Editor comments: Focus on sport cardiology

Left ventricular hypertrophy in world class elite athletes is associated with signs of improved cardiac autonomic regulation

Intense and regular physical exercise is responsible for various cardiac changes (electrical, structural, and functional) that represent a physiological adaptation to exercise training. This remodelling, commonly referred to as ‘athlete’s heart’, includes a complex network of mechanisms (structural, neurohumoral, autonomic, metabolic, and regulatory), which ultimately lead to a marked biventricular increase in cardiac output during exercise.¹

The autonomic nervous system is involved in this process through parasympathetic withdrawal and sympathetic activation.

Among the techniques used to assess vagal and sympathetic modulation of the sino atrial node, the measurement of resting or post-exercise heart rate variability (HRV) has the advantage of being simple, economical, and non-invasive. However, HRV is strongly influenced by age and gender and only a limited number of studies have attempted to find a relationship between physiological cardiac hypertrophy and HRV-derived variables. To overcome these issues, Oggionni et al.² studied whether in elite athletes the physiological increase in cardiac mass is accompanied by an improvement of autonomic performance, as assessed by post-exercise vagal indices and a novel unitary Autonomic Nervous System Index for sports (ANSIs). The authors showed that elite athletes with physiological cardiac hypertrophy presented a selective profile of indices of autonomic nervous system performance, characterized by increases of markers of vagal recovery and of the novel unitary ANSIs, while HRV and spectral indices seemed to be unmodified.

Cardiac structure and function in response to a multi-stage marathon over 4486 km

Regular exercise is one of the cornerstones of therapeutic lifestyle changes for producing optimal cardiovascular (CV) and overall health.³ However, as with any pharmacological agent, a safe upper-dose limit potentially exists, beyond which the adverse effects may outweigh its benefits. Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long-distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. However, the hypothesis that excessive endurance exercise may induce adverse CV remodelling warranted further investigations.

In this issue of the journal, Klenk et al.⁴ investigated whether participation in the Trans Europe Foot Race 2009 (TEFR), an ultramarathon race held over 64 consecutive days and 4486 km, led to changes in cardiac structure and function. Cardiac magnetic resonance imaging (CMRI) was performed in 20 of 67 participating runners at three-time points [baseline scan at 294 ± 135 km (B), scan two at 1735 ± 86 km (T1), and scan three at 3370 ± 90 km (T2)] during the TEFR. The left ventricular (LV) mass increased significantly over the course of the race while no significant change was observed in functional parameters, including stroke volume (LV and right ventricles), mitral inflow, and global ventricular strain. This study does not support the hypothesis that extensive volume load over a longer period of time impairs right ventricular function leading in some endurance athletes to exercise-induced arrhythmogenic right ventricular cardiomyopathy.

Myocarditis in athletes: a clinical perspective

Myocarditis is an inflammation of the myocardium that can often be associated with cardiac dysfunction and arrhythmias and is even one of the leading causes for sudden cardiac death (SCD) in athletes. Elite athletes seem to have an increased risk for viral infection and subsequent myocarditis due to increased exposure to pathogens (worldwide travelling/international competition) or impaired immune system due to training during infections or strenuous exercise training in extreme weather conditions. Here, the review by Halle et al.⁵ summarizes the current evidence and treatment guidelines for the management of myocarditis in competitive and recreational athletes. In athletes, symptoms of myocarditis may include a decline in physical performance, fatigue, dizziness, or new-onset atrial or ventricular arrhythmias. Beyond resting electrocardiogram (ECG), cardiac biomarkers, echocardiography, and 24-h Holter ECG, diagnostic work-up should include CMRI which is able to assess inflammation, oedema, and fibrosis and therefore is a crucial tool for prognosis and sports eligibility. Athletes with an uncomplicated course and complete recovery, including normal LV function without late gadolinium enhancement (LGE), have an excellent prognosis and eligibility for sports can be attested 3 months after clinical recovery. However, in those athletes, with persistent pathological findings, even after 6 months, the risk for SCD remains increased and resuming exercise beyond recreational activities can only be recommended individually based on the course of the disease, LV function, arrhythmias, and LGE pattern in CMRI.

Left ventricular hypertrophy in athletes: how to differentiate between hypertensive heart disease and athlete’s heart

Chronically or intermittently elevated blood pressure increases systemic pressure and volume overload with an increased workload on the left ventricle and it ultimately leads to LV hypertrophy (LVH). Physical activity increases heart rate and blood pressure. Regularly performed sports or physical activities of substantial volume and intensity lead to cardiac changes referred to as ‘athlete’s heart’ that meet the criteria for LVH and may mimic the pathological remodelling of hypertension.⁶ In this case, the distinction between the athlete’s heart and arterial hypertension can be challenging. In the present issue, the review by D’Ascenzi et al.⁷ provides some imaging and clinical clues useful to distinguish between hypertensive heart disease and athlete’s heart. In brief, the authors showed that the presence of inferolateral T-wave inversion on ECG, an increase in LV mass with a reduction of LV function, an increase in atrial size accompanied by a reduced function as well as a dilatation of the aorta and an impairment of functional capacity, support the diagnosis of hypertension and are uncommon findings in athletes.

From talented child to elite athlete: the development of cardiac morphology and function in a cohort of endurance athletes from age 12 to 18

The athlete’s heart exhibits specific morphological and functional characteristics as a consequence of regular exercise training, primarily depending on the type, volume and intensity of the exercise performed. While most studies have been performed in adult athletes, altered cardiac morphology and function have been found even in preadolescent athletes.⁸ However, limited data are available from longitudinal studies, in particular during the growth and maturation of children and adolescents.⁹ In this issue, Bjerring et al.¹⁰ assessed 76 cross-country skiers at age 12, e during follow-up at age 15 and 18. Echocardiography with three-dimensional measurements and cardiopulmonary exercise testing were performed at all-time points. The authors demonstrated that the heart of young elite athletes underwent extensive changes from preadolescence to young adulthood. In fact, between ages 12 and 15, the active endurance athletes underwent eccentric remodelling while between ages 15 and 18 the endurance athletes tended towards concentric remodelling. This study highlighted the dynamic changes of athlete heart that results from interactions between growth, maturation and the training-related stimuli of pressure and volume (over)load.

Clinical correlates and outcome of the patterns of premature ventricular beats in Olympic athletes: a long-term follow-up study

Premature ventricular complexes (PVCs) are generally considered a benign ECG abnormality in the athletic population. They may, however, be the only phenotypic manifestation of an underlying disease in athletes with negative history, unremarkable physical examination, and normal resting ECG.¹¹ Traditionally, a frequency more than 2000 PVC/24 h, a short coupling interval and development of ventricular arrhythmias during exercise have been considered red flags but, recently, some investigators, have proposed evaluation of the morphology of PVC as the key factor in differentiating benign from potentially sinister PVC.

In this issue, Pelliccia et al.¹² performed a retrospective analysis to examine the clinical significance of different patterns of PVC in Olympic athletes. Cardiac disease was identified in 12% (14/118) of athletes with ‘uncommon’ PVC compared with only 1% (1/87) of those with ‘common’ PVC. Over a 6-year follow-up, cardiac diseases occurred in four athletes, all with uncommon patterns. These results support the importance of morphology in assessing the PVC and the need for comprehensive evaluation and follow-up of athletes with ‘uncommon’ patterns.

Prescribing, dosing and titrating exercise in patients with hypertrophic cardiomyopathy for prevention of comorbidities: ready for prime time

Current guidelines recommend that patients with hypertrophic cardiomyopathy (HCM) not participate in high-intensity exercise due to the increased risk of SCD. But individuals with genetic cardiomyopathies are not immune from cardiometabolic diseases, and inactivity is common in patients with HCM, likely due to fear of exercise-induced adverse events. Although several observations have demonstrated that moderate-intensity exercise may be safe in this population, little guidance is provided regarding the optimal dose or amount of physical activity for maintaining or improving CV health in HCM patients.¹³ In this context, the paper of Cavigli et al.¹⁴ is a timely initiative. The authors remark that exercise should be prescribed and titrated just like a drug in HCM patients considering individual characteristics, symptoms, past medical history, objective individual response to exercise, previous training experience, and stage of the disease.

The use of cardiac imaging in the evaluation of athletes in the clinical practice

The European Heart Rhythm Association and the European Association of Preventive Cardiology recommend a CV evaluation, including medical history, physical examination, and a 12-lead ECG for all athletes. Despite the use of transthoracic echocardiography (TTE) as a first-line evaluation tool lacks evidence of incremental diagnostic value to ECG, it is implemented by several sports associations, such as the Federation Internationale de Football Association (FIFA). In the current issue of the journal, D’Ascenzi et al.¹⁵ present a survey on how more than 600 physicians involved in the CV evaluations of athletes view the role of TTE as part of pre-participation screening (PPS). The majority (65%) of respondents used TTE as first-line screening tool, 72% repeat it at least once in the athletes’ career while, interestingly, only 28% suggested that repeated TTE should be limited to individuals with an abnormal finding. These findings clearly showed that the clinical community has moved beyond the debate about the role of ECG in the PPS and that further work should focus on the optimal use of CV imaging in risk stratification in athletes.

Yield and clinical significance of genetic screening in elite and amateur athletes

The most important goal of PPS is the identification of CV diseases associated with sudden SCD but additional benefits include early diagnosis of conditions that may pose a threat to the health of the athlete and require follow-up and treatment.¹⁶ Over the years new screening techniques, such as genetic testing, have emerged and increased our knowledge about abnormalities that may be associated with an increased risk of arrhythmias. However, although genetic testing enhanced our ability to identify individuals who are at a high risk, it also introduced new uncertainties. The relevance of new findings is frequently unknown, and the risk of a false positive test result is real and present.

In the current issue of the EJPC, Limongelli et al.¹⁷ reported their findings from a combination of PPS, advanced clinical evaluation, and genetic testing in a small group of athletes. A total of 5892 consecutive elite and amateur athletes underwent PPS, 61 with one or more clinical markers for suspected inherited cardiac disease underwent also genetic testing. A definitive (clinical or genetic) diagnosis was made in 14 athletes (23%).¹⁸ This was attributed to clinical evaluation in 6 (10%) and genetic testing in 8 (13%). The presence of >3 clinical markers (i.e. family history, ECG and/or TTE abnormalities, exercise-induced PVC) was associated with a higher probability of positive genetic diagnosis (75%), compared with the presence of two or one clinical markers.

How to manage an athlete with mitral valve prolapse

Mitral valve prolapse (MVP) is the most common valve abnormality in the general population, affecting between 2% and 3% of people and is also the most common cause of mitral valve regurgitation in athletes. The natural history of MVP is generally benign, however, in a small proportion of athletes it has been associated with an increased risk for arrhythmic SCD. Most of these patients did not have severe mitral regurgitation. Moreover, ventricular and supraventricular arrhythmias are common in athletes with MVP. Therefore, risk stratification for SCD is particularly challenging in athletes diagnosed with MVP. The ‘How to article’ by Cavarretta¹⁹ aims to help the physicians in distinguishing athletes with MVP at high risk of arrhythmic events from those at a lower risk. In this analysis, the authors defined MVP and its presentation in athletes, reviewed physical and echocardiographic findings of this abnormality, and identified high-risk features carrying an adverse prognosis. Furthermore, they outlined consensus recommendations regarding the participation of athletes in competitive sports with MVP and mitral regurgitation. In brief, there are several markers that may be associated with a heightened risk of SCD including a family history, T-wave inversion in the inferior leads on the 12-lead ECG; polymorphic ventricular arrhythmias on Holter monitoring or stress ECG, severe mitral regurgitation, mitral annular disjunction, and bileaflet prolapse on echocardiography; myocardial fibrosis in the LV inferolateral basal region and in papillary muscles detected by CMRI.

Conflict of interest: none declared.

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