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can reveal changes associated with cardiac disease&#46; However&#44; ECG changes in athletes are common and usually reflect structural and electrical remodeling of the heart as an adaptation to regular physical training &#40;known as athlete&#39;s heart&#41;&#46; On the other hand&#44; abnormalities on a young athlete&#39;s ECG can also be an expression of an underlying disease that may carry a risk of sudden cardiac death &#40;SCD&#41; during sports&#46; Lack of knowledge of the &#8216;normal&#8217; ECG changes in athletes may lead to a diagnostic odyssey with an unfavorable cost&#8211;benefit ratio&#44; and often limits participation in sports to athletes whose ECG patterns are within the normal pattern&#46; Many of the ECG changes seen in athletes may overlap with patterns considered pathological in other subgroups of individuals&#44; and this is one of the main limitations of ECG screening in this population &#8211; the high number of false positives&#46; Alternatively&#44; signs of potentially lethal cardiovascular disorders may be misinterpreted as normal variants of an athlete&#39;s ECG&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Current European Society of Cardiology &#40;ESC&#41; guidelines include an ECG&#44; besides physical examination&#44; as a prescreening test for athletes&#46; However&#44; concern has focused in particular on the availability of practitioners qualified to interpret ECGs and the burden of false-positive results&#46; The American Heart Association &#40;AHA&#41; and the ESC have both published recommendations for the interpretation of the ECG in athletes&#46;<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">2&#44;3</span></a> The present review presents a summary of the most frequent ECG changes considered &#8216;normal&#8217; in athletes&#44; as well as a brief discussion regarding the advantages and disadvantages of ECG screening in this population&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Cardiac remodeling in athletes</span><p id="par0020" class="elsevierStylePara elsevierViewall">Athlete&#39;s heart is currently defined as a non-pathological condition in which the heart undergoes morphological and functional changes that result from a process of adaptation to intensive exercise&#46; The heart is usually enlarged and the resting heart rate is lower than normal&#46; Henschen first described the athlete&#39;s heart in 1899&#59; using only careful thoracic percussion&#44; he recognized an enlargement of the heart caused by athletic activity in cross-country skiers&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">4</span></a> He concluded that both dilation and hypertrophy were present&#44; involving both sides of the heart&#44; and that these changes were adaptive and improved performance&#46; Since then&#44; numerous descriptions and characterization of the athlete&#39;s heart have been performed with the improvements in cardiac imaging such as chest X-ray&#44; echocardiography and cardiac magnetic resonance imaging &#40;CMRI&#41;&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The cardiovascular adaptation to exercise differs with the type of conditioning&#58; endurance &#40;dynamic&#47;aerobic&#41; and strength training &#40;isometric&#47;anaerobic&#41;&#46; Some sports&#44; such as cycling and rowing&#44; combine both types of conditioning&#46; The adaptation to exercise has two distinct phases&#58; an acute and a chronic phase&#46; The acute response varies according to the type of exercise&#46; In endurance training there is a substantial increase in maximum oxygen uptake&#44; cardiac output&#44; stroke volume and systolic blood pressure&#44; associated with decreased peripheral vascular resistance&#46; On the other hand&#44; strength training causes only a mild increase in maximum oxygen uptake and cardiac output but substantial increases in blood pressure&#44; peripheral vascular resistance and heart rate&#46; Over the long term&#44; the cardiovascular adaptation to aerobic exercise includes increased maximum oxygen uptake &#40;due to increased cardiac output&#41; and an increase in arteriovenous oxygen difference&#44; while strength exercise results in little or no increase in oxygen uptake&#46; Thus&#44; endurance exercise predominantly produces volume load in the left ventricle and strength training mainly causes pressure load&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">5</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Cardiac remodeling secondary systematic training &#40;endurance or strength&#41; is not uniform&#46; In fact&#44; only 50&#37; of trained athletes actually show evidence of cardiac remodeling &#40;change in atrial and ventricular dimensions associated with normal systolic and diastolic function&#44; with or without increased left ventricular wall thickness&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">6</span></a> Left ventricular enlargement &#40;&#62;60 mm&#41; occurs in &#8764;15&#37; of highly trained athletes&#44; and can be accompanied by an increase in absolute left ventricular wall thickness&#46;<a class="elsevierStyleCrossRefs" href="#bib0200"><span class="elsevierStyleSup">6&#44;7</span></a> These changes are dynamic in nature&#44; develop rapidly after initiation of vigorous exercise&#44; and are reversible with cessation of training&#46; Although the changes in athlete&#39;s heart overlap significantly with age- and gender-matched sedentary controls&#44; an important point to consider when examining a young athlete is the type of exercise&#44; since endurance&#47;aerobic training produces the most marked changes&#44;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">8</span></a> and the pattern and extent of physiologically increased left ventricular mass varies with the nature of sports training&#46; The most extreme increases in cavity dimension or wall thickness have been observed in athletes practicing rowing&#44; skiing&#44; cycling and swimming&#46;<a class="elsevierStyleCrossRefs" href="#bib0215"><span class="elsevierStyleSup">9&#44;10</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Normal electrocardiographic changes in athletes</span><p id="par0035" class="elsevierStylePara elsevierViewall">Many preparticipation screening programs for sports include an ECG&#46; Physicians responsible for the interpretation of these ECGs should be able to distinguish those changes that result from physiological adaptation to exercise&#44; that are not pathological and reflect electrical and structural remodeling and autonomic nervous system adaptations to sustained physical activity&#46; Up to 60&#37; of athletes demonstrate ECG changes as a reflection of adaptation to exercise&#46; Normal ECG changes are described in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#46; The extent of these changes depends on the athlete&#39;s ethnicity&#44; age&#44; gender and level of training&#44; as well as the type of training and even the type of sport&#46; All these factors should be considered when looking at an athlete&#39;s ECG&#46; Sports physicians and cardiologists should be aware of the normal changes on the ECGs of athletes&#44; since a wrong diagnosis can have a significant impact on the life of a young athlete&#46; At one extreme of the spectrum of ECG changes reflecting electrical remodeling&#44; physicians may even indicate complete cessation of all sports&#44; even if cardiac imaging &#40;echocardiography or CMRI&#41; shows no changes&#46; The ESC guidelines for interpretation of the 12-lead ECG in the athlete divide changes on an athlete&#39;s ECG into two groups&#58; Group 1 &#8211; common and training-related and Group 2 &#8211; uncommon and training-unrelated&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a> Normal ECG changes may be summarized as follows&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">&#8226;</span><p id="par0040" class="elsevierStylePara elsevierViewall">Sinus bradycardia&#44; sinus arrhythmia&#44; first-degree atrioventricular &#40;AV&#41; block and junctional escape rhythm</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">&#8226;</span><p id="par0045" class="elsevierStylePara elsevierViewall">Incomplete right bundle branch block &#40;iRBBB&#41;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">&#8226;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Early repolarization</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">&#8226;</span><p id="par0055" class="elsevierStylePara elsevierViewall">Isolated QRS voltage criteria for left ventricular hypertrophy</p></li></ul></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall">These normal&#44; and exercise-related&#44; ECG changes should be distinguished from much more uncommon&#44; and pathological&#44; changes such as ST-T repolarization abnormalities &#40;T-wave inversion&#44; ST-segment depression&#41;&#44; pathological Q waves&#44; left or right axis deviation&#44; intraventricular conduction defects&#44; ventricular pre-excitation&#44; right ventricular hypertrophy and Brugada-like repolarization changes&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Sinus bradycardia and asymptomatic sinus pauses greater than 2 s &#40;particularly during sleep&#41; are common in athletes and are due to increased vagal tone&#46; In the absence of symptoms such as fatigue&#44; syncope or dizziness&#44; a heart rate &#62;30 bpm should be considered normal in a well-trained athlete&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">11</span></a> Additionally&#44; up to 55&#37; of well-trained athletes may have sinus arrhythmia&#44; caused by an exaggerated response to inspiration and expiration&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">12</span></a> A junctional rhythm occurs when the depolarization rate of the AV node is faster than the sinus rate&#59; however&#44; sinus rhythm resumes with increasing heart rate&#46; Increased vagal activity may also cause first-degree AV block &#40;up to 35&#37; of cases&#41; and Mobitz-type I second-degree AV block &#40;up to 10&#37; of cases&#41;&#44; and these changes resolve with faster heart rates during exercise&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">13</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Incomplete right bundle branch block &#40;iRBBB&#41; &#40;defined as a QRS duration &#60;120 ms and a right bundle branch block pattern&#41; is also a very common finding in athletes &#40;35&#37;&#8211;50&#37;&#41; compared with less than 10&#37; in young healthy controls&#44;<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">2&#44;14</span></a> and is reversible with deconditioning&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">14</span></a> This right ventricular conduction delay is possibly caused by enlarged right ventricular &#40;RV&#41; cavity size and RV remodeling&#44; resulting in increased conduction time&#44; and not by a delay within the specialized conduction system&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">15</span></a> The occurrence of iRBBB in an asymptomatic athlete with a negative family history and physical examination does not require further evaluation&#46; Although typical iRBBB is uncommon in arrhythmogenic right ventricular cardiomyopathy &#40;ARVC&#41;&#44; particular attention should be paid to ST-T abnormalities in patients with iRBBB because ARVC may present with iRBBB with T-wave inversion in the mid-precordial leads beyond V2&#44; low limb-lead voltages and premature ventricular beats with a left bundle branch block pattern&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Early repolarization has long been recognized as a common&#44; idiopathic and benign finding in young individuals&#46; Its prevalence is estimated to be 1&#37;&#8211;2&#37; in the general population&#44; with a clear male preponderance&#44;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">16</span></a> and it is observed in 50&#37;&#8211;80&#37; of young athletes&#8217; ECGs&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">17</span></a> Early repolarization is associated with the increased vagal tone observed in athletes and is a reversible phenomenon that disappears with deconditioning&#46; The most common pattern seen in Caucasians is an elevated ST segment with an upward concavity&#44; ending in a positive &#40;&#8216;peaked and tall&#8217;&#41; T wave&#46; These changes are more marked in V3&#8211;4&#44; but maximal ST-segment displacement may also be seen in V5&#44; V6&#44; I and aVL or in the inferior leads &#40;II&#44; III and aVF&#41;&#46; Early repolarization can be markedly different in athletes of African&#8211;Caribbean descent&#44; in whom an elevated ST segment with an upward convexity is followed by a negative T wave in V2&#8211;V4 &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46; If not interpreted in the appropriate context&#44; an ECG with such changes in an African&#8211;Caribbean athlete may lead to misinterpretation of the ECG&#44; with a consequent misdiagnosis and possibly withdrawal from sports&#46; Normal repolarization changes in African&#8211;Caribbean athletes do not extend beyond V4&#46; Thus&#44; T-wave inversion in the lateral leads &#40;V5&#8211;V6&#41; is always considered an abnormal finding and requires additional testing to rule out hypertrophic cardiomyopathy &#40;HCM&#41; or other cardiomyopathies&#46; These changes are modulated by the autonomic nervous system and vary with heart rate&#46; Slowing of heart rate exaggerates ST-segment elevation whereas sinus tachycardia reduces and can even eliminate early repolarization changes&#46; Late QRS slurring or notching with horizontal ST-segment elevation in the inferolateral leads has been associated with an increased risk of arrhythmic death in one study of middle-aged&#44; non-athletic Finnish citizens&#46;<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">18</span></a> However&#44; a significant percentage of young competitive athletes &#40;25&#37;&#8211;30&#37;&#41; show early repolarization with similar morphological features in either the inferior or lateral leads&#44;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">19</span></a> a finding that is related to increased vagal tone&#46; The currently available data are too scarce to assume a cause&#8211;effect relationship between this ECG pattern and the risk of malignant ventricular arrhythmias&#59; however&#44; in athletes presenting with syncope or cardiac arrest which remains unexplained after a detailed clinical work-up aimed to exclude cardiac causes and neuromediated mechanisms&#44; the ECG pattern of early repolarization in the inferior and&#47;or lateral leads&#44; particularly when associated with prominent terminal QRS slurring&#44; should raise the suspicion of underlying idiopathic ventricular fibrillation&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0080" class="elsevierStylePara elsevierViewall">As described previously&#44; cardiac remodeling in athletes&#44; among other changes&#44; is associated with an increase in absolute left ventricular wall thickness&#44; ventricular mass and increased chamber dimensions&#46; These changes may be reflected on the 12-lead ECG as an isolated increase in QRS amplitude&#44; with normal QRS axis&#44; normal atrial and ventricular activation patterns and normal ST-segment and T-wave repolarization&#46; Many factors can affect the QRS voltage in athletes&#44; which is higher in males&#44; black individuals and athletes engaged in endurance sports such as cycling&#44; skiing and rowing&#47;canoeing&#46; Although anything between the left ventricular myocardium and the surface electrodes will affect QRS voltage&#44; the presence of higher QRS voltage&#44; without ST-T segment abnormalities&#44; reflects the physiological LV hypertrophy associated with training and is benign&#46; Other non-voltage criteria for LV hypertrophy&#44; such as atrial enlargement&#44; left axis deviation or a strain pattern of repolarization &#40;ST-segment depression in V5&#8211;6&#44; I and aVL&#41;&#44; are not usually seen in athletes and should raise the suspicion of an underlying pathology&#44; such as aortic valve disease&#44; hypertension&#44; or HCM&#46; Although HCM can present with isolated increased QRS voltage this is a very uncommon finding&#46;<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">20</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Abnormal and training-unrelated electrocardiogram changes</span><p id="par0085" class="elsevierStylePara elsevierViewall">The most common causes of athlete deaths are HCM &#40;up to 36&#37; of cases&#41; and coronary artery anomalies&#44; together accounting for a little over 50&#37; of SCD in competitive athletes&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">21</span></a> Other causes include dilated cardiomyopathy &#40;DCM&#41;&#44; ARVC &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41; and cardiac ion-channel diseases such as long QT syndrome and Brugada syndrome &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; The ECG may disclose changes associated with these conditions &#40;inverted T waves and ST-segment depression&#44; pathological Q waves&#44; Brugada-like repolarization changes and others&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46; Such abnormalities are uncommon in athletes &#40;&#60;5&#37;&#41; and&#44; when present&#44; should always raise the suspicion of an underlying cardiac disease&#59; further work-up is thus mandatory&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a> ECG abnormalities of structural heart diseases that manifest with left ventricular hypertrophy&#44; such as HCM&#44; hypertensive heart disease or aortic stenosis&#44; overlap only marginally with training-related ECG changes&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a> An isolated QRS voltage criterion for LV hypertrophy is a very unusual pattern in pathological causes of LV hypertrophy such as HCM or hypertensive heart disease&#59; in these patients&#44; one or more additional non-voltage criteria such as atrial enlargement&#44; left axis deviation&#44; ST-segment and T-wave abnormalities&#44; and pathological Q-waves are usually present&#44; unlike in the physiological LV hypertrophy of athletes&#46; HCM is a common genetic disease present in 1&#58;500 of adults&#44;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">22</span></a> although it appears to be less common in competitive athletes &#40;1&#58;1000&#8211;1&#58;1500&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">23</span></a> HCM can be diagnosed with the ECG &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41; in combination with echocardiography or CMRI&#46; However&#44; up to 6&#37; of HCM patients have a normal ECG&#59; this subset of patients appear to have a less severe phenotype with better cardiovascular outcomes&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">24</span></a> Based on these premises&#44; the European guidelines for interpretation of 12-lead ECG in the athlete recommend that&#44; regardless of personal and family history&#44; athletes with non-voltage criteria for LV hypertrophy should undergo echocardiographic evaluation to exclude underlying structural heart disease&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0090" class="elsevierStylePara elsevierViewall">Other ECG changes&#44; if present in a young athlete&#44; should prompt further investigation to exclude cardiac disease&#46; These include resting or exercise-induced ST-segment depression&#44; right atrial enlargement and right ventricular hypertrophy&#44; T-wave inversion&#44; intraventricular conduction abnormalities &#40;complete bundle branch block and hemiblock&#41;&#44; abnormal QT interval &#40;long or short&#41; and Brugada-like ECG abnormalities&#46; Special attention should be paid to T-wave inversion&#44; which is not&#44; as once believed&#44; a common and training-related ECG change&#59; the presence of T-wave inversion of &#62;2 mm in two or more adjacent leads in an athlete is a non-specific warning sign of a potential cardiovascular disease at risk of SCD during sports&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a> This finding may represent the initial phenotypic expression of an underlying cardiomyopathy&#44; prior to the development of morphological changes detectable on cardiac imaging&#46; T-wave inversion in the inferior &#40;II&#44; III and aVF&#41; and&#47;or lateral &#40;I&#44; aVL&#44; V5 and V6&#41; leads should raise the suspicion of ischemic heart disease&#44; aortic valve disease&#44; hypertensive cardiomyopathy&#44; HCM or LV non-compaction&#44;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">25</span></a> and post-pubertal persistence of T-wave inversion beyond V1 may reflect an underlying congenital heart defect with RV pressure and volume overload&#44; ARVC<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">26</span></a> or&#44; uncommonly&#44; an inherited ion-channel disease&#46; Knowing that &#62;2 mm T-wave inversion may identify athletes at risk for subsequent development of structural heart disease underscores the importance of continued clinical surveillance and follow-up with serial ECG and echocardiograms&#46; Currently&#44; the significance of minor T-wave changes such as flat and&#47;or minimally inverted &#40;&#60;2 mm&#41; T waves in two or more leads &#40;mostly inferior and&#47;or lateral&#41; is unclear&#44; and there is also no consensus regarding the presence of biphasic T waves&#46; However&#44; if the negative portion of the T wave is &#62;1 mm in depth in two or more leads &#40;excluding leads V1&#44; aVR and V1&#41;&#44; it is reasonable to consider this pattern as abnormal until more data are obtained&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">27</span></a> As described above&#44; special attention should be paid to athletes of African&#47;Caribbean descent in whom early repolarization is manifested as an elevated ST segment with upward convexity followed by a negative T wave &#40;which can be profound&#41; in V2 through V4&#46; This finding is not considered abnormal and should be distinguished from other pathological patterns such as the presence of T-wave inversions in V1 through V4 with a flattened ST segment&#44; as occurs in ARVC&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">28</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Preparticipation screening of athletes</span><p id="par0095" class="elsevierStylePara elsevierViewall">Any screening program should be designed to take into account the frequency of the event&#44; change or abnormality that it is desired to prevent or detect&#46; Sudden cardiac death in athletes is an infrequent event&#44; and only a very small proportion of those participating in sports are in fact at risk because of unsuspected cardiovascular disease&#46; Screening programs should be driven by sound scientific principles based on evidence-based data and not by reaction to catastrophic events &#40;such as the death of an athlete on the field&#41;&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">The conditions most frequently responsible for sudden death in young athletes are HCM&#44; a relatively common condition in the general population &#40;1&#58;500<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">29</span></a>&#41;&#44; and coronary artery anomalies&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">21</span></a> Other&#44; much rarer&#44; conditions include ion channelopathies such as Brugada syndrome and long and short QT syndrome&#44; ARVC&#44; DCM and Marfan syndrome&#46; These may amount to an estimated combined prevalence of 0&#46;3&#37; in general athlete populations&#46; However&#44; these diseases do not always cause changes on the ECG&#44; which substantially reduces the sensitivity of the exam&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">The greatest disadvantage of preparticipation screening of young athletes&#8217; ECGs for abnormalities that may disclose a cardiac disease is the high number of false positives&#46; Unawareness of the changes regarded as normal on young athletes&#8217; ECGs can lead to these being classified as abnormal in up to 50&#37; of athletes&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">2</span></a> Knowledge of the ECG changes associated with the type and intensity of exercise&#44; race&#44; age and gender can be expected to lower the traditionally high number of false positives&#44; thus reducing unnecessary investigations&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">In 1996&#44; the American Heart Association &#40;AHA&#41; issued a scientific statement advocating universal cardiovascular preparticipation screening for high school and college athletes in an attempt to identify those at increased risk of cardiovascular events&#46;<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">30</span></a> The recommendations included a 12-point complete history and physical examination &#40;including brachial artery blood pressure measurement&#41; before competitive sports and reserved noninvasive testing such as a 12-lead ECG&#44; echocardiogram&#44; exercise testing&#44; and cardiovascular consultation for athletes in whom any abnormality was detected&#46; More recently&#44; the AHA issued a scientific statement on the assessment of the 12-lead ECG as a screening test for detection of cardiovascular disease in healthy general populations of young people&#46;<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">31</span></a> The authors argue that&#44; currently&#44; there is insufficient information available to support the view that universal screening with 12-lead ECGs in asymptomatic young people &#40;including competitive athletes&#41; for cardiovascular disease is appropriate&#46; The authors acknowledge that the ECG can promote detection of specific cardiovascular diseases and thereby benefit some individuals in a screening environment&#44; but cannot be regarded as an ideal or effective test when applied to large healthy populations&#44; and endorse the more widespread dissemination of automated external defibrillators&#46;<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">31</span></a> However&#44; to recommend abandoning screening in favor of improving resuscitation is not the best formula for progress&#46; Another argument against the feasibility of such a screening program is the absence of infrastructure for routine ECG screening that covers all the population of young athletes&#46; Such an infrastructure should include experienced physicians specializing in sports medicine who are able to correctly interpret a large volume of young athletes&#8217; ECGs&#44; taking into consideration the normal and abnormal ECG changes in this population&#44; and refer cases considered abnormal according to current ESC and AHA recommendations for further cardiovascular evaluation&#46;<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">2&#44;3</span></a> The working group acknowledges&#44; however&#44; that screening with 12-lead ECGs&#44; in association with comprehensive history-taking and physical examination&#44; may be considered in relatively small cohorts of young healthy people 12&#8211;25 years of age&#44; provided that the known and anticipated limitations of the 12-lead ECG as a population screening test are recognized&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">However&#44; the prescreening strategy of the ESC and the International Olympic Committee differs significantly from the American approach in that universal 12-lead rest ECGs are recommended for athletes &#60;35 years&#46; This recommendation relies heavily on the 25-year Italian experience of systematic ECG preparticipation screening of competitive athletes&#44; a program that started in 1982&#46; According to Corrado et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">32</span></a> the annual incidence of SCD in athletes decreased from 3&#46;6 deaths per 100<span class="elsevierStyleHsp" style=""></span>000 person-years &#40;1 death per year per 27<span class="elsevierStyleHsp" style=""></span>777 athletes&#41; in 1979&#8211;1981 to 0&#46;4 deaths per 100<span class="elsevierStyleHsp" style=""></span>000 person-years &#40;1 death per year per 250<span class="elsevierStyleHsp" style=""></span>000 athletes&#41; in 2003&#8211;2004&#44; an 89&#37; reduction&#44; with no change in mortality rates among the unscreened nonathletic population&#46; Although this is the largest report to date on SCD in athletes&#44; there are important limitations that should be taken into account&#46;<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">33</span></a> The study was a population-based observational report and not a temporally controlled comparison of screening versus non-screening in athletes&#59; a separate analysis of the routine use of ECGs compared with more limited screening in identifying athletes at increased risk is not provided&#59; the annual death rate before the initiation of the program was 1 per year per 27<span class="elsevierStyleHsp" style=""></span>000 athletes&#44; which is relatively high compared with other studies&#59; the lowest annual death rate achieved with screening was 0&#46;4 deaths per 100<span class="elsevierStyleHsp" style=""></span>000 person-years &#40;similar to the 0&#46;44 sudden deaths per 100<span class="elsevierStyleHsp" style=""></span>000 person-years reported for high school and college athletes in the USA from 1983 to 1993<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">34</span></a>&#41;&#59; and the event rates in the Italian study included all events&#44; not those that occurred only with exertion&#46;</p><p id="par0120" class="elsevierStylePara elsevierViewall">Considering that the most common cause of SCD in athletes is HCM&#44; this supports the strategy of ECG screening&#44; since HCM can be reliably identified&#44; or at least suspected&#44; with an ECG in most HCM patients&#46; In this particular case only a very small subset &#40;&#8764;6&#37;&#41; of patients with HCM&#44; those with a normal ECG&#44; would be missed&#46; This group appears to have a better prognosis compared to HCM patients with ECG changes&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">24</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">The efficacy and efficiency of screening with ECG in athletes has not yet been fully demonstrated&#46; As stated above&#44; the efficiency of a screening program depends on the frequency of the condition or event for which it was designed to identify&#44; and sudden death in an athlete&#44; which has a high media profile&#44; is a rare event&#46; The ECG is not an ideal method for screening due to the high numbers of false positives and false negatives&#44; and obviously the cost-effectiveness of this strategy depends on the specific health-care system in which it is implemented&#46; The ECG is intended only as the first line in the screening process&#59; it is not expected or claimed to be absolutely &#8220;diagnostic&#8221;&#46; Moreover&#44; conditions that can cause SCD&#44; such as coronary artery anomalies or catecholaminergic polymorphic ventricular tachycardia&#44; cannot be reliably identified by the currently recommended ECG screening&#44; and identifying an athlete with a genetically based SCD condition may serve many others in the family&#46; This is not just about preventing death on the athletic field&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">To conclude&#44; a large number of young athletes present with ECG changes&#44; most resulting from adaptation to exercise&#44; and only a very small number actually have changes that are considered abnormal and that prompt further investigation&#46; Athletes with ECG changes due to cardiac adaptation to physical exertion should be reassured that they can continue to participate in competitive sports without additional investigation&#44; in the absence of symptoms or a family history of cardiac disease or premature SCD&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conflicts of interest</span><p id="par0135" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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          "titulo" => "Introduction"
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        5 => array:2 [
          "identificador" => "sec0010"
          "titulo" => "Cardiac remodeling in athletes"
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        6 => array:2 [
          "identificador" => "sec0015"
          "titulo" => "Normal electrocardiographic changes in athletes"
        ]
        7 => array:2 [
          "identificador" => "sec0020"
          "titulo" => "Abnormal and training-unrelated electrocardiogram changes"
        ]
        8 => array:2 [
          "identificador" => "sec0025"
          "titulo" => "Preparticipation screening of athletes"
        ]
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          "identificador" => "sec0030"
          "titulo" => "Conflicts of interest"
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          "titulo" => "References"
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    "fechaRecibido" => "2015-05-29"
    "fechaAceptado" => "2015-09-13"
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          "clase" => "keyword"
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          "palabras" => array:3 [
            0 => "Athlete&#39;s heart"
            1 => "Electrocardiographic screening"
            2 => "Sudden death"
          ]
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          "clase" => "keyword"
          "titulo" => "Palavras-chave"
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          "palabras" => array:3 [
            0 => "Cora&#231;&#227;o de atleta"
            1 => "Rastreio de ECG"
            2 => "Morte s&#250;bita"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Young athletes are considered the healthiest group in society&#46; Although rare&#44; there are still reports of sudden death or cardiac arrest on the playing fields&#46; Clinical evaluation is of paramount importance for the identification of possible pathological states that confer increased risk of these events&#46; Interpretation of the electrocardiogram of young athletes can help identify changes associated with heart disease that might preclude the participation in sports&#46; In this context&#44; it is essential to recognize the electrocardiographic patterns that represent the structural and electrical remodeling resulting from continued adaptation to exercise&#44; and which thus do not increase the risk of adverse events during exercise&#46; The European Society of Cardiology &#40;ESC&#41; and the American Heart Association &#40;AHA&#41; have issued consensus documents summarizing which electrocardiographic abnormalities should be considered &#8216;physiological&#8217;&#44; resulting from adaptation to exercise &#40;&#8216;athlete&#39;s heart&#8217;&#41;&#44; and which should be considered pathological and thus require further study&#46; However&#44; the two societies have different approaches with respect to the electrocardiographic screening of athletes&#46; This paper provides a brief review of current evidence regarding the electrocardiographic findings considered normal and abnormal in athletes&#44; and presents the arguments of the ESC and AHA for electrocardiographic screening in this population&#46;</p></span>"
      ]
      "pt" => array:2 [
        "titulo" => "Resumo"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Os jovens atletas s&#227;o considerados como o grupo mais saud&#225;vel da sociedade&#46; Apesar de raros&#44; surgem ainda relatos de morte s&#250;bita ou paragem cardiorrespirat&#243;ria nos campos de jogo&#46; A avalia&#231;&#227;o cl&#237;nica reveste-se de primordial import&#226;ncia para a identifica&#231;&#227;o de eventuais estados patol&#243;gicos que confiram risco acrescido destes eventos&#46; A interpreta&#231;&#227;o do eletrocardiograma destes jovens atletas pode permitir identificar altera&#231;&#245;es associadas a patologia card&#237;aca que condicione ou n&#227;o a pr&#225;tica do exerc&#237;cio f&#237;sico&#46; Neste contexto&#44; torna-se essencial reconhecer os padr&#245;es eletrocardiogr&#225;ficos que representam a remodelagem estrutural e el&#233;trica resultantes da adapta&#231;&#227;o ao exerc&#237;cio continuado&#44; e que por sua vez n&#227;o acarretam risco acrescido de eventos adversos durante a pr&#225;tica de exerc&#237;cio&#46; As Sociedades Europeia e Americana de Cardiologia emitiram documentos de consenso que procuram resumir quais as altera&#231;&#245;es eletrocardiogr&#225;ficas consideradas como &#171;fisiol&#243;gicas&#187; e resultantes da adapta&#231;&#227;o ao exerc&#237;cio &#40;cora&#231;&#227;o de atleta&#41; e quais as altera&#231;&#245;es consideradas como patol&#243;gicas e que portanto implicam o estudo subsequente dos casos em que s&#227;o identificadas&#46; Estas sociedades apresentam&#44; no entanto uma abordagem diferente no que se refere ao rastreio eletrocardiogr&#225;fico de atletas&#46; Este artigo fornece uma breve revis&#227;o da evid&#234;ncia atual referente aos achados eletrocardiogr&#225;ficos considerados como normais e anormais em atletas&#44; assim como apresenta as argumenta&#231;&#245;es das Sociedades Europeia e Americana de Cardiologia referentes ao rastreio eletrocardiogr&#225;fico nesta popula&#231;&#227;o&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">ECG of an athlete of African&#8211;Caribbean descent showing an elevated ST segment with upward convexity followed by T-wave inversion in V2&#8211;4&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">ECG of a young female with right ventricular arrhythmogenic dysplasia showing T-wave inversion&#44; without ST-segment elevation&#44; in V1&#8211;V4&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">ECG of a male showing early&#44; high take-off &#40;&#62;2 mm&#41; down-sloping ST elevation &#40;coved type&#41; in V1&#8211;2 gradually descending into an inverted T wave&#44; suggestive of Brugada pattern&#46;</p>"
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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">ECG of a young male elite athlete with apical variant hypertrophic cardiomyopathy&#44; showing symmetric T-wave inversion in V3&#8211;V6 and ST elevation with J-point elevation in V2&#8211;V3&#44; suggestive of early repolarization&#46;</p>"
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        "fuente" => "Adapted from Drezner et al&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">27</span></a>"
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                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">1&#46; Sinus bradycardia &#40;&#8805;30 bpm&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">2&#46; Sinus arrhythmia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">3&#46; Ectopic atrial rhythm&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">4&#46; Junctional escape rhythm&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">5&#46; First-degree AV block &#40;PR interval &#62;200 ms&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">6&#46; Mobitz type I &#40;Wenckebach&#41; AV block&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">7&#46; Incomplete right bundle branch block&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">8&#46; Isolated QRS voltage criteria for LVH<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">9&#46; Early repolarization &#40;ST elevation&#44; J-point elevation&#44; J waves&#44; or terminal QRS slurring&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">10&#46; Convex &#40;&#8216;domed&#8217;&#41; ST segment elevation combined with T-wave inversion in leads V1&#8211;V4 in black&#47;African&#47;Caribbean athletes&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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              "identificador" => "tblfn0005"
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              "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Except QRS voltage criteria for LVH occurring with any non-voltage criteria for LVH such as left atrial enlargement&#44; left axis deviation&#44; ST segment depression&#44; T-wave inversion or pathological Q waves&#46;</p>"
            ]
          ]
        ]
        "descripcion" => array:1 [
          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Normal ECG changes in athletes&#46;</p>"
        ]
      ]
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          "leyenda" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">ARVD&#58; arrhythmogenic right ventricular dysplasia&#59; CAD&#58; coronary artery disease&#59; DCM&#58; dilated cardiomyopathy&#59; HCM&#58; hypertrophic cardiomyopathy&#59; LBBB&#58; left bundle branch block&#59; RA&#58; right atrial&#59; RBBB&#58; right bundle branch block&#59; RV&#58; right ventricular&#46;</p>"
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                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Abnormality&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Criteria for further evaluation&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Potential diagnosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">ST-segment depression&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">&#62;0&#46;5 mm below PR isoelectric line between J-junction and beginning of the T wave in V4&#8211;6&#44; I and aVL OR &#62;1 mm in any lead&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">HCM&#44; DCM&#59; CAD&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">RA enlargement and RV hypertrophy&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">P-wave amplitude 2&#46;5 mm&#59; Sokolow&#8211;Lyon voltage criteria for RV hypertrophy&#58; R &#40;V1&#41;&#43;S &#40;V5&#41; &#62;10&#46;5 mm OR R &#62;7 mm in V1 OR R&#47;S ratio &#62;1 in V1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">HCM&#59; congenital heart disease with RV pressure or volume overload&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">T-wave inversion&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">&#8805;1 mm in leads other than III&#44; aVR and V1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">HCM&#59; CAD&#59; DCM&#59; ARVD&#59; pre-excitation syndrome&#59; aortic valve disease&#59; systemic hypertension&#59; LV non-compaction&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Q waves&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">&#62;3 mm in depth and&#47;or &#62;40 ms duration in any lead except aVR&#44; III&#44; I and aVL&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">HCM&#59; CAD&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">LBBB&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">QRS &#62;120 ms and LBBB pattern&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">DCM&#59; CAD&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">RBBB&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">QRS &#62;120 ms and RBBB pattern&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">ARVD&#59; Brugada syndrome&#59; congenital heart disease&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">QTc interval&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">&#62;470 ms in males or &#62;480 ms in females&#59; &#60;340 ms in any athlete&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Long or short QT syndrome&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Brugada pattern&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Early&#44; high take-off &#40;&#62;2 mm&#41;&#44; and downsloping ST-segment elevation &#40;&#8216;J-wave&#8217;&#41; of either the coved &#40;negative T-wave&#41; or &#8216;saddle-back&#8217; &#40;positive T-wave&#41; type in V1&#8211;2&#47;V3&#46; Consider provocation testing with flecainide to unmask the diagnostic type 1 Brugada pattern&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Brugada syndrome&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Abnormal ECG changes in athletes and potential diagnoses&#46;</p>"
        ]
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    ]
    "bibliografia" => array:2 [
      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
          "identificador" => "bibs0005"
          "bibliografiaReferencia" => array:34 [
            0 => array:3 [
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              "etiqueta" => "1"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Sudden death in athletes"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "J&#46; Puig"
                            1 => "J&#46; Freitas"
                            2 => "O&#46; Costa"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:7 [
                        "tituloSerie" => "Rev Port Cardiol"
                        "fecha" => "1994"
                        "volumen" => "13"
                        "paginaInicial" => "59"
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