrocardiography (ECG) was launched in Italy. The aim of this article is to examine whether this 25-year screening program should be considered a valid and advisable public health strategy. The analysis of data coming from the long-running Italian experience indicates that ECG screening has provided adequate sensitivity and specificity for detection of potentially lethal cardiomyopathy or arrhythmias and has led to substantial reduction of mortality of young competitive athletes by approximately 90%. Screening was feasible thanks to the Italian Health System, which is developed in terms of health care and prevention services, and because of the limited costs of cardiovascular evaluation in the setting of a mass program. On the basis of current scientific evidence the implementation of a mass-screening program aimed to prevent athletic-field sudden cardiac death should be at least carefully considered by public health administrators worldwide.
In some highly trained athletes, the thickness of the left ventricular wall may increase as a consequence of exercise training and resemble that found in cardiac diseases associated with left ventricular hypertrophy, such as hypertrophic cardiomyopathy. In these athletes, the differential diagnosis between physiologic and pathologic hypertrophy may be difficult.
To address this issue, we measured left ventricular dimensions with echocardiography in 947 elite, highly trained athletes who participated in a wide variety of sports.
The thickest left ventricular wall among the athletes measured 16 mm. Wall thicknesses within a range compatible with the diagnosis of hypertrophic cardiomyopathy (greater than or equal to 13 mm) were identified in only 16 of the 947 athletes (1.7 percent); 15 were rowers or canoeists, and 1 was a cyclist. Therefore, the wall was greater than or equal to 13 mm thick in 7 percent of 219 rowers, canoeists, and cyclists but in none of 728 participants in 22 other sports. All athletes with walls greater than or equal to 13 mm thick also had enlarged left ventricular end-diastolic cavities (dimensions, 55 to 63 mm).
On the basis of these data, a left-ventricular-wall thickness of greater than or equal to 13 mm is very uncommon in highly trained athletes, virtually confined to athletes training in rowing sports, and associated with an enlarged left ventricular cavity. In addition, the upper limit to which the thickness of the left ventricular wall may be increased by athletic training appears to be 16 mm. Therefore, athletes with a wall thickness of more than 16 mm and a nondilated left ventricular cavity are likely to have primary forms of pathologic hypertrophy, such as hypertrophic cardiomyopathy.
The cardiovascular system adapts to exercise. With conditioning, the heart modifies its physiologic and morphologic structure. When those changes occur in athletes seeking clearance for sports participation, they comprise the athletic heart syndrome. With detraining, many of those modifications normalize, which is a diagnostic feature of the athletic heart syndrome. It is important for practitioners who care for athletes to be cognizant of those adaptations and to differentiate them from pathologic changes that may warrant restriction from sports participation or place the athlete at risk for sudden cardiac death.
The 1996 American Heart Association consensus panel recommendations stated that pre-participation cardiovascular screening for young competitive athletes is justifiable and compelling on ethical, legal, and medical grounds. The present article represents the consensus statement of the Study Group on Sports Cardiology of the Working Group on Cardiac Rehabilitation and Exercise Physiology and the Working Group on Myocardial and Pericardial diseases of the European Society of Cardiology, which comprises cardiovascular specialists and other physicians from different European countries with extensive clinical experience with young competitive athletes, as well as with pathological substrates of sudden death. The document takes note of the 25-year Italian experience on systematic pre-participation screening of competitive athletes and focuses on relevant issues, mostly regarding the relative risk, causes, and prevalence of sudden death in athletes; the efficacy, feasibility, and cost-effectiveness of population-based pre-participation cardiovascular screening; the key role of 12-lead ECG for identification of cardiovascular diseases such as cardiomyopathies and channelopathies at risk of sudden death during sports; and the potential of preventing fatal events. The main purpose of the consensus document is to reinforce the principle of the need for pre-participation medical clearance of all young athletes involved in organized sports programmes, on the basis of (i) the proven efficacy of systematic screening by 12-lead ECG (in addition to history and physical examination) to identify hypertrophic cardiomyopathy-the leading cause of sports-related sudden death-and to prevent athletic field fatalities; (ii) the potential screening ability in detecting other lethal cardiovascular diseases presenting with ECG abnormalities. The consensus document recommends the implementation of a common European screening protocol essentially based on 12-lead ECG.
Background: Although cardiovascular screening is recommended for athletes before participating in sports, the role of 12-lead electrocardiography (ECG) remains uncertain. To date, no prospective data that compare screening with and without ECG have been available. Objective: To compare the performance of preparticipation screening limited to medical history and physical examination with a strategy that integrates these with ECG. Design: Cross-sectional comparison of screening strategies. Setting: University Health Services, Harvard University, Cambridge, Massachusetts. Participants: 510 collegiate athletes who received cardiovascular screening before athletic participation. Measurements: Each participant had routine history and examination-limited screening and ECG. They received transthoracic echocardiography (TTE) to detect or exclude cardiac findings with relevance to sports participation. The performance of screening with history and examination only was compared with that of screening that integrated history, examination, and ECG. Results: Cardiac abnormalities with relevance to sports participation risk were observed on TTE in 11 of 510 participants (prevalence, 2.2%). Screening with history and examination alone detected abnormalities in 5 of these 11 athletes (sensitivity, 45.5% [95% CI, 16.8% to 76.2%]; specificity, 94.4% [CI, 92.0% to 96.2%]). Electrocardiography detected 5 additional participants with cardiac abnormalities (for a total of 10 of 11 participants), thereby improving the overall sensitivity of screening to 90.9% (CI, 58.7% to 99.8%). However, including ECG reduced the specificity of screening to 82.7% (CI, 79.1 % to 86.0%) and was associated with a false-positive rate of 16.9% (vs. 5.5% for screening with history and examination only). Limitation: Definitive conclusions regarding the effect of ECG inclusion on sudden death rates cannot be made. Conclusion: Adding ECG to medical history and physical examination improves the overall sensitivity of preparticipation cardiovascular screening in athletes. However, this strategy is associated with an increased rate of false-positive results when current ECG interpretation criteria are used.
The European Society of Cardiology (ESC) recently published revised criteria for ECG interpretation in the athlete.
To examine the performance of the 2010 ESC ECG criteria in a population of athletes undergoing preparticipation cardiovascular disease screening.
University athletes (n=508) underwent routine medical history/physical examination and ECG before athletic participation. Transthoracic echocardiography (TTE) was also performed on each participant to detect or exclude cardiac findings with relevance to sport participation. Screening test statistics were calculated to determine the performance of the 2010 ESC criteria, and the performance of the 2010 criteria was compared with the 2005 criteria.
Application of the 2010 ESC criteria, compared with the 2005 criteria, reduced the number of participants with abnormal ECG findings from 83/508 (16.3%) to 49/508 (9.6%). The reduction in the number of abnormal ECGs was driven by the reclassification of participants with isolated QRS voltage criteria for left ventricular hypertrophy from abnormal to normal. Of the 49 participants with abnormal ECGs, 14/49 (29%) had a single ECG abnormality and 35/49 (71%) had two or more abnormalities. The use of the 2010 criteria was associated with improved specificity (reduction in the false positive rate) and preserved sensitivity when compared with the 2005 criteria.
Application of the 2010 ESC criteria for ECG interpretation in the athlete improves the accuracy of an ECG-inclusive preparticipation screening strategy by reducing the rate of false positive ECGs.
Top-level training is associated with morphological and functional changes in the heart. Left atrial (LA) enlargement can be regarded as a physiologic adaptation to exercise conditioning. Athletes show an improvement in myocardial diastolic properties and supernormal left ventricular (LV) diastolic function. The aims of the study were to assess diastolic function by pulsed Doppler tissue imaging (DTI) and to analyze the role of LA in athletes by speckle tracking echocardiography (STE).
Twenty-three male elite soccer players underwent a complete echocardiographic analysis. Twenty-six age-matched healthy sedentary men were used as controls. Measured variables included LA indexed volumes, DTI of the LV, peak atrial longitudinal strain, and peak atrial contraction strain (PACS).
LA areas and indexed volumes were significantly higher in athletes (P < 0.001). Athletes had a higher peak E velocity (P < 0.001), a lower A peak (P < 0.01), and a higher peak E/A ratio (P < 0.0001); a higher Em peak (P < 0.001), a lower Am peak (P < 0.01), and a higher Em/Am ratio (P < 0.0001). Global PACS was lower in athletes compared with controls (P < 0.0001) and strongly correlated with mitral Am (r = 0.55; P < 0.0001), mitral Em (r =-0.41; P < 0.001), heart rate (r =-0.38; P < 0.01), and LA area (r = 0.18; P < 0.05).
Athletes showed a shift in the pattern of ventricular filling period toward early diastole as seen through DTI analysis of the diastolic properties of LV and STE analysis of LA function. DTI is a useful tool to analyze the improved myocardial diastolic properties of athletes and STE may elucidate the role of LA in the context of athlete's heart remodeling.
Sudden deaths in young competitive athletes are highly visible events with substantial impact on the physician and lay communities. However, the magnitude of this public health issue has become a source of controversy.
To estimate the absolute number of sudden deaths in US competitive athletes, we have assembled a large registry over a 27-year period using systematic identification and tracking strategies. A total of 1866 athletes who died suddenly (or survived cardiac arrest), 19+/-6 years of age, were identified throughout the United States from 1980 to 2006 in 38 diverse sports. Reports were less common during 1980 to 1993 (576 [31%]) than during 1994 to 2006 (1290 [69%], P<0.001) and increased at a rate of 6% per year. Sudden deaths were predominantly due to cardiovascular disease (1049 [56%]), but causes also included blunt trauma that caused structural damage (416 [22%]), commotio cordis (65 [3%]), and heat stroke (46 [2%]). Among the 1049 cardiovascular deaths, the highest number of events in a single year was 76 (2005 and 2006), with an average of 66 deaths per year (range 50 to 76) over the last 6 years; 29% occurred in blacks, 54% in high school students, and 82% with physical exertion during competition/training, whereas only 11% occurred in females (although this increased with time; P=0.023). The most common cardiovascular causes were hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%).
In this national registry, the absolute number of cardiovascular sudden deaths in young US athletes was somewhat higher than previous estimates but relatively low nevertheless, with a rate of <100 per year. These data are relevant to the current debate surrounding preparticipation screening programs with ECGs and also suggest the need for systematic and mandatory reporting of athlete sudden deaths to a national registry.
These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia.
Cardiac enlargement in athletes was already recognised by the end of the 19th century through percussion of the chest in cross country skiers, and was later confirmed by use of radiography and evidence from necropsy. The advent of echocardiography allowed investigators to gain a better insight into the heart of athletes, and these findings were in general confirmed by other techniques such as magnetic resonance imaging. The present review will focus on the impact of different sports and training on cardiac structure and function, and on electrocardiographic alterations associated with athlete’s heart.
### Left ventricle
#### Cross sectional studies
Physical exercise is associated with haemodynamic changes and alters the loading conditions of the heart. In dynamic exercise the emphasis is on movement with no or minimal development of force. The main haemodynamic features are increases in heart rate and stroke volume, the two components of cardiac output. Systemic vascular resistance drops but the net result is a slight to moderate rise in blood pressure. The load on the heart is predominantly that of volume. In static exercise force is developed with no or minimal movement. The haemodynamic consequences involve a slight elevation of cardiac output, caused by the increase of heart rate, and a more pronounced rise of blood pressure, resulting in a pressure load on the heart. From a theoretical point of view the haemodynamic alterations and the ventricular loading conditions during exercise could, in the long run, lead to left ventricular hypertrophy (LVH). Volume load would lead to enlargement of the left ventricular internal diameter and a proportional increase of wall thickness; this type of adaptation is termed eccentric LVH. The pressure load would induce thickening of the ventricular wall with unchanged internal dimension, or concentric LVH. It was suggested that these cardiac adaptations serve to normalise wall stress.
Individual studies showed that cardiac adaptations …
Previous studies that determined the normal limits for the paediatric ECG had their imperfections: ECGs were recorded at a relatively low sampling rate, ECG measurements were conducted manually, or normal limits were presented for only a limited set of parameters. The aim of this study was to establish an up-to-date and complete set of clinically relevant normal limits for the paediatric ECG.
ECGs from 1912 healthy Dutch children (age 11 days to 16 years) were recorded at a sampling rate of 1200 Hz. The digitally stored ECGs were analysed using a well-validated ECG computer program. The normal limits of all clinically relevant ECG measurements were determined for nine age groups. Clinically significant differences were shown to exist, compared with previously established normal limits. Sex differences could be demonstrated for QRS duration and several amplitude measurements.
These new normal limits differ substantially from those commonly used and suggest that diagnostic criteria for the paediatric ECG should be adjusted.
Establishment of upper normal limits of physiological hypertrophy in response to physical training is important in the differentiation of physiological and pathological left ventricular hypertrophy. The genetic differences that exist in the adaptive response of the heart to physical training and the causes of sudden cardiac death in young athletes indicate the need for population-specific normal values. Between September 1994 and December 2001, 442 (306 male, 136 female) elite British athletes from 13 sports were profiled. Standard two-dimensional guided M-mode and Doppler echocardiography were employed to evaluate left ventricular morphology and function. Eleven (2.5%) athletes, competing in a range of sports including judo, skiing, cycling, triathlon, rugby and tennis, presented with a wall thickness >13 mm, commensurate with a diagnosis of hypertrophic cardiomyopathy. Eighteen (5.8%) male athletes presented with a left ventricular internal diameter during diastole (LVIDd) >60 mm, with an upper limit of 65 mm. Of the 136 female athletes, none where found to have a maximum wall thickness >11 mm. Left ventricular internal diameter was <60 mm in all female athletes. Systolic and diastolic function were within normal limits for all athletes. Upper normal limits for left ventricular wall thickness and LVIDd are 14 mm and 65 mm for elite male British athletes, and 11 mm and 60 mm for elite female British athletes. Values in excess of these should be viewed with caution and should prompt further investigation to identify the underlying mechanism.
Objectives:
In the present study we assessed the distribution and clinical significance of left atrial (LA) size in the context of athlete's heart and the differential diagnosis from structural heart disease, as well as the proclivity to supraventricular arrhythmias.
Background:
The prevalence, clinical significance, and long-term arrhythmic consequences of LA enlargement in competitive athletes are unresolved.
Methods:
We assessed LA dimension and the prevalence of supraventricular tachyarrhythmias in 1,777 competitive athletes (71% of whom were males), free of structural cardiovascular disease, that were participating in 38 different sports.
Results:
The LA dimension was 23 to 50 mm (mean, 37 +/- 4 mm) in men and 20 to 46 mm (mean, 32 +/- 4 mm) in women and was enlarged (i.e., transverse dimension > or = 40 mm) in 347 athletes (20%), including 38 (2%) with marked dilation (> or = 45 mm). Of the 1,777 athletes, only 14 (0.8%) had documented, symptomatic episodes of either paroxysmal atrial fibrillation (n = 5; 0.3%) or supraventricular tachycardia (n = 9; 0.5%), which together occurred in a similar proportion in athletes with (0.9%) or without (0.8%; p = NS) LA enlargement. Multivariate regression analysis showed LA enlargement in athletes was largely explained by left ventricular cavity enlargement (R2 = 0.53) and participation in dynamic sports (such as cycling, rowing/canoeing) but minimally by body size.
Conclusions:
In a large population of highly trained athletes, enlarged LA dimension > or = 40 mm was relatively common (20%), with the upper limits of 45 mm in women and 50 mm in men distinguishing physiologic cardiac remodeling ("athlete's heart") from pathologic cardiac conditions. Atrial fibrillation and other supraventricular tachyarrhythmias proved to be uncommon (prevalence < 1%) and similar to that in the general population, despite the frequency of LA enlargement. Left atrial remodeling in competitive athletes may be regarded as a physiologic adaptation to exercise conditioning, largely without adverse clinical consequences.
Sudden death of competitive athletes is rare. However, they continue to have an impact on both the lay and medical communities. These deaths challenge the perception that trained athletes represent the healthiest segment of modern society. There is an increasing frequency of such reported deaths worldwide and the visibility of this issue is underlined by the high-profile nature of each case. Differential diagnosis between pathological and the physiologic (nonpathological) responses to high levels of physical training has become clinically more important. The purpose of this review is to highlight the main echocardiograph characteristics related to different types of training/sports participation and to highlight already recognized and newer concepts in their clinical assessment.