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To describe the overlap between structural abnormalities typical of arrhythmogenic right ventricular cardiomyopathy (ARVC) and physiological right ventricular adaptation to exercise and differentiate between pathologic and physiologic findings using CMR. We compared CMR studies of 43 patients (mean age 49 ± 17 years, 49% males, 32 genotyped) with a definitive diagnosis of ARVC with 97 (mean age 45 ± 16 years, 61% males) healthy athletes. CMR was abnormal in 37 (86%) patients with ARVC, but only 23 (53%) fulfilled a major or minor CMR criterion according to the TFC. 7/20 patients who did not fulfil any CMR TFC showed pathological finding (RV RWMA and fibrosis in the LV or LV RWMA). RV was affected in isolation in 17 (39%) patients and 18 (42%) patients showed biventricular involvement. Common RV abnormalities included RWMA (n = 34; 79%), RV dilatation (n = 18; 42%), RV systolic dysfunction (≤ 45%) (n = 17; 40%) and RV LGE (n = 13; 30%). The predominant LV abnormality was LGE (n = 20; 47%). 22/32 (69%) patients exhibited a pathogenic variant: PKP2 (n = 17, 53%), DSP (n = 4, 13%) and DSC2 (n = 1, 3%). Sixteen (16%) athletes exceeded TFC cut-off values for RV volumes. None of the athletes exceeded a RV/LV end-diastolic volume ratio > 1.2, nor fulfilled TFC for impaired RV ejection fraction. The majority (86%) of ARVC patients demonstrate CMR abnormalities suggestive of cardiomyopathy but only 53% fulfil at least one of the CMR TFC. LV involvement is found in 50% cases. In athletes, an RV/LV end-diastolic volume ratio > 1.2 and impaired RV function (RVEF ≤ 45%) are strong predictors of pathology.

Background: Physiological cardiac remodelling in highly trained athletes may overlap with dilated cardiomyopathy (DCM). Objectives: The aim of this study was to investigate the role of the electrocardiogram (ECG) in differentiating between physiological and pathological remodelling. Methods: The study population consisted of 30 patients with DCM who revealed a pathogenic variant at genetic testing and 30 elite athletes with significant cardiac remodelling defined by a left ventricular (LV) end-diastolic diameter >62 mm and/or LV ejection fraction between 45% and 50%. Results: The ECG was abnormal in 22 (73%) patients with DCM. The most common abnormalities were low voltages (n = 14, 47%), lateral T-wave inversion (TWI) (n = 6, 20%), ventricular ectopic beats (n = 5, 17%) and anterior TWI (n = 4, 13). Two athletes revealed an abnormal ECG: complete left bundle branch block (LBBB) in one case and atrial flutter in the other. The sensitivity, specificity and accuracy of the ECG in differentiating DCM from physiological adaptation to exercise in athletes was 73% (confidence interval [CI]: 54%-88%), 93% (CI: 78%-99%) and 0.83 (CI: 0.71-0.92) respectively. Conclusions: While the ECG is usually normal in athletes exhibiting significant LV dilatation and/or systolic dysfunction, this test is often abnormal in patients with DCM harbouring a pathogenic variant. Low voltages in the limb leads and lateral TWI are the most common abnormalities.

Aims Physiological cardiac remodelling in highly trained athletes may overlap with dilated cardiomyopathy (DCM). The aim of this study was to investigate the role of the ECG in differentiating between physiological and pathological remodelling. Methods and results The study population consisted of 30 patients with DCM who revealed a pathogenic variant at genetic testing and 30 elite athletes with significant cardiac remodelling defined by a left ventricular (LV) end-diastolic diameter > 62 mm and/or LV ejection fraction between 45% and 50%. The ECG was abnormal in 22 (73%) patients with DCM. The most common abnormalities were low voltages (n = 14, 47%), lateral TWI (n = 6, 20%), ventricular ectopic beats (n = 5, 17%) and anterior TWI (n = 4, 13). Two athletes revealed an abnormal ECG: complete left bundle branch block (LBBB) in one case and atrial flutter in the other. The sensitivity, specificity and accuracy of the ECG in differentiating DCM from physiological adaptation to exercise in athletes was 73% [confidence interval (CI: 54–88%), 93% (CI: 78–99%), and 0.83 (CI: 0.71–0.92), respectively. Conclusions While the ECG is usually normal in athletes exhibiting significant LV dilatation and/or systolic dysfunction, this test is often abnormal in patients with DCM harbouring a pathogenic variant. Low voltages in the limb leads and lateral TWI are the most common abnormalities.

Background Recognizing the etiology of sudden cardiac arrest (SCA) has an enormous impact on the management of victims and their immediate families. A significant proportion of SCA survivors with a structurally normal heart are not offered a diagnosis and there is no clear consensus on the type and duration of follow‐up. We aimed to assess the utility of a multidisciplinary approach in optimizing diagnosis of cardiac arrest etiology during follow‐up. Methods and Results We retrospectively assessed 327 consecutive SCA survivors (mean age 61.9±16.2 years, 80% men) who underwent secondary prevention implantable cardioverter defibrillators between May 2015 and November 2018. The initial diagnosis was recorded at the time of admission and follow‐up diagnosis was deduced from subsequent clinic records, investigations, and outcomes of multidisciplinary team meetings. Structural heart disease accounted for 282 (86%) of SCAs. Forty‐five (14%) patients had a structurally normal heart and underwent comprehensive testing and follow‐up (mean duration 93±52 weeks). On initial evaluation, 14/45 (31%) of these received a diagnosis, rising to 29/45 (64%) with serial reviews during follow‐up. Discussion in multidisciplinary team meetings and imaging reassessment accounted for 47% of new diagnoses. No additional diagnoses were made beyond 96 weeks. Nineteen (5.8%) fatalities occurred in the entire cohort, exclusively in patients with structural heart disease. Conclusions Systematic comprehensive testing combined with multidisciplinary expert team review of SCA survivors without structural heart disease improves the yield and time to diagnosis compared with previously published studies. This approach has positive implications in the management of SCA survivors and their families.

The Authors’ reply We are grateful to Dr Stuart1 for his interest in our paper.2 We agree entirely that our dilated cardiomyopathy (DCM) cohort were indeed highly selected. Most individuals with DCM do not have the capacity to exercise intensively and would not fit in the differential diagnosis of an athlete’s heart with borderline or mildly reduced left ventricular (LV) ejection fraction. For the purposes of this study, we sought to identify individuals with a mild form of DCM who were motivated to and could exercise intensively for a prolonged …

Background: Anterior T-wave inversion (ATWI) on electrocardiography (ECG) in young white adults raises the possibility of cardiomyopathy, specifically arrhythmogenic right ventricular cardi...

ObjectiveDistinguishing early dilated cardiomyopathy (DCM) from physiological left ventricular (LV) dilatation with LV ejection fraction MethodsThirty-five asymptomatic active males with DCM, 25 male athletes in the ‘grey zone’ and 24 male athletes with normal LV ejection fraction underwent N-terminal pro-brain natriuretic peptide (NT-proBNP) measurement, ECG and exercise echocardiography. Grey-zone athletes and patients with DCM underwent cardiovascular magnetic resonance (CMR) and Holter monitoring.ResultsLarger LV cavity dimensions and lower LV ejection fraction were the only differences between grey-zone and control athletes. None of the grey-zone athletes had abnormal NT-proBNP, increased ectopic burden/complex arrhythmias or pathological late gadolinium enhancement on CMR. These features were also absent in 71%, 71% and 50% of patients with DCM, respectively. 95% of grey-zone athletes and 60% of patients with DCM had normal ECG. During exercise echocardiography, 96% grey-zone athletes increased LV ejection fraction by >11% from baseline to peak exercise compared with 23% of patients with DCM (p63% in 92% grey-zone athletes compared with 17% patients with DCM (p11% from baseline to peak exercise or achieve a peak LV ejection fraction >63% had sensitivity of 77% and 83%, respectively, and specificity of 96% and 92%, respectively, for predicting DCM.ConclusionComprehensive assessment using a cascade of routine investigations revealed that exercise stress echocardiography has the greatest discriminatory value in differentiating between grey-zone athletes and asymptomatic patients with DCM. Our findings require validation in larger studies.

Background The diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) is often challenging and some structural abnormalities typical of the disease may overlap with changes reflective of cardiac adaptation to exercise. Purpose The aim of the study was to assess the performance of the cardiac magnetic resonance (CMR) 2010 Task Force Criteria (TFC) in a cohort of patients with definite diagnosis of ARVC and define the overlap with a cohort of highly trained athletes of similar age and sex. Methods We compared the CMR features of 43 patients (mean age 49±17 years, 49% males, 32 (74%) genotyped) with a definite diagnosis of ARVC according to the revised TFC to 97 (mean age 45±16 years, 61% males) highly-trained athletes of similar age and sex, in whom cardiac disease was excluded after comprehensive work-up. Results The CMR was abnormal in 37 (86%) patients. The right ventricle (RV) was affected in isolation in 17 (39%) patients, with 18 (42%) patients exhibiting biventricular involvement and 2 (5%) patients showing isolated left ventricular (LV) involvement. The most common RV abnormalities were regional wall motion abnormalities (RWMA) (n=34; 79%), RV dilatation fulfilling a major or minor volume TFC (n=18; 42%), impaired systolic function (RV ejection fraction (EF) ≤45%: n=17; 40%) and myocardial fibrosis (n=13; 30%). The predominant LV abnormality was myocardial fibrosis (n=20; 47%), with a small proportion of patients exhibiting RWMA (n=6; 14%) and impaired systolic function (LVEF Conclusions The great majority (86%) of patients with ARVC demonstrates structural abnormalities suggestive of cardiomyopathy on CMR but only 53% fulfills any of the CMR TFC. Only a small proportion (16%) of older athletes demonstrate significant RV dilatation that overlaps with the volume criteria for ARVC, in juxtaposition to younger athletes who exhibit a greater degree of overlap. The emergence of ARVC as a biventricular disease provides an opportunity to re-evaluate the diagnostic criteria and include LV involvement in conjunction with RV involvement to improve diagnostic accuracy. Acknowledgement/Funding CRY (Cardiac Risk in the Young) charity

Background The diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) is often challenging and structural abnormalities typical of the disease may overlap with changes reflective of cardiac adaptation to exercise. The aim of the study was to assess the performance of the cardiac magnetic resonance (CMR) 2010 Task Force Criteria (TFC) in a cohort of patients with definite diagnosis of ARVC and define the overlap with a cohort of highly trained athletes of similar age and sex. Methods We compared the CMR features of 43 patients (mean age 49±17 years, 49% males, 32 (74%) genotyped) with a definite diagnosis of ARVC according to the revised TFC to 97 (mean age 45±16 years, 61% males) highly-trained athletes of similar age and sex, where cardiac disease was excluded after comprehensive work-up. Results The CMR was abnormal in 37 (86%) patients. The RV was affected in isolation in 17 (39%) patients, with 18 (42%) patients exhibiting biventricular involvement and 2 (5%) patients showing isolated left ventricular involvement. The most common RV abnormalities were regional wall motion abnormalities (RWMA) (n=34; 79%), RV dilatation fulfilling a major or minor volume TFC (n=18; 42%), impaired systolic function (RVEF ≤45%: n=17; 40%) and myocardial fibrosis (n=13; 30%). The predominant LV abnormality was myocardial fibrosis (n=20; 47%), with a small proportion of patients exhibiting RWMA (n=6; 14%) and impaired systolic function (LVEF Twenty-three (53%) patients fulfilled a major (n=14; 32%) or a minor (n=9; 21%) CMR TFC. Sixteen (16%) athletes exceeded the cut-off values for RV volumes used as a major (n=10; 10%) or a minor (n=6; 6%) TFC with an inverse relationship between age and RV volumes (r=-0.41, p=0.001). None of the athletes fulfilled the TFC for RV ejection fraction. Applying the CMR TFC to the ARVC patient population, showed a sensitivity of 33% for the major and 28% for the minor criteria. Applying the RV volume and systolic function TFC values in the entire study population, showed a sensitivity of 53%, a specificity between 83% and an accuracy of 0.68. Please see (Figure 1). Conclusion The great majority (86%) of patients with ARVC demonstrate structural abnormalities suggestive of cardiomyopathy on CMR but only 53% fulfil any of the CMR TFC. A small proportion (16%) of older athletes demonstrate significant RV dilatation that overlaps with the volume criteria for ARVC. The emergence of ARVC as a biventricular disease provides an opportunity to re-evaluate the diagnostic criteria and include LV involvement in conjunction with RV involvement to improve diagnostic accuracy. Conflict of Interest no

Introduction: Athletes can exhibit abnormal electrocardiogram (ECG) phenotypes that require further evaluation prior to competition. These are apparently more prevalent in high-intensity endurance sports. The purpose of this study was to assess the association between ECG findings in athletes and intensity of sport and level of competition. Methods: A cohort of 3423 competitive athletes had their ECGs assessed according to the Seattle criteria (SC). The presence of abnormal ECGs was correlated with: (1) intensity of sport (low/moderate vs. at least one high static or dynamic component); (2) competitive level (regional vs. national/international); (3) training volume (≤20 vs. >20 hours/week); (4) type of sport (high dynamic vs. high static component). The same endpoints were studied according to the ‘Refined Criteria’ (RC). Results: Abnormal ECGs according to the SC were present in 225 (6.6%) athletes, more frequently in those involved in high-intensity sports (8.0% vs. 5.4%; p=0.002), particularly in dynamic sports, and competing at national/international level (7.1% vs. 4.9%; p=0.028). Training volume was not significantly associated with abnormal ECGs. By multivariate analysis, high-intensity sport (OR 1.55, 1.18-2.03; p=0.002) and national/international level (OR 1.50, 95% CI 1.04-2.14; p=0.027) were independent predictors of abnormal ECGs, and these variables, when combined, doubled the prevalence of this finding. According to the RC, abnormal ECGs decreased to 103 (3.0%), but were also more frequent in high-intensity sports (4.2% vs. 2.0%; p20 horas/semana); 4) tipo de desporto (elevados componentes dinâmico versus estático). Os mesmos endpoints foram estudados pelos Refined Criteria (RC). Resultados: De acordo com os SC, 225 (6,6%) atletas tinham alterações patológicas, mais frequentes nos envolvidos em desportos de elevada intensidade (8,0 versus 5,4%; p=0,002), sobretudo dinâmica, e em nível nacional/internacional (7,1 versus 4,9%; p=0,028). O volume de treino não esteve significativamente associado a estas alterações. Em análise multivariada, desporto de elevada intensidade (OR 1,55, IC 95% 1,18-2,03; p=0,002) e o nível nacional/internacional (OR 1,50, IC 95% 1,04-2,14; p=0,027) foram preditores independentes de ECG anormais, variáveis que combinadas duplicaram a prevalência. Com os RC o número de ECG patológicos decresceu para 103 (3,0%), também mais frequentes nos desportos de elevada intensidade (4,2 versus 2,0%; p

Objectives The purpose of this study was to determine the potential value of a novel marker for the severity of structural heart disease and the risk of arrhythmia. Background The ventricular ectopic QRS interval (VEQSI) has been shown to identify structural heart disease and predict mortality in an unselected population. In ischemic heart disease (IHD), risk stratification for sudden death is imperfect. We hypothesized that VEQSI would identify patients with prior myocardial infarction (MI) compared with healthy subjects and distinguish IHD patients who have suffered life-threatening events from those without prior significant ventricular arrhythmia. Methods The 12-lead Holter recordings from 189 patients with previous MI were analyzed: 38 with prior ventricular tachycardia/ventricular fibrillation (MI-VT/VF) (66 ± 9 years; 92% male); 151 without prior significant ventricular arrhythmia (MI-no VT/VF) (64 ± 11 years; 74% male). These were compared with 60 healthy controls (62 ± 7 years; 70% male). All ventricular ectopic beats were reviewed and maximal VEQSI duration (VESQI max) was recorded as the duration of the longest ventricular ectopic beat. Results VEQSI max was longer in post-MI patients compared with normal controls (185 ± 26 ms vs. 164 ± 16 ms; p 198 ms had 86% sensitivity, 85% specificity, 62% positive predictive value, and 96% negative predictive value for identifying patients with prior life-threatening events (odds ratio: 37.4; 95% confidence interval: 13.0 to 107.5). Conclusions VEQSI max >198 ms distinguishes post-MI patients with prior life-threatening events from those without prior significant ventricular arrhythmia. This may be a useful additional index for risk stratification in IHD.

Background\ud High false positive rates and the subsequent cost of additional investigations provide a major obstacle to screening young athletes for cardiac disease with an electrocardiogram (ECG). However, the actual cost of ECG has never been assessed systematically in a large cohort of athletes.\ud Objective\ud This study investigated the financial implications associated with ECG interpretation in athletes according to the 2010 European Society of Cardiology (ESC) and the more contemporary Seattle and refined ECG interpretation criteria.\ud Methods\ud Between 2011 and 2014, 4,925 previously unscreened athletes aged 14-35 years were prospectively evaluated with history, physical examination and an ECG interpreted with the 2010 ESC recommendations. Athletes with abnormal results underwent secondary investigations, the costs of which were based on the UK National Health Service Tariffs. The impact on cost after applying the Seattle and refined criteria was evaluated retrospectively.\ud Results\ud 1,072 (21.8%) athletes revealed an abnormal ECG based on the 2010 ESC recommendations. 11.2% athletes required echocardiography, 1.7% exercise stress test, 1.2% Holter, 1.2% cardiac MRI and 0.4% other tests. The Seattle and refined criteria reduced the number of positive ECGs to 6.0% and 4.3% respectively. 15 (0.3%) athletes were diagnosed with potentially serious cardiac disease using all three criteria. The overall cost of de-novo screening using the 2010 ESC recommendations amounted to $539,888, equating to $110 per athlete and $35,993 per serious diagnosis. The Seattle and refined criteria reduced the cost to $92 and $87 per athlete screened and $30,251 and $28,510 per serious diagnosis respectively, representing a 21% cost saving per athlete screened.\ud Conclusion\ud Contemporary ECG interpretation criteria are associated with significant cost reductions for a de-novo screening program in athletes which may be cost permissive for some financially endowed sporting organisations.

Background Accurate knowledge of causes of sudden cardiac death (SCD) in athletes and its precipitating factors is necessary to establish preventative strategies. Objectives This study investigated causes of SCD and their association with intensive physical activity in a large cohort of athletes. Methods Between 1994 and 2014, 357 consecutive cases of athletes who died suddenly (mean 29 ± 11 years of age, 92% males, 76% Caucasian, 69% competitive) were referred to our cardiac pathology center. All subjects underwent detailed post-mortem evaluation, including histological analysis by an expert cardiac pathologist. Clinical information was obtained from referring coroners. Results Sudden arrhythmic death syndrome (SADS) was the most prevalent cause of death (n = 149 [42%]). Myocardial disease was detected in 40% of cases, including idiopathic left ventricular hypertrophy (LVH) and/or fibrosis (n = 59, 16%); arrhythmogenic right ventricular cardiomyopathy (ARVC) (13%); and hypertrophic cardiomyopathy (HCM) (6%). Coronary artery anomalies occurred in 5% of cases. SADS and coronary artery anomalies affected predominantly young athletes (≤ 35 years of age), whereas myocardial disease was more common in older individuals. SCD during intense exertion occurred in 61% of cases; ARVC and left ventricular fibrosis most strongly predicted SCD during exertion. Conclusions Conditions predisposing to SCD in sports demonstrate a significant age predilection. The strong association of ARVC and left ventricular fibrosis with exercise-induced SCD reinforces the need for early detection and abstinence from intense exercise. However, almost 40% of athletes die at rest, highlighting the need for complementary preventive strategies.

We are grateful for interest shown in our article. Harrell and colleagues propose that myocardial bridging may be a potential explanation for the increased prevalence of coronary atherosclerosis in male masters athletes. We agree that this is an interesting concept. As expected, we observed an element of myocardial bridging in a small proportion of our athletes and control subjects but did not report this in our article. Although it is conceivable that myocardial bridging may cause atherosclerotic plaque proximal to the bridge, our observations do not substantiate this particular theory as a possible mechanism of atherosclerosis in masters athletes. Male masters athletes had a higher prevalence of atherosclerosis affecting ≥2 vessels compared with controls (23 [21.7%] versus 2 [3.7%]; P =0.0024) and a higher proportion of multiple plaques (25 [23.6%] versus 2 [3.7%]; P =0.0014).1 The diffuse pattern of atherosclerosis noted in some of the athletes is difficult to reconcile with a single …

Pre-participation cardiovascular screening of young athletes with electrocardiography (ECG) is practiced by several major sporting organizations. A primary argument against this practice is the workload and cost associated with secondary investigations due to the high number of abnormal ECGs. We

Background: Studies in middle-age and older (masters) athletes with atherosclerotic risk factors for coronary artery disease report higher coronary artery calcium (CAC) scores compared with sedentary individuals. Few studies have assessed the prevalence of coronary artery disease in masters athletes with a low atherosclerotic risk profile. Methods: We assessed 152 masters athletes 54.4±8.5 years of age (70% male) and 92 controls of similar age, sex, and low Framingham 10-year coronary artery disease risk scores with an echocardiogram, exercise stress test, computerized tomographic coronary angiogram, and cardiovascular magnetic resonance imaging with late gadolinium enhancement and a 24-hour Holter. Athletes had participated in endurance exercise for an average of 31±12.6 years. The majority (77%) were runners, with a median of 13 marathon runs per athlete. Results: Most athletes (60%) and controls (63%) had a normal CAC score. Male athletes had a higher prevalence of atherosclerotic plaques of any luminal irregularity (44.3% versus 22.2%; P =0.009) compared with sedentary males, and only male athletes showed a CAC ≥300 Agatston units (11.3%) and a luminal stenosis ≥50% (7.5%). Male athletes demonstrated predominantly calcific plaques (72.7%), whereas sedentary males showed predominantly mixed morphology plaques (61.5%). The number of years of training was the only independent variable associated with increased risk of CAC >70th percentile for age or luminal stenosis ≥50% in male athletes (odds ratio, 1.08; 95% confidence interval, 1.01–1.15; P =0.016); 15 (14%) male athletes but none of the controls revealed late gadolinium enhancement on cardiovascular magnetic resonance imaging. Of these athletes, 7 had a pattern consistent with previous myocardial infarction, including 3(42%) with a luminal stenosis ≥50% in the corresponding artery. Conclusions: Most lifelong masters endurance athletes with a low atherosclerotic risk profile have normal CAC scores. Male athletes are more likely to have a CAC score >300 Agatston units or coronary plaques compared with sedentary males with a similar risk profile. The significance of these observations is uncertain, but the predominantly calcific morphology of the plaques in athletes indicates potentially different pathophysiological mechanisms for plaque formation in athletic versus sedentary men. Coronary plaques are more abundant in athletes, whereas their stable nature could mitigate the risk of plaque rupture and acute myocardial infarction.

Sudden cardiac death (SCD) is defined as a non-traumatic, non-violent and unexpected fatality resulting from sudden cardiac arrest within 6 h of previously witnessed normal health.[1][1] The majority of victims are elderly patients with a history of coronary artery disease or heart failure. However

Methods 77 healthy volunteers with no known cardiovascular condition underwent CMR at 1.5T (Siemens, Avanto). Mid ventricular short axis native T1 maps by MOLLI (with T1* reconstruction in addition) and ShMOLLI were acquired. Hematocrit (Hct), iron profile and lipid profile were acquired immediately prior to the scan. CVI42 (Calgary, Canada) was used for analysis of the maps. A ROI was drawn in the blood pool on the MOLLI T1 map, avoiding papillary muscles and was copied on to the MOLLI T1* and ShMOLLI T1.

The purpose of this study was to determine the potential value of a novel marker for the severity of structural heart disease and the risk of arrhythmia.The ventricular ectopic QRS interval (VEQSI) has been shown to identify structural heart disease and predict mortality in an unselected population. In ischemic heart disease (IHD), risk stratification for sudden death is imperfect. We hypothesized that VEQSI would identify patients with prior myocardial infarction (MI) compared with healthy subjects and distinguish IHD patients who have suffered life-threatening events from those without prior significant ventricular arrhythmia.The 12-lead Holter recordings from 189 patients with previous MI were analyzed: 38 with prior ventricular tachycardia/ventricular fibrillation (MI-VT/VF) (66 ± 9 years; 92% male); 151 without prior significant ventricular arrhythmia (MI-no VT/VF) (64 ± 11 years; 74% male). These were compared with 60 healthy controls (62 ± 7 years; 70% male). All ventricular ectopic beats were reviewed and maximal VEQSI duration (VESQI max) was recorded as the duration of the longest ventricular ectopic beat.VEQSI max was longer in post-MI patients compared with normal controls (185 ± 26 ms vs. 164 ± 16 ms; p 0.001) and in MI-VT/VF patients with prior life-threatening events compared with MI-no VT/VF patients without prior life-threatening events (214 ± 20 ms vs. 177 ± 22 ms; p 0.001). Multivariate analysis established VEQSI max as the strongest independent marker for prior serious ventricular arrhythmia. VEQSI max198 ms had 86% sensitivity, 85% specificity, 62% positive predictive value, and 96% negative predictive value for identifying patients with prior life-threatening events (odds ratio: 37.4; 95% confidence interval: 13.0 to 107.5).VEQSI max198 ms distinguishes post-MI patients with prior life-threatening events from those without prior significant ventricular arrhythmia. This may be a useful additional index for risk stratification in IHD.

Accurate knowledge of causes of sudden cardiac death (SCD) in athletes and its precipitating factors is necessary to establish preventative strategies.This study investigated causes of SCD and their association with intensive physical activity in a large cohort of athletes.Between 1994 and 2014, 357 consecutive cases of athletes who died suddenly (mean 29 ± 11 years of age, 92% males, 76% Caucasian, 69% competitive) were referred to our cardiac pathology center. All subjects underwent detailed post-mortem evaluation, including histological analysis by an expert cardiac pathologist. Clinical information was obtained from referring coroners.Sudden arrhythmic death syndrome (SADS) was the most prevalent cause of death (n = 149 [42%]). Myocardial disease was detected in 40% of cases, including idiopathic left ventricular hypertrophy (LVH) and/or fibrosis (n = 59, 16%); arrhythmogenic right ventricular cardiomyopathy (ARVC) (13%); and hypertrophic cardiomyopathy (HCM) (6%). Coronary artery anomalies occurred in 5% of cases. SADS and coronary artery anomalies affected predominantly young athletes (≤ 35 years of age), whereas myocardial disease was more common in older individuals. SCD during intense exertion occurred in 61% of cases; ARVC and left ventricular fibrosis most strongly predicted SCD during exertion.Conditions predisposing to SCD in sports demonstrate a significant age predilection. The strong association of ARVC and left ventricular fibrosis with exercise-induced SCD reinforces the need for early detection and abstinence from intense exercise. However, almost 40% of athletes die at rest, highlighting the need for complementary preventive strategies.

Introduction/Objective: Around 90% of patients with HCM have an abnormal ECG; however there is paucity of data on the ECG in DCM. Approximately 14% athletes show an LV cavity >60mm and 1-2% reveal a borderline low LVEF which overlaps with DCM. The role of ECG in facilitating the differentiation between physiologic LV enlargement and DCM has not been investigated. We sought to ascertain the utility of the various ECG screening criteria in differentiating physiology from pathology in a cohort of individuals with LV dilatation. Methods: 89 individuals with a dilated LVEDD (43 asymptomatic athletes from cardiac screening (male=37, female=6) and 46 non-ischaemic DCM NYHA class I from a cardiomyopathy clinic (males=33, female=13) were included. Fourty (87%) of the DCM patients were on a beta-blocker. The 2010 ESC, ‘Seattle’ and the novel ‘Refined’ screening criteria were applied to the most recent ECG in both cohorts to assess whether ECG screening would have accurately raised suspicion of pathology. Results: Using the ESC criteria 11 DCM patients had a normal ECG and 6 had group 1 changes; therefore 40.0% of DCM patients would have been considered to have an ECG compatible with athletic training. Excluding sinus bradycardia, the most common group 1 change was early repolarisation. The sensitivity and specificity of the ESC criteria for detecting pathology in our cohort was 63.0% and 69.0% respectively. The sensitivity and specificity of the ‘Seattle’ criteria is 50% and 76.7%. The ‘Refined’ criteria was less sensitive at 41.3% but had a higher specificity of 79.2%. Conclusions: It is often assumed the ECG is abnormal in patients with a dilated cardiomyopathy. In our cohort 40% of the ECGs in our DCM patients would have not prompted further investigation if seen at pre-participation screening. This study demonstrates the ECG is not a particularly useful investigation in distinguishing physiological from pathological LV dilatation.

Introduction: T wave inversion (TWI) is the electrical hallmark of primary cardiomyopathies which are substrates for sudden death in young athletes. Such repolarization anomalies can feature on the ECG of an apparently healthy athlete and pose major diagnostic dilemmas in sports cardiology. Athletes are reluctant to detrain during the season. Hypothesis: This study hypothesized that detraining would affect TWI in athletes. Methods: Between 2013-2014, 36 professional footballers demonstrated TWI at mid-season ECG screenings (trained period). They were followed up during the "off-season" after a period of detraining (6-8 weeks). TWI was defined as –0.1 mV or greater 2 or more contiguous leads: anterior leads-V2-V3/4; inferior-II,III,aVF; or lateral-beyond V4 +/-aVL. Comparisons were drawn by 2 independent cardiologists, between trained and detrained ECGs. All players were also investigated for an underlying cardiomyopathy. Results: *Athletes were male, aged 24.5+/-2.7 years. *27 (75%) were Afro-Caribbean and 25% Caucasian (p=0.0141). *TWI was most common in the anterior leads (n=20, 55%), followed by inferior (n=10, 28%) and lateral (n=6, 17%) as in the bar chart. *No Caucasian player had TWI laterally. *After detraining, 16 players demonstrated resolution of anterior TWI (80%, p=0.0293), 8 in inferior leads (80%, p=0.2353) and 4 in the lateral leads (67%, p=0.638) (Figures 1a & b). *All players with abnormal TWI according to consensus guidelines were evaluated with no cardiomyopathy identified. Conclusions: In athletes who detrained during the 'off-season', we observed resolution of TWI in the majority of athletes (both Afro-Caribbean and Caucasian) after a relatively brief period of detraining which may be a physiological phenomenon. This was statistically significant in the anterior leads. However, TWI in the inferior and/or lateral leads should always raise the suspicion of an underlying cardiomyopathy, especially if persistent after detraining.

Introduction: The benefits of regular moderate exercise are well documented, however, there is a burgeoning group of veteran athletes who have been exercising vigorously since youth and the impact of life long intensive exercise on the heart is unknown. Hypothesis: Life-long intensive exercise may promote adverse cardiac remodelling. Methods: A large cohort of veteran athletes and gender, age and Framingham matched controls were studied comprehensively to investigate any detrimental effects of chronic life-long intensive exercise among veteran athletes. Veteran athletes were defined as >40 years of age and having competed in multiple endurance events over a 10 year period. Controls were recruited from University staff. All individuals were subjected to a cardiopulmonary exercise test, 24 hour Holter monitor, cardiac MRI (CMR) and CT coronary angiography. Results: A total of a 178 veteran athletes (m=128 f=50, mean age:54.8) and 123 controls (m=75 f=48, mean age 55.3) were recruited. Athletes demonstrated enlargement of all chamber sizes compared to sedentary controls on CMR. A significant proportion of male athletes (17.5%) exhibited myocardial fibrosis compared to none of the sedentary men (p=0.008) although this difference wasn’t observed in females (2.5% vs 0%, p=1.0). In 45% of cases fibrosis was subendocardial in distribution suggesting a prior ischaemic event. Male athletes with myocardial fibrosis had a 15% prevalence of ventricular tachycardia on a 24hour ECG compared to 1.06% of fibrosis free athletes (p=0.017). Compared to controls, male athletes had a higher prevalence of atherosclerosis (28.2% ≥2vessel disease vs 3.45%, p=0.009). Female athletes had similar indices of atherosclerosis compared to controls but they did demonstrate a U shaped relationship between V02 max and atherosclerosis: The lower and upper tertile of V02 Max had a higher prevalence of atherosclerosis (20%, and 26.7%) than those in the middle tertile(6.7%). Conclusions: Long term endurance exercise is associated with adverse cardiac remodelling. Myocardial fibrosis is common in male veteran athletes and is associated with ventricular tachycardia. Chronic endurance exercise also promotes atherosclerosis in males and females and this is likely to be dose dependent.

The short QT syndrome is a cardiac channelopathy characterised by accelerated repolarisation which manifests as a short QT interval on the ECG. The definition of a short QT interval is debated, ranging from390 to ≤320 ms, and its clinical significance in healthy young individuals is unknown. We assessed the prevalence and medium-term significance of an isolated short QT interval in a diverse young British population.Between 2005 and 2013, 18 825 apparently healthy people aged 14-35 years underwent cardiovascular evaluation with history, physical examination and ECG. QT intervals were measured by cardiologists using 4 recommended guidelines (Seattle 2013, Heart Rhythm Society 2013, European Society of Cardiology 2010 and American Heart Association 2009).The prevalence of a short QT interval was 0.1% (26 patients, ≤320 ms), 0.2% (44 patients, ≤330 ms), 7.9% (1478 patients,380 ms), 15.8% (2973 patients,390 ms). Male gender and Afro-Caribbean ethnicity had the strongest association with short QT intervals. Athletes had shorter QT intervals than non-athletes but athletic status did not predict short QT intervals. Individuals with short QT intervals ≤320 ms did not report syncope or a sinister family history, and during a follow-up period of 5.3±1.2 years, there were no deaths in this group.The prevalence of a short QT interval depends on the recommended cut-off value. Even at values ≤320 ms, there was an excellent medium-term prognosis among 14 people followed. We conclude that a definition of ≤320 ms is realistic to prevent overdiagnosis and excessive investigations.

The benefits of exercise are irrefutable. Individuals engaging in regular exercise have a favourable cardiovascular risk profile for coronary artery disease and reduce their risk of myocardial infarction by 50%. Exercise promotes longevity of life, reduces the risk of some malignancies, retards the onset of dementia, and is as considered an antidepressant. Most of these benefits are attributable to moderate exercise, whereas athletes perform way beyond the recommended levels of physical activity and constantly push back the frontiers of human endurance. The cardiovascular adaptation for generating a large and sustained increase in cardiac output during prolonged exercise includes a 10-20% increase in cardiac dimensions. In rare instances, these physiological increases in cardiac size overlap with morphologically mild expressions of the primary cardiomyopathies and resolving the diagnostic dilemma can be challenging. Intense exercise may infrequently trigger arrhythmogenic sudden cardiac death in an athlete harbouring asymptomatic cardiac disease. In parallel with the extraordinary athletic milieu of physical performances previously considered unachievable, there is emerging data indicating that long-standing vigorous exercise may be associated with adverse electrical and structural remodelling in otherwise normal hearts. Finally, in the current era of celebrity athletes and lucrative sport contracts, several athletes have succumbed to using performance enhancing agents for success which are detrimental to cardiac health. This article discusses the issues abovementioned, which can be broadly classified as the good, bad, and ugly aspects of sports cardiology.

Annexin-1 is an anti-inflammatory protein that plays an important homeostatic role in innate immunity; however, its potential actions in the modulation of adaptive immunity have never been explored. Although inactive by itself, addition of annexin-1 to stimulated T cells augmented anti-CD3/CD28-mediated CD25 and CD69 expression and cell proliferation. This effect was paralleled by increased nuclear factor-κB (NF-κB), nuclear factor of activated T cells (NFATs), and activator protein-1 (AP-1) activation and preceded by a rapid T-cell receptor (TCR)–induced externalization of the annexin-1 receptor. Interestingly, differentiation of naive T cells in the presence of annexin-1 increased skewing in Th1 cells; in the collagen-induced arthritis model, treatment of mice with annexin-1 during the immunization phase exacerbated signs and symptoms at disease onset. Consistent with these findings, blood CD4+ cells from patients with rheumatoid arthritis showed a marked up-regulation of annexin-1 expression. Together these results demonstrate that annexin-1 is a molecular “tuner” of TCR signaling and suggest this protein might represent a new target for the development of drugs directed to pathologies where an unbalanced Th1/Th2 response or an aberrant activation of T cells is the major etiologic factor.

Exercise confers a plethora of health benefits that are well documented, whereas physical inactivity is a leading risk factor for cardiovascular morbidity and mortality. The dose of physical activity required to achieve these benefits is relatively modest and equates to jogging at a pace of 15min per mile for 20-30min daily. In the current era, most athletes engage in a volume and intensity of exercise that is at least 5-10-fold greater than the general recommendations for physical activity. Such practice is evidenced by the fact that many sportsmen have achieved athletic feats that were considered impossible only 2 decades ago. Numerous studies in retired athletes have consistently shown a reduced incidence of heart disease and an increased longevity of life. Occasionally, however, intense exercise is associated with sudden deaths in athletes harboring quiescent yet potentially sinister cardiac diseases. Despite the visibility afforded by such catastrophes, the reputation of exercise remains unscathed because most deaths can be accounted for by an underlying cardiac abnormality where exercise is a mere trigger for a fatal arrhythmia rather than the actual cause of death. More recently, there have been an emerging number of reports suggesting that intense exercise may have an adverse impact on an otherwise normal heart. This article will review the morbidity and mortality associated with sport and pose the question whether one can have "too much of a good thing."

Introduction Anterior T wave inversion (ATWI) on an electrocardiogram (ECG) of an adult white individual raises the possibility of an underlying cardiomyopathy. While European consensus guidelines recommend that ATWI beyond V1 warrants further investigation, the prevalence and significance of ATWI has never been reported in a large white asymptomatic population. Objective This study investigated the prevalence and significance of ATWI in a large cohort of young, white adults including athletes. This was an observational study with a mean follow-up period of 18.1 months. Setting Several UK elite sporting organizations conduct ECG based pre-participation screening of athletes through the charitable organization, Cardiac Risk in the Young (CRY) for young and apparently healthy individuals. Follow-up of individuals with abnormalities at preliminary assessment is provided at a tertiary centre for inherited heart conditions and sports cardiology. Participants 14,646 subjects aged 16–35 years were evaluated including 4,720 (32%) females and 2,958 (20%) athletes. All individuals underwent health questionnaire, physical examination and 12-lead ECG. Main Measures ATWI was defined as T wave inversion in 2 or more contiguous anterior leads (V1-V4) and investigated comprehensively to elucidate underlying cardiac pathology. ATWI >-0.1 mV or in 2 or more contiguous leads was considered abnoraml except in V1/III. Results 338 individuals (2.3%) exhibited ATWI. Those with ATWI were of similar age compared with subjects without ATWI (21.2 (± 5.4) years vs. 21.7 (± 5.3) years). Both groups had a similar mean body surface area. ATWI was more common in females compared with males (n = 203; 4.3% vs n = 135; 1.4%: p Univariate predictors of ATWI were female gender and athletic status. Stepwise multiple linear regression identified female gender (hazard ratio 3.1, 95% CI 1.96–4.90, p Conclusions and implications Anterior T wave inversion confined to V1/ V2 may be a normal variant or physiological phenomenon in asymptomatic white individuals without a relevant family history. Conversely, ATWI beyond V2 is rare, particularly in males and may warrant investigation. The results of this study will have a significant impact on ECG interpretation in young white athletes and non-athletes.

Deaths of young athletes from cardiac disease are uncommon but receive considerable media attention and intermittently galvanize debates about cardiac screening prior to participation in sports. Both the American Heart Association (AHA) and European Society of Cardiology (ESC) endorse preparticipation screening in athletes; however, there is disagreement about the best approach. The AHA recommends history and physical examination; this approach is pragmatic and relatively inexpensive but has poor sensitivity because most athletes are asymptomatic and physical examination identifies only a minority of those at risk of sudden cardiac death. The inclusion of the electrocardiogram in accordance with the recommendations of the ESC improves sensitivity for detection of serious cardiac disease but is associated with an unacceptably high false-positive rate, in part because of the overlap between the electrical manifestations of athletic training and the cardiomyopathies. For young athletes with normal electrocardiogram results, echocardiography contributes minimally to the diagnosis of serious cardiac diseases. Given all the complexities, cardiac screening of young athletes should be voluntary not mandatory and conducted by highly experienced physicians who fully understand the cardiovascular adaptation to intensive exercise.

Most GPs will encounter at least one case of sudden arrhythmic death syndrome (SADS) during their career. They may have to evaluate a young person at risk of SADS or offer support and screening to family members. SADS is the term used to describe an unexpected death in individuals with no prior history of cardiac disease and where no underlying pathology is identified despite a comprehensive post-mortem evaluation and toxicology screen. in England alone, SADS is responsible for 544 deaths per year, with a mean age of 32 years and a male predominance. Among the 100,000 cases of sudden cardiac death in the UK per year, SADS makes up around 4%, but this proportion is significantly higher in younger cohorts (13% of sudden cardiac deaths in those aged less than 35). Most cases of SADS are the result of inherited cardiac ion channel abnormalities of the heart which predispose to fatal arrhythmias. These include Brugada syndrome, long QT syndrome, short QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Most individuals remain asymptomaticand are diagnosed incidentally on routine ECG testing or family screening. Syncope or cardiac arrest may be the first manifestation, All first-degree relatives of SADS victims should be referred for comprehensive evaluation in an expert setting. In studies of families of SADS victims evaluation of blood relatives identified a hereditary arrhythmogenic syndrome in almost 50% of families, thereby providing a likely cause of ath and preventing further tragedies.

We are grateful to Dr. Karam and colleagues for their interest in our paper. Their letter focuses on the circumstances of sudden cardiac death (SCD) in our athletes. Previous reports suggest over 80% of SCDs in athletes occur during or immediately after exercise. In contrast, we observed that a

Aims Obesity is a rising public health problem and widely known risk factor for cardiovascular diseases. The relationship between obesity and sudden cardiac death (SCD) is unclear and based on small cohort studies. The aim of the study was to determine the main features and aetiologies in a large cohort of SCD occurred in obese subjects Methods Between 1994 and 2014, 3684 consecutive cases of SCD were referred to our cardiac pathology centre. In 1954 body mass index (BMI) data were available; obesity was defined by a BMI ≥ 30. All subjects underwent macroscopic and microscopic post-mortem evaluation by an expert cardiac pathologist. Clinical information were obtained from the referring coroners. Results Four hundred ninety-one patients (25%) were obese. The average heart weight (HW) in obese patients was 505 ± 170 g and 186 (38%) had a HW of more than 500 g. Obese patients were older at death (39 ± 14 vs 35 ± 16 years in non-obese, p Conclusions Various conditionsunderlie SCD inobese patients, with a prevalence of SADS, ILVH and CAD. The degree of hypertrophy measured by heart weight appears in excess even after correction for body size, postulating its possible pathogenetic role in the development of fatal arrhythmias. Almost one in four young obese sudden death victims shows some degree of CAD, underscoring the need for primary prevention in this particular subgroup.

Introduction High false positive rates and subsequent costs of additional investigations provide major obstacles to state-sponsored screening of young athletes for cardiac disease with ECG. However, the actual cost of ECG screening in large cohorts of athletes has never been assessed systematically. We investigated the financial implications of ECG screening in young athletes in the UK, and evaluated the impact of modification of ECG interpretation criteria on cost. Methods Between 2011–14, 4,925 athletes (14–35 years) were consecutively assessed through a charity screening programme with history, physical examination and an ECG interpreted with the ESC criteria by a cardiologist at a cost of £35 per athlete. Athletes with abnormal results underwent additional tests at hospitals in their geographic vicinity at the discretion of the hospital cardiologist. The cost of additional tests were based on the UK National Health Service tariffs. A cost-projection model to evaluate cost-effectiveness was conducted based on (1) our costs, (2) UK sports participation statistics and (3) data from an Italian study which reported a 3.6/100,000/years reduction in incidence of sudden cardiac death in athletes screened with ECG over 20 years (Figure 1). The Seattle and refined criteria for ECG interpretation were applied to the cohort retrospectively. Results The majority of athletes were male (83%) and Caucasian (85%). 26 sports were represented. 1.6% had an abnormal history or physical examination. 21.8% had an abnormal ECG according to the ESC criteria. 11.2% athletes required echocardiography, 1.9% exercise testing, 1.4% holter, 1.2% cardiac MRI and 0.2% required other tests after 30 month follow-up. The Seattle and refined criteria reduced the abnormal ECG rate to 6% and 4.3% respectively. 15 athletes (0.3%) were identified with potentially sinister cardiac disease by all 3 criteria. Following further tests, the cost of screening with the ESC criteria amounted to £72 per athlete screened and £23,750 per condition detected. The Seattle and refined criteria reduced costs to £61 and £58 per athlete respectively, and £20,160 and £18,976 per condition detected (Figure 2). 20 years of annual screening would save 1,667 lives at a cost of £3.5 million per life saved with the ESC criteria; the Seattle and refined criteria reduced the cost to £3 million and £2.8 million per life saved respectively. Conclusions The impressive 20% cost saving associated with ECG modification will be welcomed by organizations that mandate screening for their athletes. However, ECG screening is expensive considering the large number of young athletes that would require screening and the low event rate in such populations. Further ECG modification and physician education is required for such practices to be achievable or sustainable at a state-level.

Annexin-1 is a well-known endogenous anti-inflammatory protein that modulates the activation of cells of the innate immune system such as neutrophils and macrophages. We have recently reported a positive role for the exogenous protein on T cell differentiation, however, whether such a role holds true for the endogenous protein has yet to be determined. This aspect has been investigated here finding that Annexin-1-deficient T cells display an impaired activation and proliferation in response to anti-CD3 plus anti-CD28 stimulation. Furthermore, differentiation of T cells from Annexin-1-deficient mice in Th0/Th1/Th2 or Th17 skewing conditions demonstrated an increased Th2 phenotype compared to cells from control littermates. Similar results were obtained when we analyzed the Th1/Th2 profile of lymph node cells obtained from mice immunized with keyhole limpet hemocyanin or the inflammatory infiltrate in mouse model of allergic inflammation. These results demonstrate a novel modulatory role of endogenous Annexin-1 in TCR signaling and T cell differentiation and suggest this protein might play a dual and complementary role in the innate and adaptive immune response.

Purpose Recommendations for interpretation of the athlete’s electrocardiogram (ECG) has evolved in recent years, namely with the European Society of Cardiology (ESC, 2010), Seattle (2013) and more recently, the Refined (2014) criteria. A principle aim of these developments has been to improve the sensitivity and specificity for identification of young athletes at risk of sudden cardiac death and reduce false-positive rates. Whether these criteria are effective in adolescents is yet to be validated. Our study aimed to compare these criteria in a large cohort of adolescent (aged 14–17 years) athletes. Methods Between July 1998–August 2012, 7993 adolescent, professional male footballers aged between 14 and 17, were assessed through pre-participation screening. This included a history, examination, 12-lead ECG and echocardiogram. A retrospective analysis of the ECG data was undertaken with the application of the ESC, Seattle and Refined criteria. Results Athletes were aged 16.1 ± 1.5 years and were all male. 87.8% were Caucasian, 10.3% were Afro-Caribbean and the remainder being Oriental and South-East Asians. 1017 (12.7%) subjects were deemed to have an abnormal ECG when the ESC criteria were applied. This compared with 312 (3.9%) athletes against the Seattle criteria (p Conclusions/implications Recent developments of recommendations for interpretation of the athlete’s ECG, most significantly through the Refined criteria, shows a reduction in the number of adolescent athletes deemed to have cardiac abnormalities. Our results suggest that current screening criteria are applicable in adolescent athletes as well as older counterparts. The Refined criteria will further improve the specificity of screening and therefore reduce the burden posed by high false-positive rates.

Background Pre-participation cardiovascular evaluation is being recommended by a growing number of sporting bodies and scientific organisations in an attempt to identify athletes harbouring quiescent cardiac conditions which put them at risk of exercise-related sudden cardiac death (SCD). However cardiac adaptation to exercise may itself result in ECG patterns that overlap with those observed in several cardiac conditions, including hypertrophic cardiomyopathy (HCM), the leading cause of SCD in athletes worldwide. This raises significant challenges for physician’s involved in ECG-based pre-participation cardiovascular evaluation of athletes with respect to distinguishing physiological from pathological ECG changes. Data demonstrates that cardiac conditions such as hypertension may modulate the HCM phenotype. However the effect of exercise on the HCM phenotype remains unknown. We compared the ECGs and echocardiographic parameters of athletes with HCM to sedentary HCM patients and healthy athletes to establish whether physical activity modifies the phenotype in HCM. Methods The presenting ECGs of 103 young (14–35) consecutive asymptomatic athletes with HCM identified through pre-participation or familial evaluation were compared to the presenting ECGs of 106 sedentary HCM patients (14–40) and 110 consecutive healthy young athletes. Echocardiographic characteristics indicating disease severity and patterns of left ventricular hypertrophy (LVH) were also compared. Results Sedentary HCM patients were older than the athlete groups (Table 1). All 3 groups contained a similar number Afro-Caribbean individuals (30.2% sedentary HCM vs. 33.0% athletes with HCM vs. 30.9% healthy athletes, p > 0.05), the remainder being Caucasian. Athletes with HCM exhibited significantly more repolarisation changes (specifically T-wave inversions [TWIs] and deep TWIs) in addition to voltage criteria for LVH compared to sedentary HCM patients and healthy athletes (p Conclusions Athletes with HCM exhibit more ECG repolarisation changes compared to sedentary HCM patients and healthy athletes, suggesting that exercise modifies the ECG phenotype in HCM. Virtually all athletes with HCM revealed TWIs, rendering softer ECG changes such as axis deviation and atrial enlargement less relevant to the detection of HCM in athletes. These results should be taken into consideration when devising criteria for interpretation of an athlete’s ECG.

Purpose Anterior T wave inversion (V1-V4) is the hallmark of arrhythmogenic right ventricular cardiomyopathy (ARVC). However, it is widely perceived that anterior T wave inversion is also common in female individuals. Previous studies in small cohorts of female athletes have demonstrated a highly variable prevalence of anterior T wave inversion of up to 14%. This study investigated the prevalence and significance of anterior T wave inversion in a large, unselected cohort of female athletic and non-athletic individuals who underwent cardiac screening. Methods Between May 2007 and September 2013, 17,708 individuals (n = 5,234; 29.6% females) aged 14–35 underwent cardiac screening with health questionnaire, 12-lead ECG and consultation with a cardiologist. Further evaluation was dictated by initial results. The ECGs of female subjects were analysed placing emphasis on the presence of anterior T wave inversion, defined as T wave inversion in ≥2 contiguous anterior leads. Results T wave inversion was present in 322 (6.2%) females, the majority confined to the anterior leads; 73% anterior, 14% lateral, 13% inferior. Anterior T wave inversion was more prevalent in competitive athletes compared to non-athletes (7.02 vs 3.78%, p 16 years of age. The majority of anterior T wave inversion (n = 171; 73%) was confined to leads V1-V2, with only 1.2% of females exhibiting T wave inversion beyond V2, raising the suspicion of ARVC. Multivariate analysis identified black ethnicity as the sole, independent predictor for the presence of anterior T wave inversion (OR 3.1, 95% CI 1.2–8.4, p = 0.03). Conclusion In the largest unselected cohort of females to date, the overall prevalence of anterior T wave inversion was higher (4.5%) than those in previously reported studies. This was also the case for females of Caucasian ethnicity. Anterior T wave inversion persisted in a considerable proportion of females >16 years, excluding the ‘juvenile’ pattern. Although we did not identify ARVC in any females with anterior T wave inversion, given the low prevalence of T wave inversion beyond V2, particularly in Caucasian individuals (1.06%), such patterns not be considered a normal finding and should trigger further clinical evaluation.