Athlete’s Heart: A Multimodal Approach – From Physiological to Pathological Cardiac Adaptations

By Antonello D’Andrea and Eduardo Bossone

Athlete's Heart: A Multimodal Approach – From Physiological to Pathological Cardiac Adaptations provides a complete overview of all adaptations of the heart to sport practice by highlighting the different diagnosis between athlete’s heart and pathological remodeling. Written by international experts in the field, chapters discuss ECG findings, echocardiogram data, cardiac magnetic resonance and new forms of multimodality imaging, providing readers with evidence-based guidance on how to differentiate athlete's heart from cardiomyopathies.

Athlete's heart is the term given to a constellation of cardiac structural, functional and electrical remodeling that accompanies regular athletic training. Due to the substantial phenotypic overlap between electrical and structural changes observed in the physiological athletic heart remodeling and pathological changes resulted from inherited or acquired cardiomyopathies, distinguishing between adaptive and maladaptive cardiovascular response to exercise is a challenging task.

• Presents a comprehensive overview of exercise-induced cardiac adaptations
• Provides practical aspects for a differential diagnosis between a physiological and a pathological cardiac remodeling
• Includes new imaging technics, with a special focus on multi-modality imaging, such as exercise echocardiography, and new echocardiographic modalities (3D Strain)

• Language: English
• Publisher: Academic Press
• Release date: May 3, 2023
• ISBN: 9780323952224

Antonello D’Andrea

Dr. Antonello D’Andrea is Director of the Complex Unit of Cardiology and Intensive Care at the Umberto I Hospital Nocera Inf and Head of the ICU of the Cardiology Department of the Second University of Naples, Italy. His research interests include non-invasive diagnostic cardiology in the acute and chronic patients, left ventricular hypertrophy and athlete's heart. He is the author of numerous manuscripts, chapters and reviews addressing changes induced by different sport activities in the heart’s structure and cardiac response.

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Chapter 1: What is athlete’s heart?

Antonello D’Andreaa,b; Andreina Carboneb; Eduardo Bossonec    a Unit of Cardiology and Intensive Coronary Care, Umberto I Hospital, Nocera Inferiore, Italy

b Division of Cardiology, Department of Translational Medical Sciences, University of Campania Luigi Vanvitelli, Monaldi Hospital, Naples, Italy

c Public Health Department, University of Naples Federico II, Naples, Italy

Abstract

Strenuous exercise training can determine cardiac remodeling, often referred to as the athlete’s heart, characterized by increased left ventricular mass, cavity dimensions, and wall thickness with normal systolic and diastolic function. The physiological mechanisms of athlete’s heart are various and are not fully known. Sometimes, there may be some overlap between physiological and pathological conditions, some of which might be related to sudden cardiac death (SCD) (hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, dilated cardiomyopathy, etc.). The differentiation between physiological and pathological cardiac anomalies in athletes is mandatory because an incorrect diagnosis has important consequences, such as exclusion from competitive sport, false reassurance, and missed opportunity for effective therapeutic intervention. For this reason, preparticipation cardiovascular screening aimed at the identification of pathological conditions in athletes, to prevent morbidity and SCD. However, the best strategies remain controversial. The inclusion of the 12‑lead electrocardiogram (ECG) in the initial screening is a source of debate. Familiar and personal medical history and physical examination are the first steps of preparticipation screening. Italian and European guidelines recommend performing an ECG, as the initial screening of athletes, whereas the United States and American Heart Association positions are against national mandatory screening with ECGs in athletes. The purpose of this chapter is to define athlete’s heart, summarize the most important causes of sudden cardiac death in athletes, and establish the diagnostic pathways to achieve eligibility in competitive sports.

Keywords

Athlete’s heart; Sudden cardiac death; Sport eligibility

1: Introduction

Vigorous exercise training determines profound effects on cardiac structure and function, often referred to as the athlete’s heart, characterized by increased left ventricular mass (LVM), cavity dimensions, and wall thickness with normal systolic and diastolic function [1]. The actual evidence suggests that there may be some overlap between physiological and pathological conditions, some of which are related to sudden cardiac death (SCD). During dynamic exercise, the rise in pressure and volume determines an increase in the wall stress of both ventricles and in the atria [2–4]. Furthermore, ventricular afterload increases with exercise intensity in a near-linear manner, increasing progressively with exercise load [3–5]. The duration of physical efforts represents the second major determinant of the entity of cardiac remodeling [4]. For this reason, endurance athletes have greater cardiac remodeling than athletes from team or sprint sports [4,6]. The differences in cardiac remodeling may be attributed to both hemodynamic conditions created from a variety of static and dynamic exercise components and the time of exposure to exercise load [4]. A diagnostic gray zone between physiological remodeling and cardiac alterations exists at the extremes of athletic cardiac remodeling, and questions arise as to whether the observed increase in cardiac dimensions is proportional to the amount of exercise conditioning [1]. The differentiation between physiological and pathological changes in athletes is mandatory because an incorrect diagnosis has important consequences, such as exclusion from competitive sports, false reassurance, and missed opportunities for effective therapeutic intervention.

2: Athlete’s heart: Should we need a more specific definition?

Athlete’s heart is defined as a benign increase in cardiac mass, with specific circulatory and cardiac morphological alterations, that represents a physiological adaptation to systematic training [7]. A more consistent definition of athlete is essential for understanding the heterogeneity regarding the degree of cardiac changes as a result of exercise training and to better differentiate physiological and pathological remodeling [4]. If the cardiac remodeling is consistent with the level of training, further examinations may not be required. However, it can be extremely difficult to estimate the degree of expected remodeling given the broad ranges published in the literature [4]. The Michell criteria have been used to explain cardiac remodeling in athletes categorizing sports according to the relative amount of static and dynamic exercise [4,6]. Beaudry et al. proposed a simple model of the athlete’s heart, defined by two variables of exercise intensity and duration [4]. Briefly, the entity of myocardial adaptation is proportional to the hemodynamic stress (amount of intensity) and the time in which this stress is applied (duration and frequency of training). However, this is a simplified model of a more complex system in which also genetic factors and environmental issues play an important role. For example, cardiac remodeling is probably less marked in women than in men [8], and electrical and structural adaptations appear to be more evident in black compared with white athletes [9–11]. Furthermore, other genetic features, such as the age and cumulative years of exercise exposure, may have a role in the entity of cardiac remodeling [4].

3: SCD in athletes: The entity of the problem

SCD associated with sports is a rare but catastrophic event. Strenuous exercise training may be a trigger of ventricular tachyarrhythmias, usually ventricular fibrillation (VF) or ventricular tachycardia degenerating in VF, in predisposed individuals [12]. SCD associated with sport is defined as sudden and unexpected death occurring during, or shortly after exercise training in an apparently healthy individual [13]. The real incidence of SCD in athletes is uncertain [13]. As a general estimate, 1 to 2 of 100,000 athletes between the age of 12 and 35 years experienced SCD each year [12,14–17]. The most reliable data are those resulting from Italian studies [12,18,19], retrospective US cohort studies [17], a prospective observational study in high school [20], and studies in active US military recruits [21]. Italian data show a three times higher incidence of SCDs in athletes than in nonathletes [12]. However, in a Danish study, the incidence of SCD is similar in competitive and recreational sports [22]. The incidence is 2–25 times higher in men than in females and increases with age, being 5–10 times higher in athletes over 35 years old [12,14,16,17,20,23]. Sport-related SCD is more frequent in black athletes (5.5/100,000) and male basketball players (10/100,000) [14,23]. There is a great interest in the early identification of at-risk athletes to minimize the risk of SCD, and the preparticipation evaluation (PPE) is a reasonable strategy to identify subjects at risk, although debated and controversial.

3.1: Cardiac conditions associated with SCD

SCD in young athletes is usually caused by genetic or congenital structural cardiac disorders [12,22,24–27]. In young athletes (<35 years/old), inherited cardiac conditions predominate, with hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricle cardiomyopathy (ARVC), and anomalous origin of a coronary artery being the most common causes of sport-related SCD in young [28]. In athletes >35 years of age, more than 80% of all SCD is due to atherosclerotic coronary artery disease, and vigorous physical activity is associated with an increased risk of the acute coronary syndrome and SCD [24]. The most common causes of SCD are summarized in Table 1. These conditions are variable depending on the age and geographical factors of the studied population [13].

Table 1

HCM, hypertrophic cardiomyopathy; DCM, dilated cardiomyopathy; LVNC, left ventricle noncompaction; ARVC, arrhythmogenic right ventricle cardiomyopathy; WPW, Wolff-Parkinson-White.

4: Preparticipation cardiovascular screening in athletes

Preparticipation cardiovascular screening aimed at the identification of anomalies associated with SCD and is supported by major international medical societies [13,24,29–31]. However, the best strategies remain controversial. The inclusion of the 12‑lead ECG in the initial screening is a source of debate. In particular, the American Heart Association (AHA) recommends taking accurate medical and familial history and physical examination, whereas the European Society of Cardiology (ESC) recommends routine execution of a 12‑lead ECG [7]. Further evaluations (exercise ECG, cardiovascular imaging tests, etc.) are recommended in symptomatic and/or high cardiovascular risk patients [24]. In Italy since 1982, athletes had to undergo a clinical evaluation to obtain eligibility for competitive sports. The recommendations of Comitato Organizzativo Cardiologico per l’Idoneità allo Sport (COCIS) organization represent the pillar of the screening program in Italian athletes [32].

4.1: Clinical and familial history

A comprehensive clinical history is critical to identify athletes with underlying medical conditions that may interfere with participation in sports. Particular attention should be given to the personal and family cardiac histories [7,13]. Ideally, a parent should be present at the preparticipation clinical evaluation to provide historical details for athletes younger than 18 years [7]. The first element to be taken into consideration is the entity of the sport (type of sport, intensity, duration of training, and competitions), to correlate it with subsequent clinical, electrocardiographic, and echocardiographic findings [32]. The family history should be evaluated, in particular the presence of heart disease in the first-degree relatives, including sudden unexplained deaths or sudden deaths before age 50 related to heart problems, heart disease in childhood, drowning/predrowning or accidents unexplained, which may indicate the presence of genetic cardiovascular disorders [32]. In the personal medical history, in addition to any previous pathological conditions, the evaluation of the presence of risk factors for coronary artery disease (especially in master athletes who are at higher risk of atherosclerotic coronary heart disease) and the use of cardiotoxic substances such as alcohol and drugs (especially cocaine) are recommended [32]. Warning signs and symptoms (chest pain from exertion, syncope or presyncope, palpitations, excessive dyspnea or fatigue disproportionate to the level of exercise, unexplained seizures) reported by the athlete should lead to further diagnostic investigations [7,32]. The AHA proposed a 14-points screening questionnaire as part of a comprehensive history-taking and physical examination to detect or raise suspicion of genetic/congenital cardiovascular abnormalities [7] (Table 2). Furthermore, the Italian COCIS 2017 proposed a structured checklist for anamnesis [32].

Table 2

a Parental verification is recommended for high school and middle school athletes.

b Judged not to be of neurocardiogenic (vasovagal) origin; of particular concern when occurring during or after physical exertion.

c Refers to heart murmurs judged likely to be organic and unlikely to be innocent; auscultation should be performed with the patient in both the supine and standing positions (or with Valsalva maneuvre), specifically to identify murmurs of dynamic left ventricular outflow tract obstruction.

d Preferably taken in both arms.

Adapted from Maron BJ, Friedman RA, Kligfield P, Levine BD, Viskin S, Chaitman BR, et al. Assessment of the 12-lead electrocardiogram as a screening test for detection of cardiovascular disease in healthy general populations of young people (12-25 years of age): a scientific statement from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol 2014;64(14):1479–514.

4.2: Cardiovascular physical examination

The cardiovascular evaluation should be performed in a quiet room to facilitate auscultation. A brief visual inspection of the precordium to evaluate for asymmetry and abnormal impulses is recommended. Precordial palpation can detect thrills, abnormal apical impulse location, and parasternal heave. The physician then should carefully auscultate to identify the first and second heart sounds, extra heart sounds, and murmurs. A fixed split of a second heart sound can be a sign of an atrial septal defect, and a paradoxical split (i.e., narrowing on inspiration) can be a sign of severe aortic stenosis, hypertrophic cardiomyopathy, or left bundle branch block [33]. Murmurs should be characterized based on timing, location, character, and intensity. Dynamic auscultation (e.g., squat-to-stand and Valsalva maneuvres) can further clarify the murmur type. Squatting increases venous return to the heart, thereby increasing left ventricular blood volume, chamber size, and stroke volume [32]. In contrast, standing and the Valsalva maneuvre decrease venous return, thereby decreasing left ventricular size and stroke volume. Increased stroke volume causes murmurs to become louder with squatting and quieter with standing or the Valsalva maneuvre. However, if a murmur is softer when the patient squats or is louder or longer when he or she returns to a standing position or during the Valsalva maneuvre, hypertrophic cardiomyopathy or mitral valve prolapse should be suspected