Maria Sanz de la Garza

Inter-individual variability in right ventricle adaptation after an endurance race.

Background Right ventricle (RV) dysfunction has been described in athletes after endurance races. We aimed to understand and characterize the RV response to endurance exercise, the impact of individual variability and the effects of the amount of exercise. Methods and results Echocardiography was performed in 55 healthy adults at baseline and after a three-stage trail race: short (14 km; n = 17); medium (35 km; n = 21); and long (56 km; n = 17). Standard and speckle tracking echocardiographic assessment of the RV was performed with global and separate analysis of the RV basal (inflow) and apical regions. Although no change was observed in the short distance runners, the RV systolic deformation decreased significantly (p < 0.05) after both the medium length and long races (Δ% RV global strain −7.6 ± 20.1 and −8.7 ± 21.8, respectively) with significant RV dilatation (Δ% RV volume +10.6 ± 9.9 and +15.3 ± 12.8, respectively). The RV basal segment made a major contribution to stroke volume during exercise, showing larger increases in size and strain compared with the apex. Various patterns of RV adaptation to exercise, ranging from increases in both RV segmental strains and sizes to an insufficient increase in size and a decrease in strain, were identified; this individual variability was not correlated with prior training. Conclusion An acute RV impairment was demonstrated after a trail-running race and was related to the amount of exercise. A high inter-individual variability was observed. Differences in RV adaptation patterns were independent of prior training, suggesting the influence was due to other individual factors.

Gender influence on the adaptation of atrial performance to training

Abstract Background: High-intensity training has been associated with atrial remodelling and arrhythmias in men. Our purpose was to analyse atrial performance in female endurance athletes, compared to male athletes and controls. Methods: This was a cross-sectional study. We included four groups: female athletes, females controls, male athletes and male controls. Left (LA) and right atrial (RA) volumes and function were assessed using 2D and speckle-tracking echocardiography to determine peak atrial strain-rate at atrial (SRa) and ventricular contraction (SRs), as surrogates of atrial contractile and reservoir function, respectively. ANOVA and Bonferroni’s statistical tests were used to compare variables among groups. Results: We included 82 subjects, 39 women (19 endurance athletes, 20 controls) and 43 men (22 endurance athletes, 21 controls). Mean age was similar between groups (36.6 ± 5.6 years). Athletes had larger bi-atrial volumes, compared to controls (women, LA 27.1 vs. 15.8 ml/m2, p < 0.001; RA 22.31 vs. 14.2 ml/m2, p = 0.009; men, LA: 25.0 vs. 18.5 ml/m2, p = 0.003; RA 30.8 vs. 21.9 ml/m2, p < 0.001) and lower strain-rate (women, LASRa −1.60 vs. −2.18 s−1, p < 0.001; RASRa −1.89 vs. −2.38 s−1, p = 0.009; men, LASRa −1.21 vs. −1.44 s−1, p = 1; RASRa −1.44 vs. −1.60 s−1, p = 1). However, RA indexed size was lower and bi-atrial deformation greater in female athletes, compared to male athletes. Conclusions: The atria of both male and female athletes shows specific remodelling, compared to sedentary subjects, with larger size and less deformation at rest, particularly for the RA. Despite a similar extent of remodelling, the pattern in women had greater bi-atrial myocardial deformation and smaller RA size.

Prevention of sudden death in adolescent athletes: Incremental diagnostic value and cost-effectiveness of diagnostic tests

Introduction Pre-participation screening in athletes attempts to reduce the incidence of sudden death during sports by identifying susceptible individuals. The objective of this study was to evaluate the diagnostic capacity of the different pre-participation screening points in adolescent athletes and the cost effectiveness of the programme. Methods Athletes were studied between 12–18 years old. Pre-participation screening included the American Heart Association questionnaire, electrocardiogram, echocardiogram, and stress test. The cost of test was established by the Catalan public health system. Results Of 1650 athletes included, 57% were men and mean age was 15.09 ± 1.82 years. Positive findings were identified as follows: in American Heart Association questionnaire 5.09% of subjects, in electrocardiogram 3.78%, in echocardiogram 4.96%, and in exercise test 1.75%. Six athletes (0.36%) were disqualified from participation and 10 (0.60%) were referred for interventional treatment. Diagnostic capacity was assessed by the area under the curve for detection of diseases that motivated disqualification for sport practice (American Heart Association questionnaire, 0.55; electrocardiogram, 0.72; echocardiogram, 0.88; stress test, 0.57). The cost for each athlete disqualified from the sport for a disease causing sudden death was €45,578. Conclusion The electrocardiogram and echocardiogram were the most useful studies to detect athletes susceptible to sudden death, and the stress test best diagnosed arrhythmias with specific treatment. In our country, pre-participatory screening was cost effective to detect athletes who might experience sudden death in sports.

Molecular disturbance underlies to arrhythmogenic cardiomyopathy induced by transgene content, age and exercise in a truncated PKP2 mouse model.

Arrhythmogenic cardiomyopathy (ACM) is a disorder characterized by a progressive ventricular myocardial replacement by fat and fibrosis, which lead to ventricular arrhythmias and sudden cardiac death. Mutations in the desmosomal gene Plakophilin-2 (PKP2) accounts for >40% of all known mutations, generally causing a truncated protein. In a PKP2-truncated mouse model, we hypothesize that content of transgene, endurance training and aging will be determinant in disease progression. In addition, we investigated the molecular defects associated with the phenotype in this model. We developed a transgenic mouse model containing a truncated PKP2 (PKP2-Ser329) and generated three transgenic lines expressing increasing transgene content. The pathophysiological features of ACM in this model were assessed. While we did not observe fibro-fatty replacement, ultrastructural defects were exhibited. Moreover, we observed transgene content-dependent development of structural (ventricle dilatation and dysfunction) and electrophysiological anomalies in mice (PR interval and QRS prolongation and arrhythmia induction). In concordance with pathological defects, we detected a content reduction and remodeling of the structural proteins Desmocollin-2, Plakoglobin, native Plakophilin-2, Desmin and β-Catenin as well as the electrical coupling proteins Connexin 43 and cardiac sodium channel (Nav1.5). Surprisingly, we observed structural but not electrophysiological abnormalities only in trained and old mice. We demonstrated that truncated PKP2 provokes ACM in the absence of fibro-fatty replacement in the mouse. Transgene dose is essential to reveal the pathology, whereas aging and endurance training trigger limited phenotype. Molecular abnormalities underlay the structural and electrophysiological defects.

Characterizing the spectrum of right ventricular remodelling in response to chronic training

The significance and spectrum of reduced right ventricular (RV) deformation, reported in endurance athletes, is unclear. To comprehensively analyze the cardiac performance at rest of athletes, especially focusing on integrating RV size and deformation to unravel the underlying triggers of this ventricular remodelling. Hundred professional male athletes and 50 sedentary healthy males of similar age were prospectively studied. Conventional echocardiographic parameters of all four chambers were obtained, as well as 2D echo-derived strain (2DSE) in the left (LV) and in the RV free wall with separate additional analysis of the RV basal and apical segments. Left and right-sided dimensions were larger in athletes than in controls, but with a disproportionate RA enlargement. RV global strain was lower in sportsmen (−26.8 ± 2.8% vs −28.5 ± 3.4%, p < 0.001) due to a decrease in the basal segment (−22.8 ± 3.5% vs −25.8 ± 4.0%, p < 0.001) resulting in a marked gradient of deformation from the RV inlet towards the apex. By integrating size, deformation and stroke volume, we observed that the LV working conditions were similar in all sportsmen while a wider variability existed in the RV. Cardiac remodelling in athletes is more pronounced in the right heart cavities with specific regional differences within the right ventricle, but with a wide variability among individuals. The large inter-individual differences, as well as its acute and chronic relevance warrant further investigation.