Athlete’s Heart

DR. ARZALAN BAIG

Objectives

 Introduction to Athlete’s Heart.

 Structural cardiac adaptations.
 Electrophysiologic cardiac adaptations.
 Emerging Issues in the cardiac care of athletes.
 ESC Recommendations for Eligibility and Disqualification of athletes.
Definition

 The terms “athlete’s heart,” “athlete’s heart syndrome,” or “exercise-induced cardiac

remodeling” refer to the structural, functional, and electrical adaptations that occur with
prolonged and intense exercise training.
Morganorth’s Hypothesis

 Morganroth initially put forward the concept of sport-specific cardiac remodeling in the
1970s.
 Divergent cardiac adaptation for dynamic and static sports became known as the
Morganroth hypothesis.
Morganorth’s Hypothesis

 Dynamic Training:
 During dynamic exercise, in order to meet demand, the cardiovascular system responds through
two principal mechanisms: increased cardiac output (CO) and reduced peripheral vascular
resistance (PVR).
 The increase in preload and CO during endurance exercise creates a volume overload (isotonic)
stress on the heart.
 End-diastolic volume increases in trained athletes, which augments CO during exercise.
 Therefore, characteristic findings in the highly trained endurance athlete include resting
bradycardia and a balanced increase in left ventricular (LV) dimensions and wall thickness
(eccentric hypertrophy).
Eccentric LVH
Morganorth’s Hypothesis

 Static Training:
 According to the Morganroth hypothesis, strength training will result in an increase in LV wall
thickness that is not matched by an increase in LV chamber dimension (concentric hypertrophy).
 The increase in PVR is accompanied by only a limited increase in CO and, therefore, strength
exercise mainly creates a pressure overload (isometric) stress on the heart.
Concentric LVH
Classification of Sports
Structural Cardiac Adaptations

 Left Ventricle:
 Volume overload stress, produces dilation of the left ventricle, accompanied by a balanced
increase in wall thickness (eccentric hypertrophy).
 In a large series of young healthy athletes (n = 1,309), representing 38 different sporting
disciplines, LVEDD ranged from 38 to 66 mm (mean 48 mm) in women and 43 to 70 mm (mean
55 mm) in men. More than 40% of male athletes had LVEDD exceeding 54 mm, and 14% had
very pronounced dilation exceeding 60 mm.
 A recent meta-analysis reported a mean LVEDD of 55 mm (95% CI: 54 to 56) and 52.4 mm
(95% CI: 51.2 to 53.6) in endurance- and resistance-trained athletes, respectively.
Structural Cardiac Adaptations

 Diagnostic challenge in differentiating athlete’s heart from pathologic changes (i.e., dilated
cardiomyopathy) becomes evident, by an occasionally observed low-normal or mildly reduced
LV ejection fraction (EF) in highly trained endurance athletes.
 When faced with a diagnostic dilemma in an apparently healthy athlete with LV dilation and
reduced EF, it can be useful to perform an exercise test to demonstrate normal myocardial
recruitment and supranormal exercise capacity.
 In addition, the healthy endurance athlete with LV dilation will invariably have four-chamber
dilation, normal diastolic function, and eccentric hypertrophy. Abnormal diastolic function or
findings isolated to the left ventricle, on the other hand, suggest pathology.
Structural Cardiac Adaptations

 The normal distribution of LV septal wall thickness has been investigated in several large series
of athletes.
 Because of phenotypic overlap with mild hypertrophic cardiomyopathy (HCM), athletes with a
septal wall thickness of 13 to 15 mm are often considered to be in a diagnostic “gray zone.”
 In such cases, other echocardiographic parameters are often useful to differentiate physiologic
LVH from HCM.
Structural Cardiac Adaptations

 In athletes, septal wall thickness is typically accompanied by an increase in LV size (>55 mm).
Importantly, LV chamber size appears to remain <50 mm even in HCM patients that participate in
competitive sports against medical advice.
 An LV size >55 mm in HCM patients, on the other hand, is usually due to progressive myocardial
fibrosis and thinning, accompanied by systolic dysfunction and heart failure symptoms. Such
advanced HCM is typically not compatible with participation in competitive sports.
 Furthermore, physiologic LVH is usually accompanied by normal parameters of diastolic
function and is not asymmetric.
 Myocardial deformation assessment using speckle tracking echocardiography is an emerging tool
that may be a useful adjunct in differentiating HCM from athlete’s heart. Typically, strain is
normal in the athlete, while there is a reduction in strain at the site of greatest hypertrophy and
fibrosis in HCM.
Structural Cardiac Adaptations

 When the suspicion for HCM remains high, despite initial reassuring ECHO findings, contrast-
enhanced echocardiograph or MRI can be used. Cardiac MRI is also useful to identify
asymmetric areas of hypertrophy and to identify scar using delayed gadolinium enhancement.
 Furthermore, MRI, in conjunction with echo, can be used to identify abnormalities of the mitral
valve apparatus, which is seen in up to 75% of patients with HCM.
 If the diagnosis remains uncertain despite extensive imaging workup, detraining (i.e., exercise
reduction or abstinence) may be used as a diagnostic tool.
Structural Cardiac Adaptations

 Right Ventricle:
 Pressure overload–induced cardiac remodeling, seen in strength training, is usually limited to the
left ventricle by virtue of mitral valve shielding.
 Endurance exercise–induced cardiac remodeling, on the other hand, affects all cardiac chambers
including the right ventricle.
 In a recent study of 102 endurance athletes, RV chamber dilation exceeded the upper limit of
normal in >50%. Importantly, the RV enlargement was accompanied by LV dilation in almost all
cases.
 Isolated RV dilation, on the other hand, is rare in athletes and should raise the suspicion for a
pathologic process (e.g., arrhythmogenic right ventricular cardiomyopathy [ARVC]).
Structural Cardiac Adaptations

 Left Atrium:
 Left atrial (LA) enlargement (>40 mm anterior–posterior dimension by echocardiography) is
common in athletes as a result of increased preload.
 An upper limit of 45 mm in women and 50 mm in men has been suggested to differentiate
athlete’s heart from pathologic conditions
 The left atrium responds to exercise-induced increases in preload by augmenting reservoir and
conduit functions although LA active emptying is lower in athletes. Similarly, speckle tracking
echocardiography exhibits normal reservoir function and reduced active contribution of the
atrium to ventricular filling at rest.
 Reduced reservoir function and unbalanced enlargement of the atria are features more consistent
with pathology.
Structural Cardiac Adaptations

 Aorta:
 Volume and pressure overloads during endurance and strength exercise, respectively, place a
significant hemodynamic stress on the aorta.
 A recent meta-analysis showed that the aortic root diameter measured at the sinus of Valsalva
and the aortic valve annulus was 3.2 and 1.6 mm greater in athletes (n = 5,580) compared to
matched nonathletic controls (n = 727).
 Marked aortic root dilation (>4 cm) is unusual in athletes and should raise the suspicion for an
underlying pathologic process.
Electrophysiologic cardiac adaptations

 Exercise-induced cardiac remodeling not only affects cardiac structure and mechanical
function but can also induce profound cardiac electrophysiologic changes.

 Normal and abnormal ECG findings in athletes according to the international criteria are
shown in Figure. An additional category of “borderline” changes is now used; features
seen in isolation are considered benign but if there is more than one borderline feature,
further evaluation is recommended.
Common ECG Findings

 Sinus bradycardia (up to 91%) – may be less than 50 beats / minute, reflects
predominance of vagal tone , may exhibit junctional escape rhythm.
 Sinus arrhythmia.
 1st and 2nd (type I) degree AV block (10% - 33%).
 Left ventricular hypertrophy (up to 76%).
 Incomplete RBBB (up to 51%) – QRS width between .10 and .12 seconds.
 Early repolarization – mild J-point and ST segment elevation, differential diagnosis –
Brugada Syndrome, elevated J-point swoops into a negative T-wave.
 Premature atrial & ventricular contractions.
Ventricular Arrhythmias and Athletes

 In one study, 355 competitive athletes with frequent PVCs on screening ECG and/or a history
of palpitations were further evaluated using 24-hour Holter monitoring.
 Athletes were subsequently divided into three groups based on the total number of PVCs
and/or presence of non-sustained ventricular tachycardia (NSVT).
 Group A (n = 71; >2,000 PVCs /24 hour and/or ≥1 episode of NSVT/24 hour), group B (n =
153, ≥100 to <2,000 PVCs and no NSVT), and group C (<100 PVCs and no NSVT).
 In 7% (n = 26) of athletes, a cardiac abnormality was identified (mitral valve prolapse with
mild mitral regurgitation in 11, ARVC in 7, myocarditis in 4, and dilated cardiomyopathy in
4). The prevalence of cardiac abnormalities was 30%, 3%, and 0% in groups A through C,
respectively, suggesting that the presence of >2,000 PVCs/24 hour and/or NSVT in an athlete
should trigger further evaluation
Causes of SCD in Athletes

 Long QT syndrome QT interval longer than .44 seconds

• Predisposition to Torsades de Pointes, a type of V-tach
• Hank Gathers died in 1990 while playing basketball (went off meds).
 Hypertrophic Cardiomyopathy of the Left Ventricle
• Symptoms: chest pain, dyspnea, syncope
• Predisposition to V-Tach
 Arrhythmogenic Cardiomyopathy of the Right Ventricle
• Familial condition where RV myocardium is replace by fibro-fatty tissue
• Predisposition to V-tach
 Congenital Coronary Artery Anomalies
• Pete Maravich – had no left coronary artery – died of MI at 40 years of age
Voltage criteria for LVH

 Voltage criteria for LVH are common in athletes and present in up to 70% of male
athletes.
 Increased QRS voltage criteria, when present in isolation, do not warrant further
investigation.
 However, in the presence of pathologic Q-waves, ST-depression, T-wave inversion (TWI),
or symptoms, LVH on ECG warrants further investigation.
 Voltage criteria for RVH are present in up to 12% of athletes.
 Similarly, voltage criteria for RA and LA enlargement are also common in athletes.
LVH

LVH in an athlete Pathological LVH “strain” pattern

Repolarization Changes

 ERP is present in up to 90% of athletes and is considered a normal variant in

asymptomatic athletes. ERP may develop before, and independent of, LVH.
 TWI is present in approximately 5% of white athletes and in up to 25% of black athletes.
 The international criteria only consider TWI to be abnormal if T-waves are >1 mm in
depth in more than two leads, excluding V1, III, and aVR (except in black athletes where
V2 to V4 are also excluded). TWI should be considered abnormal if extending beyond V2
in white athletes, beyond V4 in black athletes, or if it is accompanied by Q-waves or ST-
depression
Prolonged QT and Athletes

 Athletes have slightly longer QT-intervals compared to nonathletes, which has been
primarily attributed to LVH. It has been reported that 6% of athletes have a corrected QTc
exceeding the upper limit of normal (470 in men and 480 in women).
 QT-intervals are notoriously difficult to measure in athletes because of the common
presence of sinus arrhythmia and U-waves.
 Prolonged QTc in isolation (i.e., in the absence of other long QT syndrome criteria) only
has a positive predictive value of 7%. Further evaluation is therefore essential, and the
diagnosis should not be made solely based on the ECG
Risk of Excessive Exercise

 Individuals with unrecognized cardiac disease there is an increased risk of an adverse

cardiac event during strenuous exercise.
 Proposed mechanisms are that repeated high-intensity exercise, without sufficient
recovery time, results in inflammation, myocardial injury, and accelerated atherosclerosis,
ultimately leading to fibrosis and adverse cardiac remodeling.
 Several studies have shown that sinoatrial node disease, advanced heart block, and atrial
fibrillation are more common in veteran athletes compared to sedentary peers.
Emerging Issues in the Cardiac Care of
Athletes

 Atrial Fibrillation:
 In contrast to this reduction in AF with moderate physical activity, the incidence of AF in the
Cardiovascular Health Study in those exercising at the highest level was not different from that
in inactive subjects.
 Other studies have demonstrated higher rates of AF among participants in endurance events who
ran the most races or had the most years of exercise training.
 Possible mechanisms for this relationship include increased atrial size, changes in autonomic
tone, or increased inflammation,
Emerging Issues in the Cardiac Care of
Athletes

 Accelerated Atherosclerosis:
 Several reports suggest that long-term endurance athletes have increased coronary artery
calcification (CAC) scores compared to their sedentary counterparts.
 Our approach should be to evaluate the athlete for exercise-induced ischemia, treat ASCVD risk
factors aggressively, especially with lipid-lowering agents, and provide reassurance.
Emerging Issues in the Cardiac Care of
Athletes

 Myocardial Fibrosis:
 At least three studies have detected the presence of late gadolinium enhancement (LGE) with
cardiac MRI in 12% to 50% of veteran endurance athletes.
 The presence of LGE suggests that prolonged exercise training produces myocardial fibrosis, but
this possibility requires more extensive study for confirmation and determination of its
significance.
Emerging Issues in the Cardiac Care of
Athletes

 Non Compaction Cardiomyopathy:

 Noncompaction cardiomyopathy (NCCM) results from an arrest of process of trabecular
regression and is characterized by a hypertrabeculated left ventricle with a thin, subepicardial,
compacted layer.
 NCCM can produce myocardial dysfunction, systemic emboli from the deep ventricular pits, and
SCD.
 NCCM presenting in adults is inherited in an autosomal dominant pattern, but an X-linked
pattern is seen in pediatric patients.
 Obtaining a careful family history and reviewing the myocardial images, with special attention
to LV systolic function and thickness of the compacted layer is paramount.
Emerging Issues in the Cardiac Care of
Athletes

 Exercise Induced ARVC:

 An evolving concept in sports cardiology is exercise-induced adverse remodeling of the right
ventricle, that is, “exercise-induced ARVC.”
 During endurance exercise, the right ventricle is subjected to the same preload as the left
ventricle. However, because the pulmonary vascular resistance (in contrast to the systemic
vascular resistance) decreases only minimally with exertion, pulmonary artery pressures may
exceed 80 mm Hg during vigorous exercise in some athletes, exerting a disproportionately large
afterload stress on the thin-walled right ventricle.
 It is supported by studies showing a correlation between post-exertional right (but not left)
ventricular dysfunction and cardiac biomarker (e.g., Troponin and B-type natriuretic peptide)
release.
Eligibility and Disqualification for athletes
with cardiac diseases

 Eligibility and disqualification recommendations for athletes with cardiac abnormalities

have been published by the ACC/AHA and ESC.
 With newer data, recommendations have been modified.
 A brief overview of ESC recommendation is as follows:
Conclusion

 Cardiovascular clinicians require a working knowledge of exercise physiology, the CV

adaptations to exercise training, and the risks and benefits of exercise to advise and
evaluate active patients appropriately.
 Clinicians should avoid overreacting to borderline findings detected on CV screening of
asymptomatic athletes, but should also avoid ignoring possible cardiac symptoms in
active individuals.
 Sports cardiology has emerged as a subspecialty of cardiology, but general cardiologists
can deal with many of the management issues and queries adequately if they understand
the CV adaptations to exercise and the most common pathologic conditions that affect
athletic patients.