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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 …

Introduction: Pathological Q waves are considered harbingers of cardiac pathology and should instigate comprehensive evaluation of athletes. Several definitions of the depth or duration of a Q wave exist, with disagreement between scientific bodies as to the most useful. Objectives: 1. Determine the prevalence of pathological Q waves in large cohorts of the general population, athletes and patients with hypertrophic cardiomyopathy (HCM). 2. Identify the most accurate Q wave criterion. Methods: ECGs were retrospectively analysed in consecutive cohorts of 10,008 healthy young athletes (14-35 years old), 2,994 healthy young non-athletes and 468 HCM patients. Results: Pathological Q waves that fulfilled at least one of the 4 individual definitions (Table 1) were identified in 0.7% athletes (n = 75), 1.2% non-athletes (n = 36) and 22.6% patients with HCM (n = 106). In the healthy athletic and non-athletic population, all pathological Q waves (n = 111) met the >3mm depth definition. In contrast, the majority of pathological Q waves in HCM patients met the ≥40msec duration definition (n = 75; 70.75%). We tested the ability of all 4 criteria to distinguish between health and disease in the entire cohort. Seattle and Refined had the best sensitivity for detecting HCM. Refined criteria however, had a significantly higher positive predictive value and 7 times lower false positive rate compared to Seattle. (Table 2) Conclusion: Pathological Q waves are present in up to 1.2% of healthy young individuals and do not correlate with physical activity. Of the proposed criteria, the Refined criteria has the lowest false positive rate and should be utilised in the context of cardiac evaluation in young athletes.

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.