Focus on exercise and sport cardiology

In contrast to the well-known beneficial effect of moderate physical activity,1,2 the pathophysiological adaptations induced by high level exercise and sports activity have gained intense attention because of the fear of the possibility of detrimental effects and permanent deterioration of cardiovascular function.3 On the other hand, the need for and effectiveness of pre-participation screening in individuals before sports activity has been the object of intense debate.4,5 In this focus issue, we have collected recent original studies which have provided contributions to these two important issues on sports cardiology and preventive medicine in general. In endurance athletes few studies have suggested that chronic excessive endurance exercise can lead to adverse structural cardiac remodelling reporting high coronary artery calcium scores, myocardial fibrosis and atrial arrhythmias. In this issue of the journal the paper by Christou et al., examining 27 runners who finished a 246 km SPARTATHLON race, adds important information to our understanding of the impact of a single episode of extreme vigorous exercise over a relatively short time frame.6 In brief, the authors showed that the main cardiac effects of ultra-long duration exercise were a decrease in left ventricular (LV) end-diastolic dimensions and an increase in LV wall thickness, as well as minimal dilation and alteration in systolic function of the right ventricle. This reduction of cardiac function did not appear to relate to myocardial necrosis but may well be attributed to reversible oedema or an inflammatory response. The past few years have seen a significant rise in paediatric athletes competing in various disciplines, training at a very high level. As in the young adult counterpart, this intense physical training could be associated with changes in cardiac morphology, called ‘athlete’s heart’. Several studies have recently investigated paediatric athlete’s heart reporting conflicting results: some authors showed similar absolute and scaled wall thicknesses between pre-adolescent athletes and controls, others demonstrated larger LV diameter and wall thickness. These differences could be explained by the variations in maturity status, the sex of the athletes and disparate sports being studied. In this regard paediatric athletes competing in endurance sports had the greatest differences in wall thickness and cardiac mass in comparison with age-matched controls.7 Beaumont et al. have now compared LV structure, function and mechanics by advanced speckle tracking echocardiography techniques in highly trained pre-adolescent soccer players and age-matched controls. The major findings from their study are that pre-pubertal soccer players showed greater circumferential strains, twist and faster diastolic lengthening in the absence of differences in wall thickness.8 The study adds important information to our understanding of paediatric athlete’s heart and highlights the utility of new echocardiography techniques such as speckle tracking echocardiography to differentiate athlete’s heart from cardiomyopathy. The cardiovascular system of endurance athletes mounts a fivefold to sevenfold increase in cardiac output to sustain sufficient oxygen delivery to exercising muscles, which is achieved through an array of physiological structural and functional cardiac adaptations, collectively known as the ‘athlete’s heart’. A growing number of studies have shown a transitory impairment in right ventricular (RV) performance after completing endurance races without LV involvement, and several authors have raised the hypothesis that this theoretically transient exercise-induced RV dysfunction could lead, over time, to permanent damage in some individuals. The predominant involvement of the right ventricle could be explained by the fact that, although the right ventricle is subjected to the same volume of venous return as the left ventricle during exercise, the reduction in pulmonary vascular resistance is considerably smaller than the reduction in systemic vascular resistance, resulting in an exponential rise in pulmonary artery pressure and in a greater than 30-fold increase in RV wall stress. However, the RV adaptation to endurance exercise differs widely among individuals and the mechanisms behind these interindividual differences are still not well understood. One suggested explanation is a larger pulmonary vascular reserve and, consequently, a lower exercise-related increase in pulmonary artery systolic pressure during exercise in some athletes.9 In this issue of the journal Sanz-de la Garza et al. has tried to elucidate this mechanism further evaluating the transpulmonary transit of agitated saline (PTAS) as a parameter of vascular reserve in 88 highly trained female and male endurance athletes. The athletes were stratified into two groups according to a high or low PTAS. The authors confirmed that high PTAS capability was associated with a significantly larger RV contractile reserve, a larger pulmonary vascular reserve and an enhanced maximal exercise capacity. Interestingly, female sex was the only significant independent determinant of high PTAS capability in the multivariate analysis.10 In the past few years several studies have investigated the aortic root dimension in elite athletes. There is a need for generating size-independent reference values for the aortic root in the athletic population. Here, the study presented by Abuli and colleagues on a cohort of 2092 athletes aged between 12 and 35 years indexed the aortic root size by two different scaling models: ratiometric and allometric scaling.11 In brief, the authors confirmed that the aortic root size in healthy trained athletes is within normal ranges established for the general population, and that sports with a high dynamic component are related to significantly larger aortic root size. Furthermore, the authors showed that allometric and ratiometric scaling to height provides almost perfect size-independent models, as shown by the lowest existing relationship with body surface area and height using these scaling methods. Numerous epidemiological studies have consistently shown an association between moderate aerobic exercise and a decreased risk of coronary heart disease and death; however, for a small number of individuals harbouring silent cardiac conditions, exercise can sometimes be associated with the risk of sudden death (i.e. the exercise paradox). Sudden cardiac death (SCD) is the most frequent medical cause of sudden death in athletes, and estimates vary widely based on the population. One of the available strategies to reduce the incidence of SCD in sports is the early identification of clinically relevant cardiovascular diseases through pre-participation evaluation (PPE). The protocol of PPE including clinical history, physical examination, and 12-lead ECG endorsed by European guidelines has been demonstrated to have superior diagnostic capability than just clinical history and physical examination, but the adoption of these recommendations among athletes competing at international level in low to middle income countries is poor.12 Here the results of questionnaires distributed during world championships in 2017 showed that only 59% of all participating athletes had a PPE, with large differences between athletes from low and middle income countries (28%) and very high income countries (74%). A clear inequality of the check-up and PPE around the world is evident and the need to improve sports care in low income regions, bearing in mind that athletes from Africa or from the Caribbean region more frequently have occult diseases of the heart.13 In recent years there has been a huge increase in master athletes (over 35 years) competing at various levels, undergoing pre-participation screening. At present, a significant amount of data exists on the athletes’ ECG interpretation in young adult athletes (16–35 years), thus allowing the differentiation of physiological ECG changes from those potentially pathological changes.14 For master athletes, ECG criteria are currently not available and it is unknown whether the criteria recommended for young athletes can be applied to master athletes. In this issue of the journal Panhuyzen-Goedkoop et al. aimed to test the effectiveness of three sets of contemporary ECG criteria (ESC 2005, Seattle and international criteria) to detect high-risk cardiac conditions in a large sample of athletes (2578, >35 years old) screened from 2006 to 2010. The authors found that 494 of the 2578 athletes (mean age 47.9 years) required second level examination and showed that ESC 2005 had the highest sensitivity, enabling them to detect more high-risk cardiac conditions (46, 1.8%) compared with Seattle (33, 1.4%) and international criteria (24, 1.3%).15 The 12-lead ECG is the cornerstone of the PPE of athletes as it is effective in detecting a number of disorders linked to SCD, including ion-channel disorders, electrical accessory pathways and cardiomyopathies. One of the main criticisms of the systematic use of ECG in PPE is the large number of false positive results. To address this issue, there have been several evidence-based refinements in ECG interpretation criteria that recognise the impact of age, ethnicity and type and intensity of sporting discipline on the electrical manifestation of the athlete’s heart. All these data have finally led to the international recommendations for electrocardiographic interpretation in athletes published in 2017. These recommendations divided the ECG findings into three groups: normal, borderline and abnormal. While an increased QRS voltage was considered a normal finding in the athletes, the observation of low QRS voltage (LQRSV) was not considered relevant. The article presented by the group of Pelliccia in this issue of the journal is the first study that focuses on the prevalence of LQRSV in athletes and on its prognostic value. The authors studied with clinical exam, ECG, echocardiography, maximal exercise test and 24-hour ECG Holter monitoring of 516 Caucasian Olympic Italian athletes. The prevalence of LQRSV was 4% slightly higher in athletes competing in skilled sports disciplines and associated with left atrial enlargement in 13% of cases. No correlation was observed between LQRSV and LV morphological patterns. Premature ventricular beats were more frequent (39%) in athletes with LQRSV than in those with normal QRS voltage (7%) but no cardiac event was reported over a follow-up period of 5 years.16 The authors concluded that, due to a higher prevalence of ventricular arrhythmias in athletes with LQRSV, a long-term follow-up with clinical evaluations and serial imaging of these athletes was justified, also bearing in mind that LQRSV may be present in patients with arrhythmogenic cardiomyopathy in an early stage of the disease. Atrial fibrillation (AF) is one of the most common arrhythmias encountered not only in the general population but also in athletes, especially in long-term middle-aged marathon runners. Over the past two decades, a growing body of evidences has revealed a complex relationship between endurance exercise and the risk of developing this arrhythmia: in particular a J-shaped relationship was identified with a reduction in AF risk in non-sedentary individuals who trained less than 20 metabolic equivalent (MET) hours/week but an increased risk in those who trained more than 20 MET hours/week.17 Atrial dilation is the major predictor of AF in athletes; in fact, high-intensity training was associated with atrial dilation and increased P-wave duration, both of which have been linked to the pathogenesis of AF. Modulating factors could include an increase in vagal tone, which itself increases the risk of AF, as well as intrinsic conduction changes genetically mediated by ion channel remodelling. On the other hand, it is controversial whether endurance sports activity also increases the burden of premature atrial beats (PABs), which represent a well-known AF trigger and risk factor. In this issue of the journal. Cipriani et al. compared the burden of PABs at 24 hours ECG monitoring off therapy in 134 healthy middle-aged endurance (30–60-year-old) competitive athletes, in 134 age and gender-matched healthy sedentary individuals and 66 middle-aged patients (20 athletes and 46 non-athletes) with ‘lone’ paroxysmal AF. The authors found no difference in the PABs burden between middle-aged athletes and controls, either with or without a history of paroxysmal AF.18 Moreover, at multivariable analysis, there was no relationship between hours of training per week or cumulative years of sports activity and higher PABs burden in healthy middle-aged athletes. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.