BACKGROUND: Assessment of the athlete\'s heart is challenging because of a phenotypic overlap between reactive physiological adaptation and pathological remodelling. The potential value of myocardial deformation remains controversial in identifying early cardiomyopathy.
OBJECTIVE: To identify the echocardiographic phenotype of athletes using advanced two-dimensional speckle tracking imaging, and to define predictive factors of subtle left ventricular systolic dysfunction.
METHODS: In total, 191 healthy male athletes who underwent a preparticipation medical evaluation at Nancy University Hospital between 2013 and 2020 were included. Clinical and echocardiographic data were compared with 161 healthy male subjects from the STANISLAS cohort. Borderline global longitudinal strain value was defined as<17.5%.
RESULTS: Athletes demonstrated lower left ventricular ejection fraction (57.9±5.3% vs. 62.6±6.4%; P<0.01) and lower global longitudinal strain (17.5±2.2% vs. 21.1±2.1%; P<0.01). No significant differences were found between athletes with and without a borderline global longitudinal strain value regarding clinical characteristics, structural echocardiographic features and exercise capacity. A borderline global longitudinal strain value was associated with a lower endocardial global longitudinal strain (18.8±1.2% vs. 22.7±1.9%; P=0.02), a lower epicardial global longitudinal strain (14.0±1.1% vs. 16.6±1.2%; P<0.01) and a higher endocardial/epicardial global longitudinal strain ratio (1.36±0.07 vs. 1.32±0.06; P<0.01). No significant difference was found regarding mechanical dispersion (P=0.46).
CONCLUSIONS: Borderline global longitudinal strain value in athletes does not appear to be related to structural remodelling, mechanical dispersion or exercise capacity. The athlete\'s heart is characterized by a specific myocardial deformation pattern with a more pronounced epicardial layer strain impairment.

\"Athlete\'s heart\" is a spectrum of morphological, functional, and regulatory changes that occur in people who practice regular and long-term intense physical activity. The morphological characteristics of the athlete\'s heart may overlap with some structural and electrical cardiac diseases that may predispose to sudden cardiac death, including inherited and acquired cardiomyopathies, aortopathies and channelopathies. Overdiagnosis should be avoided, while an early identification of underlying cardiac life-threatening disorders is essential to reduce the potential for sudden cardiac death. A step-by-step multimodality approach, including a first-line evaluation with personal and family history, clinical evaluation, 12-lead resting electrocardiography (ECG), followed by second and third-line investigations, as appropriate, including exercise testing, resting and exercise echocardiography, 24-hour ECG Holter monitoring, cardiac magnetic resonance, computed tomography, nuclear scintigraphy, or genetic testing, can be determinant to differentiate between extreme physiology adaptations and cardiac pathology. In this context, cardiovascular imaging plays a key role in detecting structural abnormalities in athletes who fall into the grey zone between physiological adaptations and a covert or early phenotype of cardiovascular disease.

Cardiovascular disease (CVD) is the most common cause of death globally in general population. Sport activity is an effective and recommended non-pharmacological method of CVD prevention. Presently, the group of people practicing sport regularly is constantly growing due to increasing awareness of its health benefits. However, vigorous-intensity exercises can reveal previously undetected disease. Master athletes over 35 years old are particularly exposed to sudden cardiac death (SCD) mainly in the course of coronary artery disease (CAD). Another common disease in veteran athletes is hypertension. It is known that regular endurance training can lower blood pressure at rest, so arterial hypertension in athletes is usually masked by adaptation to effort. Despite of normal or high-normal blood pressure in the office, the values during exercises and in ambulatory blood pressure monitoring (ABPM) can exceed the norm. Hidden hypertension have the same negative impact on cardiovascular system. It increases the risk of (1) atherosclerosis and therefore myocardial infarction or stroke, (2) left ventricular hypertrophy with diastolic and/or systolic heart failure, myocardial fibrosis and ventricular arrhythmias, (3) left atrial enlargement increasing the risk of atrial fibrillation and stroke and (4) aortic dilation/dissection. Through these complications hypertension can lead to SCD during sport activities, therefore it is important to recognize this disease early and start a proper treatment. To enable safe participation in sports competition detailed guidelines for screening were created, but they mainly concern CAD. We propose an additional scheme of screening in master athletes including the detection of hidden hypertension to prevent its consequences.

UNASSIGNED: In young athletes, the level of competitiveness in sports is increasing, as well as frequency and intensity of exercise training. Adaptations of the cardiac system to this increased workload imposed by exercise has not yet been studied sufficiently. In adults, studies point towards a shift from the functional athlete\'s heart towards pathological cardiac remodelling, with ventricular arrythmia and impaired cardiac function, that is exercise-related. This systematic review investigates cardiac adaptations to exercise in junior athletes compared to inactive controls.
UNASSIGNED: Three electronic databases (PubMed/Medline, ScienceDirect and Web of Science) were searched for studies assessing 2-dimensional transthoracic echocardiography (2D TTE) and 2-dimensional speckle tracking echocardiography (2D STE) parameters in junior athletes, aged 7-19 years, compared to inactive controls. Data was screened and extracted by two reviewers; study quality and risk of bias was assessed by three reviewers.
UNASSIGNED: Eight out of 1460 studies met all inclusion criteria, with all studies reporting results on 2D TTE and six studies reporting results on 2D STE parameters in 540 (51 girls) junior athletes and 270 (18 girls) controls. There is evidence for structural cardiac adaptations of the left ventricle and both atria in junior athletes. Results regarding left ventricular function are controversial with a tendency to improved function in dynamic exercising athletes. Left ventricular mass and relative wall thickness point towards higher values in static exercising athletes.
UNASSIGNED: Cardiac adaptations to exercise occur in children and adolescents. These adaptations are more pronounced in structural left ventricular parameters. Functional parameters are preserved or slightly improved in junior athletes but not impaired by exercise.

Soccer is the most popular sport in the world, with over 265 million active players and approximately 0.05% professional players worldwide. The Fédération Internationale de Football Association (FIFA) has made preparticipation screening recommendations which involve electrocardiography and echocardiography being performed prior to international competition. The aim of preparticipation cardiovascular screening in young athletes is to detect asymptomatic individuals with cardiovascular disease at risk of sudden cardiac death (SCD). The incidence of SCD in young athletes (age≤ 35 years) is 0.6-3.6 in 100,000 persons/year, with most deaths due to cardiovascular causes. Arrhythmogenic right ventricular cardiomyopathy (ARVC) is one of the leading causes of SCD in young athletes. It is a genetic disease characterized by progressive fibrofatty replacement of the myocardium with variable phenotypic expression. Exercise-induced cardiac remodeling in conjunction with extensive T-wave inversion raises concern for ARVC. This case report and literature review explores a potential mimic for ARVC, the role of cardiovascular screening in sport, and the use of a multimodality approach for risk stratification and management.

In a 77-year-old former world-record holding male marathoner (2:08:33.6) this study sought to investigate the impact of lifelong intensive endurance exercise on cardiac structure, function and the trajectory of functional capacity (determined by maximal oxygen consumption, V̇O2max) throughout the adult lifespan. As a competitive runner, our athlete (DC) reported performing up to 150-300 miles/wk of moderate-to-vigorous exercise, and sustained 10-15 hours/wk of endurance exercise after retirement from competition. DC underwent maximal cardiopulmonary exercise testing in 1970 (aged 27yrs), 1991 (aged 49yrs) and 2020 (aged 77yrs) to determine V̇O2max. At his evaluation in 2020, DC also underwent comprehensive cardiac assessments including resting echocardiography, and resting and exercise cardiac magnetic resonance to quantify cardiac structure and function at rest and during peak supine exercise. DC\'s V̇O2max showed minimal change from 27yrs (69.7mL/kg/min) to 49yrs (68.1mL/kg/min), although it eventually declined by 36% by the age of 77yrs (43.6mL/kg/min). DC\'s V̇O2max at 77yrs, was equivalent to the 50th percentile for healthy 20-29 year-old males and 2.4 times the requirement for maintaining functional independence. This was partly due to marked ventricular dilatation (left-ventricular end-diastolic volume: 273mLs), which facilitates a large peak supine exercise stroke volume (200mLs) and cardiac output (22.2L/min). However, at the age of 78 years, DC developed palpitations and fatigue, and was found to be in atrial fibrillation requiring ablation procedures to revert his heart to sinus rhythm. Overall, this life study of a world champion marathon runner exemplifies the substantial benefits and potential side effects of many decades of intense endurance exercise.

Arterial hypertension (AH) is one of the most common pathologic conditions and uncontrolled AH is a leading risk factor for cardiovascular disease and mortality. AH chronically causes myocardial and arterial remodelling with hemodynamic changes affecting the heart and other organs, with potentially irreversible consequences leading to poor outcomes. Therefore, a proper and early treatment of AH is crucial after the diagnosis. Beyond medical treatment, physical exercise also plays a therapeutic role in reducing blood pressure, given its potential effects on sympathetic tone, renin-angiotensin-aldosterone system, and endothelial function. International scientific societies recommend physical exercise among lifestyle modifications to treat AH in the first stages of the disease. Moreover, some studies have also shown its usefulness in addition to drugs to reduce blood pressure further. Therefore, an accurate, personalized exercise prescription is recommended to optimize the prevention and treatment of hypertension. On the other hand, uncontrolled AH in athletes requires proper risk stratification and careful evaluation to practice competitive sports safely. Moreover, the differential diagnosis between hypertensive heart disease and athlete\'s heart is sometimes challenging and requires a careful and comprehensive interpretation in order not to misinterpret the clinical findings. The present review aims to discuss the relationship between hypertensive heart disease and physical exercise, from diagnostic tools to prevention and treatment strategies.

Long-term athletic training can result in structural and conduction changes within the heart, leading to Athlete\'s heart syndrome (AHS). This syndrome is characterized by increased left ventricle (LV) dimensions, thickness, and mass. Dynamic exercise significantly contributes to these alterations, with sinus bradycardia being a common conduction abnormality, often accompanied by first-degree atrioventricular (AV) block. However, higher degrees of AV conduction abnormalities, such as second- and third-degree blocks, though rare, might occur due to parasympathetic hypertonia. Prompt evaluation is necessary to rule out underlying structural or infiltrative heart diseases. We present the case of a 66-year-old lifelong long-distance runner with marked sinus bradycardia, AV dissociation, and junctional escape rhythm, alongside left ventricular hypertrophy (LVH) and T-wave repolarization abnormalities. Subsequent studies ruled out possible pathologies, and the patient was diagnosed with AHS, characterized by cardiac remodeling and bradycardia due to prolonged cardiac loading. This case underscores the importance of clinical assessment, cardiac imaging, and exclusion of pathologic causes to distinguish normal physiological adaptations from potentially concerning conditions.

Pre-participation screening and management of congenital cardiac valvulopathy in competitive athletes can be challenging, particularly within the context of ultra-endurance disciplines. A 55-year-old female athlete without a reported history of cardiac disease exhibited clinical signs of cardiogenic pulmonary edema during a 156 km ultra-trail race. The echocardiographic assessment revealed the presence of a parachute mitral valve, with no evidence of mitral stenosis or regurgitation at rest, but it demonstrated severe dynamic mitral stenosis during exercise. In competitive athletes, the detection of rare valvulopathy should prompt a comprehensive cardiac evaluation aimed at assessing the potential for dynamic valvular dysfunction.

BACKGROUND: Left ventricular (LV) trabeculations (LVTs) are common findings in athletes. Limited information exists regarding clinical significance, management, and outcome.
OBJECTIVE: The purpose of this study is to examine the prevalence and morphologic characteristics of LVTs in elite athletes, with a focus on clinical correlates and prognostic significance.
METHODS: We enrolled 1,492 Olympic elite athletes of different sports disciplines with electrocardiogram, echocardiogram, and exercise stress test. Individuals with a definite diagnosis of LV noncompaction (LVNC) were excluded; we focused on athletes with LVTs not meeting the criteria for LVNC.
RESULTS: Four hundred thirty-five (29.1%) athletes presented with LVTs, which were more frequent in male athletes (62.1% vs 53.5%, P = .002) and Black athletes compared with Caucasian (7.1% vs 2.4%, P < .0001) and endurance athletes (P = .0005). No differences were found with relation to either the site or extent of trabeculations. Endurance athletes showed a higher proportion of LVTs and larger LV volumes (end-diastolic and end-systolic, respectively, 91.5 ± 19.8 mL vs 79.3 ± 29.9 mL, P = .002; and 33.1 ± 10 mL vs 28.6 ± 11.7 mL, P = .007) and diastolic pattern with higher E wave (P = .01) and e\' septal velocities (P = .02). Ventricular arrhythmias were found in 14% of LVTs versus 11.6% of athletes without LVTs (P = .22). Neither the location nor the LVTs\' extension were correlated to ventricular arrhythmias. At 52 ± 32 months of follow-up, no differences in arrhythmic burden were observed (11.1% in LVT athletes vs 10.2%, P = .51).
CONCLUSIONS: Left ventricular trabeculations are quite common in athletes, mostly male, Black, and endurance, likely as the expression of adaptive remodeling. In the absence of associated clinical abnormalities, such as LV systolic and diastolic impairment, electrocardiogram repolarization abnormalities, or family evidence of cardiomyopathy, athletes with LVTs have benign clinical significance and should not require further investigation.