Como eu faço no Coração de Atleta: avaliação dos diferentes tipos de adaptação ao exercício / My approach to "Athlete'S Heart": evaluation of the different types of adaptation to exercise

A prática regular de esportes pode induzir adaptações no coração, sendo essa condição comumente chamada de "coração de atleta". As alterações observadas incluem dilatação das câmaras cardíacas, aumento da espessura miocárdica, melhora do enchimento ventricular, aumento da trabeculação do ventrículo esquerdo (VE), dilatação da veia cava inferior, entre outras. Essas alterações também podem ser observadas em algumas doenças cardíacas, como cardiomiopatia (CMP) dilatada, hipertrófica e outras. Dessa forma, os exames de imagem cardíaca são fundamentais na identificação dessas alterações e na diferenciação entre o "coração de atleta" e uma possível cardiopatia.(AU)

Exercise-induced adaptation may occur in amateur and professional athletes. This condition is commonly named "athlete's heart". The alterations observed include dilation of the heart chambers, increased myocardial thickness, improved ventricular filling, increased left ventricular trabeculation, dilation of the inferior vena cava, among others. These changes can also be observed in some heart diseases, such as dilated, hypertrophic and other cardiomyopathies (CMP). Thus, cardiac imaging tests are fundamental in identifying these alterations and in differentiating between "athlete's heart" and possible heart disease. (AU)

Three-dimensional echocardiography of the athlete's heart: a comparison with cardiac magnetic resonance imaging.

Three-dimensional echocardiography (3DE) is the most accurate cardiac ultrasound technique to assess cardiac structure. 3DE has shown close correlation with cardiac magnetic resonance imaging (CMR) in various populations. There is limited data on the accuracy of 3DE in athletes and its value in detecting alterations during follow-up. Indexed left and right ventricular end-diastolic volume (LVEDVi, RVEDVi), end-systolic volume, ejection fraction (LVEF, RVEF) and left ventricular mass (LVMi) were assessed by 3DE and CMR in two-hundred and one competitive endurance athletes (79% male) from the Pro@Heart trial. Sixty-four athletes were assessed at 2 year follow-up. Linear regression and Bland-Altman analyses compared 3DE and CMR at baseline and follow-up. Interquartile analysis evaluated the agreement as cardiac volumes and mass increase. 3DE showed strong correlation with CMR (LVEDVi r = 0.91, LVEF r = 0.85, LVMi r = 0.84, RVEDVi r = 0.84, RVEF r = 0.86 p < 0.001). At follow up, the percentage change by 3DE and CMR were similar (∆LVEDVi r = 0.96 bias - 0.3%, ∆LVEF r = 0.94, bias 0.7%, ∆LVMi r = 0.94 bias 0.8%, ∆RVESVi r = 0.93, bias 1.2%, ∆RVEF r = 0.87 bias 0.4%). 3DE underestimated volumes (LVEDVi bias - 18.5 mL/m2, RVEDVi bias - 25.5 mL/m2) and the degree of underestimation increased with larger dimensions (Q1vsQ4 LVEDVi relative bias - 14.5 versus - 17.4%, p = 0.016; Q1vsQ4 RVEDVi relative bias - 17 versus - 21.9%, p = 0.005). Measurements of cardiac volumes, mass and function by 3DE correlate well with CMR and 3DE accurately detects changes over time. 3DE underestimates volumes and the relative bias increases with larger cardiac size.

A comparative study on the analysis of hemodynamics in the athlete's heart.

The pathophysiological mechanisms underlying the development of the athlete's heart are still poorly understood. To characterize the intracavitary blood flows in the right ventricle (RV) and right-ventricular outflow tract (RVOT) in 2 healthy probands, patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and 2 endurance athletes, we performed 4D-MRI flow measurements to assess differences in kinetic energy and shear stresses. Time evolution of velocity magnitude, mean kinetic energy (MKE), turbulent kinetic energy (TKE) and viscous shear stress (VSS) were measured both along the whole RV and in the RVOT. RVOT regions had higher kinetic energy values and higher shear stresses levels compared to the global averaging over RV among all subjects. Endurance athletes had relatively lower kinetic energy and shear stresses in the RVOT regions compared to both healthy probands and ARVC patients. The athlete's heart is characterized by lower kinetic energy and shear stresses in the RVOT, which might be explained by a higher diastolic compliance of the RV.

Indications and utility of cardiac genetic testing in athletes.

Sports Cardiology practice commonly involves the evaluation of athletes for genetically determined cardiac conditions that may predispose to malignant arrhythmias, heart failure, and sudden cardiac death. High-level exercise can lead to electrical and structural cardiac remodelling which mimics inherited cardiac conditions (ICCs). Differentiation between 'athlete's heart' and pathology can be challenging and often requires the whole armamentarium of available investigations. Genetic studies over the last 30 years have identified many of the genetic variants that underpin ICCs and technological advances have transformed genetic testing to a more readily available and affordable clinical tool which may aid diagnosis, management, and prognosis. The role of genetic testing in the evaluation and management of athletes with suspected cardiac conditions is often unclear beyond the context of specialist cardio-genetics centres. This document is aimed at physicians, nurses, and allied health professionals involved in the athlete's care. With the expanding role and availability of genetic testing in mind, this document was created to address the needs of the broader sports cardiology community, most of whom work outside specialized cardio-genetics centres, when faced with the evaluation and management of athletes with suspected ICC. The first part of the document provides an overview of basic terminology and principles and offers guidance on the appropriate use of genetic testing in the assessment of such athletes. It outlines key considerations when contemplating genetic testing, highlighting the potential benefits and pitfalls, and offers a roadmap to genetic testing. The second part of the document presents common clinical scenarios in Sports Cardiology practice, outlining the diagnostic, prognostic, and therapeutic implications of genetic testing, including impact on exercise recommendations. The scope of this document does not extend to a comprehensive description of the genetic basis, investigation, or management of ICCs.

Cardiac MRI findings to differentiate athlete's heart from hypertrophic (HCM), arrhythmogenic right ventricular (ARVC) and dilated (DCM) cardiomyopathy.

To provide clinically relevant criteria for differentiation between the athlete's heart and similar appearing hypertrophic (HCM), dilated (DCM), and arrhythmogenic right-ventricular cardiomyopathy (ARVC) in MRI. 40 top-level athletes were prospectively examined with cardiac MR (CMR) in two university centres and compared to retrospectively recruited patients diagnosed with HCM (n = 14), ARVC (n = 18), and DCM (n = 48). Analysed MR imaging parameters in the whole study cohort included morphology, functional parameters and late gadolinium enhancement (LGE). Mean left-ventricular enddiastolic volume index (LVEDVI) was high in athletes (105 ml/m2) but significantly lower compared to DCM (132 ml/m2; p = 0.001). Mean LV ejection fraction (EF) was 61% in athletes, below normal in 7 (18%) athletes vs. EF 29% in DCM, below normal in 46 (96%) patients (p < 0.0001). Mean RV-EF was 54% in athletes vs. 60% in HCM, 46% in ARVC, and 41% in DCM (p < 0.0001). Mean interventricular myocardial thickness was 10 mm in athletes vs. 12 mm in HCM (p = 0.0005), 9 mm in ARVC, and 9 mm in DCM. LGE was present in 1 (5%) athlete, 8 (57%) HCM, 10 (56%) ARVC, and 21 (44%) DCM patients (p < 0.0001). Healthy athletes' hearts are characterized by both hypertrophy and dilation, low EF of both ventricles at rest, and increased interventricular septal thickness with a low prevalence of LGE. Differentiation of athlete's heart from other non-ischemic cardiomyopathies in MRI can be challenging due to a significant overlap of characteristics also seen in HCM, ARVC, and DCM.

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K.

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110α (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor that regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1) swim training or 2) cardiac-specific transgenic expression of constitutively active PI3K (caPI3KTg+). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (∼21%) in heart weight normalized to tibia length vs. untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression but was comparable between genotypes. However, differences in Foxo3a, Hsp70, and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3KTg+ mice. Cardiac Akt and FoxO1 protein expressions were significantly reduced in hearts of caPI3KTg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when one is considering FoxO1 as a target for treating the diseased heart.NEW & NOTEWORTHY Regulators of exercise-induced physiological cardiac hypertrophy and protection are considered promising targets for the treatment of heart failure. Unlike pathological hypertrophy, the transcriptional regulation of physiological hypertrophy has remained largely elusive. To our knowledge, this is the first study to show that the transcription factor FoxO1 is a critical mediator of exercise-induced cardiac hypertrophy. Given that exercise-induced hypertrophy is protective, this finding has important implications when one is considering FoxO1 as a target for treating the diseased heart.

Arrhythmogenic right ventricular cardiomyopathy and sports activity: from molecular pathways in diseased hearts to new insights into the athletic heart mimicry.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disease associated with a high risk of sudden cardiac death. Among other factors, physical exercise has been clearly identified as a strong determinant of phenotypic expression of the disease, arrhythmia risk, and disease progression. Because of this, current guidelines advise that individuals with ARVC should not participate in competitive or frequent high-intensity endurance exercise. Exercise-induced electrical and morphological para-physiological remodelling (the so-called 'athlete's heart') may mimic several of the classic features of ARVC. Therefore, the current International Task Force Criteria for disease diagnosis may not perform as well in athletes. Clear adjudication between the two conditions is often a real challenge, with false positives, that may lead to unnecessary treatments, and false negatives, which may leave patients unprotected, both of which are equally inacceptable. This review aims to summarize the molecular interactions caused by physical activity in inducing cardiac structural alterations, and the impact of sports on arrhythmia occurrence and other clinical consequences in patients with ARVC, and help the physicians in setting the two conditions apart.

Differential diagnosis of arrhythmogenic cardiomyopathy: phenocopies versus disease variants.

Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease caused by mutations of desmosomal genes in about 50% of patients. Affected patients may have defective non-desmosomal genes. The ACM phenotype may occur in other genetic cardiomyopathies, cardio-cutaneous syndromes or neuromuscular disorders. A sizeable proportion of patients have non-genetic diseases with clinical features resembling ACM (phenocopies). The identification of biventricular and left-dominant phenotypic variants has made differential diagnosis more difficult because of the broader spectrum of phenocopies which requires a detailed clinical study with appropriate evaluation of most prominent and discriminatory disease features. Conditions that enter into differential diagnosis of ACM include heart muscle diseases affecting the right ventricle, the left ventricle, or both. To confirm a conclusive diagnosis of ACM, these differential possibilities need to be reasonably excluded by an accurate and targeted clinical evaluation. This article reviews the clinical and imaging features of major phenocopies of ACM and provides indications for differential diagnosis. The recent etiologic classification of Arrhythmogenic Cardiomyopathies, whose common denominator is the distinctive phenotype characterized by a hypokinetic and non-dilated ventricle with a large amount of myocardial fibrosis underlying its propensity to generate ventricular arrhythmias is also addressed.

The arrhythmogenic right ventricular cardiomyopathy in comparison to the athletic heart.

Intense exercise-induced right ventricular remodeling is a potential adaptation of cardiac function and structure. The features of the remodeling may overlap with those of a very early form of arrhythmogenic right ventricular cardiomyopathy (ARVC): at this early stage, it could be difficult to discriminate ARVC, from exercise-induced cardiac adaptation that may develop in normal individuals. The purpose of this paper is to discuss which exercise-induced remodeling may be a pathological or a physiological finding. A complete evaluation may be required to identify the pathological features of ARVC that would include potential risk of sudden cardiac death during sport or, to avoid the false diagnosis of ARVC. The most recent expert assessment of arrhythmogenic cardiomyopathy focuses on endurance athletes presenting with clinical features indistinguishable from ARVC.

Cardiovascular Magnetic Resonance and Sport Cardiology: a Growing Role in Clinical Dilemmas.

Exercise training induces morphological and functional cardiovascular adaptation known as the "athlete's heart" with changes including dilatation, hypertrophy, and increased stroke volume. These changes may overlap with pathological appearances. Distinguishing athletic cardiac remodelling from cardiomyopathy is important and is a frequent medical dilemma. Cardiac magnetic resonance (CMR) has a role in clinical care as it can refine discrimination of health from a disease where ECG and echocardiography alone have left or generated uncertainty. CMR can more precisely assess cardiac structure and function as well as characterise the myocardium detecting key changes including myocardial scar and diffuse fibrosis. In this review, we will review the role of CMR in sports cardiology.

Arrhythmogenic Cardiomyopathy and Sports Activity.

Arrhythmogenic right-ventricular cardiomyopathy (ARVC) is a genetically determined heart disease characterized by progressive myocyte death and substitution by fibrofatty tissue. Life-threatening ventricular arrhythmias may occur during the course of the disease and are distinctively triggered by sports activity: for this reason, ARVC is one of the leading causes of sudden death in the athlete. Early identification of affected athletes by preparticipation screening in the pre-symptomatic phase is essential, but differential diagnosis with the athlete's heart may be challenging. Variants with predominant involvement of the left ventricle are difficult to diagnose unless cardiac magnetic resonance is performed. Athletes with overt ARVC or asymptomatic carriers of pathological gene mutations, including those with an implantable cardioverter defibrillator, should refrain from competitive sports, while a moderate-intensity recreational physical activity appears safe.

Special Article - Exercise-induced right ventricular injury or arrhythmogenic cardiomyopathy (ACM): The bright side and the dark side of the moon.

There is still debate on the range of normal physiologic changes of the right ventricle or ventricular (RV) function in athletes. Genetic links to arrhythmogenic cardiomyopathy (ACM) are well-established. There is no current consensus on the importance of extensive exercise and exercise-induced injury to the RV. During the intensive exercise of endurance sports, the cardiac structures adapt to athletic load over time. Some athletes develop RV cardiomyopathy possibly caused by genetic predisposition, whilst others develop arrhythmias from the RV. Endurance sports lead to increased volume and pressure load in both ventricles and increased myocardial mass. The extent of volume increase and changes in myocardial structure contribute to impairment of RV function and pose a challenge in cardiovascular sports medicine. Genetic predisposition to ACM may play an important role in the risk of sudden cardiac death of athletes. In this review, we discuss and evaluate existing results and opinions. Intensive training in competitive dynamic/power and endurance sports leads to specific RV adaptation, but physiological adaptation without genetic predisposition does not necessarily lead to severe complications in endurance sports. Discriminating between physiological adaptation and pathological form of ACM or RV impairment provoked by reinforced exercise presents a challenge to clinical sports cardiologists.

Left Atrial Volume, Cardiorespiratory Fitness, and Diastolic Function in Healthy Individuals: The HUNT Study, Norway.

Background Left atrial (LA) size and cardiorespiratory fitness (CRF) are predictors of future cardiovascular events in high-risk populations. LA dilatation is a diagnostic criterion for left ventricular diastolic dysfunction. However, LA is dilated in endurance athletes with high CRF, but little is known about the association between CRF and LA size in healthy, free-living individuals. We hypothesized that in a healthy population, LA size was associated with CRF and leisure-time physical activity, but not with echocardiographic indexes of left ventricular diastolic dysfunction. Methods and Results In this cross-sectional study from HUNT (Nord-Trøndelag Health Study), 107 men and 138 women, aged 20 to 82 years, without hypertension, cardiovascular, pulmonary, or malignant disease participated. LA volume was assessed by echocardiography and indexed to body surface area LAVI (left atrial volume index). CRF was measured as peak oxygen uptake (VO2peak) using ergospirometry, and percent of age- and-sex-predicted VO2peak was calculated. Indexes of left ventricular diastolic dysfunction were assessed in accordance with latest recommendations. LAVI was >34 mL/m2 in 39% of participants, and LAVI was positively associated with VO2peak and percentage of age- and-sex-predicted VO2peak (ß [95% CI], 0.11 [0.06-0.16] and 0.18 [0.09-0.28], respectively) and weighted minutes of physical activity per week (ß [95% CI], 0.01 [0.003-0.015]). LAVI was not associated with other indexes of left ventricular diastolic dysfunction. There was an effect modification between age and VO2peak/percentage of age- and-sex-predicted VO2peak showing higher LAVI with advanced age and higher VO2peak/percentage of age- and-sex-predicted VO2peak as presented in prediction diagrams. Conclusions Interpretation of LAVI as a marker of diastolic dysfunction should be done in relation to age-relative CRF. Studies on the prognostic value of LAVI in fit subpopulations are needed.

Right ventricular mechanical pattern in health and disease: beyond longitudinal shortening.

Right ventricular (RV) function has proven to be a prognostic factor in heart failure with reduced and preserved ejection fraction and in pulmonary hypertension. RV function is also a cornerstone in the management of novel clinical issues, such as mechanical circulatory support devices or grown-up congenital heart disease patients. Despite the notable amount of circumferentially oriented myofibers in the subepicardial layer of the RV myocardium, the non-longitudinal motion directions are often neglected in the everyday assessment of RV function by echocardiography. However, the complex RV contraction pattern incorporates different motion components along three anatomically relevant axes: longitudinal shortening with traction of the tricuspid annulus towards the apex, radial motion of free wall often referred as the "bellows effect", and anteroposterior shortening of the chamber by stretching the free wall over the septum. Advanced echocardiographic techniques, such as speckle-tracking and 3D echocardiography allow an in-depth characterization of RV mechanical pattern, providing better understanding of RV systolic and diastolic function. In our current review, we summarize the existing knowledge regarding RV mechanical adaptation to pressure- and/or volume-overloaded states and also other physiologic or pathologic conditions.

The relationship between right heart and aerobic capacity in large cohort of young elite athletes.

We sought to investigate right heart remodeling and function in elite athlees, as well as the relationship between parameters of right ventricular (RV) and right atrial (RA) remodeling and indices of aerobic capacity. Elite male athletes (n = 352) underwent echocardiographic examination including the evaluation of RV and RA parameters. Maximal cardiopulmonary exercise testing was performed to measure maximal oxygen consumption (VO2max), ventilatory anaerobic threshold (VAT) and heart rate reserve (HRR). The right heart remodeling was different between groups. Soccer players had significantly higher RV and RA diameters indexed for BSA. RV filling pressure assessed by tricuspid E/e' ratio was the lowest in soccer players, suggesting somewhat better RV diastolic function. Functional capacity also varies between groups of athletes. VO2max was the highest among soccer players, somewhat lower in basketball players and and the lowest among water polo players (55.3 ± 5.6 vs. 52.1 ± 5.9 vs. 53.5 ± 4.8 ml/kg/min, p < 0.001). Age, average weekly duration of training, percentage of body fat, as well as parameters of cardiopulmonary fitness (VO2max, O2 pulse, HRR), correlated well with parameters of RV and RA structure and function in the whole study population. However, systolic blood pressure at rest, VO2max and LV mass index are independently associated with RV and RA structure, whereas duration of training shows the best association with parameters of RV systolic and diastolic function. Even though soccer, water polo and basketball belong to the same group of sports, there is a significant difference in RV and RA remodeling between these three groups. It seems that right heart adaptation is the most pronounced in soccer players, who also have the highest maximal oxygen consumption. Further studies are necessary to investigate the mechanisms of these differences.

Cardiac magnetic resonance based deformation imaging: role of feature tracking in athletes with suspected arrhythmogenic right ventricular cardiomyopathy.

Both, arrhythmogenic right ventricular cardiomyopathy (ARVC) and regular training are associated with right ventricular (RV) remodelling. Cardiac magnetic resonance (CMR) is given an important role in the diagnosis of ARVC in current task force criteria (TFC), however, they contain no cut-off values for athletes. We aimed to confirm the added value of feature tracking and to provide new cut-off values to differentiate between ARVC and athlete's heart. Healthy athletes with training of minimal 15 h/week (n = 34), patients with definite ARVC (n = 34) and highly trained athletes with ARVC (n = 8) were examined by CMR. Left and right ventricular volumes and masses were determined. Global right and left ventricular, and regional strain analysis for the RV free wall was performed using feature tracking on balanced steady-state free precession cine images. 94% of healthy athletes showed RV dilatation of the proposed TFC, 14.7% showed RV ejection fraction (RVEF) between 45-50%, none of them had RVEF < 45%. Although RVEF showed the highest accuracy in differentiating between athlete's heart and ARVC, only 37.5% of athletes with ARVC showed RVEF < 45%. The only parameters falling in the pathological range (based on our established cut-off values: > - 25.6 and > - 1.4, respectively) in all athletes with ARVC were the strain and strain rate of the midventricular RV free wall. Establishing RVEF and RV strain analysis provides an important tool to distinguish ARVC from athlete's heart. CMR based regional strain and strain rate values may help to identify ARVC even in highly trained athletes with preserved RVEF.

Diagnostic Differentiation Between Arrhythmogenic Cardiomyopathy and Athlete's Heart by Using Imaging.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cause of sudden cardiac death (SCD) in youth and athletes. In the last decade, several studies focused on right ventricular (RV) remodeling in athletes and revealed that features of the physiological adaptation of the right heart to training, such as RV dilation, may overlap with those of ARVC. Therefore, a careful multiparametric evaluation is required for differential diagnosis in order to avoid false diagnosis of ARVC or, in contrast, fail to identify the risk of causing SCD. This review summarizes physiological adaptation of the RV to exercise and describes features that could help distinguishing between athlete's heart and ARVC.

Right Heart-Pulmonary Circulation Unit in Cardiomyopathies and Storage Diseases.

Cardiomyopathies (CM) are a heterogeneous group of muscle heart diseases, divided into 3 main categories (dilated, hypertrophic, and restrictive). In addition to these subgroups, athlete's heart and hypertensive cardiopathy are both the result of heart adaptation to increased loading conditions, making it possible to include them in the CM group. Right heart involvement is clear in some CM as arrhythmogenic CM, carcinoid syndrome, and endomyocardial fibrosis, whereas in others, like hypertrophic or dilated CM, it is known that the right heart has a prognostic impact but less clear is its pathogenic role.