Background Cardiac remodelling beyond reference values is well-known in adult athlete's heart. Male endurance athletes are more prone to develop cardiac chambers and wall thickness above reference values. Cardiac remodelling is also described in adolescent athletes, but considered to be moderate compared to adults. However, few studies evaluate adolescent athlete's heart by paediatric echocardiographic reference values. Current paediatric reference values are sex-unspecific and do not include exercise data. The impact of sex and exercise on remodelling in adolescent athlete's heart remains unclear. Purpose We aimed to study the development of cardiac remodelling and potential sex differences in adolescent athletes. We hypothesized that male adolescent athletes would display greater degree of remodelling compared to female adolescent athletes. Methods Male (M) and female (F) adolescent cross-country skiers were recruited in a longitudinal cohort study. They were examined with echocardiography at age 12, 15 and 18. Data on exercise was collected at all examinations. We evaluated echocardiographic parameters by paediatric reference values (Z-score: number of standard deviations above estimated mean in the given body surface area). Echocardiographic measures were considered above upper reference value if Z-score was ≥2. Results Seventy-six athletes were examined at age 12 (48 M, 28 F), 48 at age 15 (34 M, 14 F) and 34 at age 18 (23 M, 11 F). Although Z-scores were within reference values at age 12 (Table 1), a subset of athletes displayed Z-scores ≥2 for end-diastolic intraventricular septum diameter (IVSd, M 13/48=27%, F 5/28=18%) and left ventricular posterior wall thickness (LVPWd, M 6/48=13%, F 2/28=14%). The male group demonstrated enlarged left ventricular mass (LVM) from age 15 (Figure 1). Males had greater left ventricular end-diastolic volume (LV EDV) from age 12. Additional sex differences were evident from age 15 for IVSd, LVPWd and LVM (Table 1). There was no sex difference in exercise hours. Both groups had normal myocardial function through the study period. Conclusion Cardiac remodelling beyond reference values was observed in athletes of both sexes from early adolescent age. Sex differences were evident from age 12 with further progression. Pathological values for LVM were more frequent in males. These findings suggest that sex differences in exercise-induced cardiac remodelling is more prominent in adolescents than previously reported. Sex and exercise history should be considered in questions of pathology. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The South-Eastern Norway Regional Health AuthorityCentre for Children and Youth Sport, Norwegian School of Sport Sciences
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): South-Eastern Norway Regional Health Authority OnBehalf ProCardio Center for Innovation Introduction Athlete’s Heart (AH) is characterized by cardiac remodelling as a response to exercise, but data on sex differences in adolescent athletes is limited. Purpose To study the impact of sex on development of AH in adolescent athletes. We hypothesize that male adolescent athletes develop greater morphological changes than females, also when adjusted for body surface area (BSA). Methods We recruited 12-year-old cross-country skiers of both sexes in a longitudinal cohort study. We examined them with echocardiography at age 12, 15 and 18. Results We recruited 76 athletes (48 males and 28 females). We could follow 48 participants at age 15 (34 males and 14 females), and 34 participants at age 18 (23 males and 11 females). There were no sex differences in exercise hours at any time point. Adolescent males had greater indexed LV end-diastolic volume (LV EDVi) at all time points (Figure 1). Both sexes displayed LV enlargement already at age 12, and athletes of both sexes displayed LV EDVi close to or above upper reference values for the adult population. Only males increased their indexed LV mass (LVMI) from 12 to 18 years (LVM/BSA, Δg/m²; 33 ± 27 vs 4 ± 19, P = 0.006). Male adolescent athletes increased their LVMI by 7.4 grams more and LV EDVi by 4.0 ml more than female athletes did for every 1000 hours of exercise training. Cardiac function was within normal range in both sexes throughout the study period. Conclusion Sex-related differences in cardiac adaptation to exercise are evident from early adolescence. Both sexes demonstrate cardiac remodelling, but adolescent male athletes display greater morphological changes compared to female athletes. Abstract Figure 1
Background Arrhythmogenic cardiomyopathy (AC) is an inheritable and progressive cardiomyopathy characterized by high risk of ventricular tachyarrhythmias and sudden cardiac death. Pediatric patients are underrepresented in AC publications, and the AC penetrance and incidence of cardiac events in children have yet to be determined. Current guidelines recommend initiating family screening in first-degree relatives after age 10–12 years, but the clinical value of this approach has not been systematically evaluated. Purpose We aimed to explore the incidence of severe cardiac events in pediatric patients with AC and to describe the phenotype in early-onset AC. Furthermore, we wanted to estimate the penetrance of AC disease in genotype positive pediatric family members. Methods In a single-center follow-up study, we included consecutive AC pediatric patients and genotype positive family members ≤18 years of age. The patients were followed regularly with electrocardiographic, structural and arrhythmic characteristics according to the AC 2010 Task Force Criteria (TFC). Penetrance of AC disease was defined as fulfilling definite AC diagnosis by the 2010 TFC. We defined severe cardiac events as cardiac death, heart transplantation (HTx) or severe ventricular arrhythmias (VAs) (sustained ventricular tachycardia or aborted cardiac arrest). Results We included 62 individuals (11 probands, 51 family members). Fourteen events (5 HTx, 9 VAs) occurred during 6±4 years of follow-up, giving a cumulative incidence of 23% and a yearly incidence rate of 4%. Seven (50%) events occurred in patients ≤12 years of age (Figure 1). All children who underwent heart transplantation were ≤12 years. At inclusion, 13 patients (21%) fulfilled definite AC diagnosis (10 probands, 3 family members). At end of follow-up, AC diagnosis were fulfilled in 20 (32%) patients (11 probands, 9 family members), indicating progression of disease in 7 patients. Mean age at definite AC diagnosis was 13±4 years and 8 patients (40%) were ≤12 years old (Figure 1). All patients diagnosed with AC <12 years of age had biventricular disease with mean LVEF 30±9% and right ventricular fractional area change 21±5% at end of follow-up. Among the family members, 5 (10%) had signs of AC disease at the time of genetic diagnosis. At end of follow-up, AC penetrance was 18% and 3 (6%) experienced severe cardiac events at a mean age of 13±6 years. Conclusion In a pediatric AC cohort of probands and genotype positive family members, we found a high incidence of VA and HTx. Half of the events occurred in children ≤12 years of age, supporting a markedly severe phenotype in early-onset AC. AC penetrance among pediatric family members identified by screening was high, with a significant incident of events. Our findings emphasize the high risk features of early-onset AC disease and indicate a need to start AC family screening in children at an younger age than recommended by current guidelines. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The Norwegian Research Council
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