Athletes heart a short review

Dr V S R Bhupal
ATHLETES HEART-A SHORT REVIEW

“In highly conditioned athletes, a big
heart-the literal, not the
metaphorical kind- is a sign of
health and power. But in some
cases, it can be a deadly burden.” ATHLETES HEART-A SHORT REVIEW

OVERVIEW
 DEFINITION
 HISTORY
 PHYSIOLOGY
 CHAMBER MORPHOLOGY
 12 LEAD ECGS
 ARRHYTHMIAS
 ATHLETE’S HEART AND CARDIOVASCULAR
DISEASE
 LONG TERM CONSEQUENCES

Definition
Athlete´s heart means characteristic enlargement
/hypertrophy/ of the myocardium in response to repeated
exercise stimuli
Principal features of athlete´s heart
 Cardiac enlargement to allow for increased maximal stroke
volume (SV)
 and cardiac output (Q) adaptations that drive the increase in
oxygen delivery in the trained state since no training effect is
evident in maximal heart rate (HR max)

HISTORY
 The concept that the cardiovascular system of trained
athletes differs structurally and functionally from others in
the normal general population remarkably extends over a
century.
 Henschen is credited with the first description in 1899,
using only a basic physical examination with careful
percussion to recognize enlargement of the heart caused by
athletic activity in cross-country skiers.
 Henschen concluded that both dilatation and
hypertrophy were present, involving both the left and right
sides of the heart, and that these changes were normal and
favorable: “Skiing causes an enlargement of the heart which
can perform more work than a normal heart.

 Similar observations were made during the same year by
Eugene Darling of Harvard University in university
rowers.
 In the early 1900s, Paul Dudley White studied radial
pulse rate and pattern among Boston Marathon
competitors, and was the first to report marked resting
sinus bradycardia in long distance runners.
 Early chest radiography work confirmed the physical
examination findings of Darling and Henschen by showing
global cardiac enlargement in trained athletes.

 The subsequent development of ECG enabled
widespread study of electric activity in the heart of the
trained athlete.
 Advanced echocardiographic techniques and magnetic
resonance imaging have begun to clarify important
functional adaptations that of athlete’s heart.

PHYSIOLOGY
 Cardiovascular adaptations differ with respect to the
type of conditioning:endurance training
(dynamic,isotonic, or aerobic) such as long-distance
running and swimming; and strength
training(static,isometric, power, or anaerobic) such as
wrestling, weightlifting,or throwing heavy objects.
 Sports such as cycling and rowing are examples of
combined endurance and strength exercise.

Acute response to endurance
exercise
Increase in
 maximum oxygen consumption
 cardiac output
 stroke volume
 systolic blood pressure
Decrease in
 Peripheral vascular resistance.

Acute response to strength
conditioning
Mild increase in
 oxygen consumption
 cardiac output
Substantial increase in
 Blood pressure
 peripheral vascular resistance
 heart rate.

 Long-term cardiovascular adaptation to dynamic
training produces increased maximal oxygen uptake
due to increased cardiac output and arteriovenous
oxygen difference.
 Strength exercise results in little or no increase in
oxygen uptake.
 Endurance exercise predominantly produces volume
load on the left ventricle (LV), and strength exercise
causes largely a pressure load.

The maximum oxygen consumption represents the
largest amount of oxygen a person can use while
performing dynamic exercise involving a large part of
total muscle mass. It is determined by the equation

Morganroth hypothesis, 1977
M-mode echocardiography-two different
morphological forms of athlete´s heart:
eccentric LV hypertrophy - increase in LV cavity
dimensions,proportional increase in left ventricle
wall thickeness /LVWT/ to normalise myocardial
strain, typically in pure aerobic,endurance sports
concentric LV hypertrophy - increase in LVWT
to normalise increased wall tension with rise in
pressure, typically in resistance or strength training
athletes

CHAMBER MORPHOLOGY

 Training induces cardiac remodeling in 50% of trained
athletes.
 Increased
LV,RV and LA size and volume .
 Normal
Systolic and diastolic function

 Marked enlargement of the LV chamber (60 mm)
occurs in 15% of highly trained athletes.
 This chamber enlargement may occasionally be
accompanied by a relatively mild increase in absolute
LV wall thickness that exceeds upper normal limits
(range 13 to 15 mm).

 LV remodeling may develop rapidly, or more
gradually, after the initiation of vigorous conditioning.
 Changes are reversible with cessation of training -
most impressive in endurance athletes.
 Athletes show relatively small increase 10% to 20% in
wall thickness or cavity size,and these values remain
within accepted normal limits.

Longitudinal studies of exercise training and
cardiac morphology in athletes
 LVIDd can be further augmented with training mainly with
endurance training in elite athletes despite preexisting
increase in cardiac internal dimensions

Longitudinal studies in sedentary individuals
 Exercise programs in sedentary or untrained individuals
result in significant enlargement of LV cavity, increases in
LVWT

Conclusions
1. Athletes exhibit significant cardiac adaptations
with absolute LVM increase in both endurance
and strength – trained athletes compared with
controls
2. LVM and LVMi are larger in endurance-trained
athletes compared with strengths-trained
athletes
3. Volume of training influences the degree of increase
in LVM in endurance athletes

IMPACT OF VARIOUS VARIABLES
ON LV DIMENSIONS

 Left atrial remodeling is present in highly trained
athletes, most commonly those in combined static and
dynamic sports (cycling and rowing), and is associated
with LV cavity enlargement and volume overload.
 Increased transverse left atrial dimensions (40 mm)
are present in 20% of athletes and more substantially
enlarged dimensions (45 mm) are evident in 2%.

 Left atrial enlargement is benign and largely confined
to training in endurance sports, is rarely associated
with atrial fibrillation(1% of cases).

12 LEAD ECGS
 A spectrum of abnormal ECG patterns is present in
40% of trained athletes, occurring 2-fold more
commonly in men than women, and particularly in
those participating in endurance sports.

The Athlete’s Heart & ECG
Common abnormalities seen in an athlete
• 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

38 year old male distance runner with sinus bradycardia (42 bpm) with periods
of junctional rhythm (red arrows)

41 year old male distance runner with J-point and ST-segment elevation (arrows)
depicting early repolarization

LVH in an athlete
Patholigical LVH
Note “strain” pattern in lateral precordial leads

Early repolarization pattern of
Brugada Syndrome (elevated ST-segment
goes into a negative T-wave
in V1 and V2)
Early repolarization pattern of
an athlete (note voltage criteria
for LVH is borderline)
Brugada Syndrome predisposes one
to Ventricular Tachycardia /
Ventricular FibrillatioAnTH.LETES HEART-A SHORT REVIEW

Causes of Sudden Death 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

 Distinctly abnormal and bizarre ECGs, intuitively
suggestive of cardiac disease, are encountered in an
important minority of elite athletes (15%).
 Majority of such ECGs represent extreme
manifestations of physiological athlete’s heart.

ARRHYTHMIAS

 Ambulatory (Holter) ECG monitoring in trained
athletes documented substantial ectopy with frequent
premature beats and complex ventricular
tachyarrhythmias (including couplets and bursts of
nonsustained ventricular tachycardia) in many
individuals.
 These findings suggest that a variety of arrhythmias
are part of the athlete’s heart spectrum .

 Such rhythm disturbances have not been associated
with adverse clinical events and are usually abolished
or substantially reduced after relatively brief periods of
deconditioning .
 Even in athletes with heart disease, resolution of
ventricular tachyarrhythmias with deconditioning is
common and may represent a potential mechanism by
which sudden death risk is reduced by withdrawal of
these individuals from training and competition

 A few observational studies have reported mild-to
moderate post race elevations in biochemical cardiac-specific
markers (plasma cardiac troponin T and I)
suggestive of transient myocardial injury in some
participants after prolonged and strenuous endurance
athletic events, such as triathlons and marathons.
 At present, there is no evidence that these subclinical
findings are associated with permanent clinical
consequences.
 Some studies have also identified transient and reversible
systolic and diastolic dysfunction after extreme athletic
events.

Athlete’s Heart and Cardiovascular
Disease
 Distinguishing physiologically based athlete’s heart
from a variety of structural heart diseases is important
because-
 This may represent the basis for disqualification from
competitive sports to reduce the risk of sudden death.
 High risk athletes may become candidates for an
implantable defibrillator and prophylactic prevention
of sudden death.

 2% of elite adult male athletes have been reported to
show modestly increased LV wall thickness of 13 to 15
mm, which defines a “gray zone” of overlap between
the extreme expressions of athlete’s heart and a mild
HCM Phenotype.
 This ambiguity can be resolved by the application of a
number of noninvasive parameters, such as -
1)reduced cardiac mass with short deconditioning
periods (best assessed with serial magnetic resonance
imaging)
2)absolute LV diastolic dimension 55 mm

 HCM diagnosis would be favored by-
-Abnormal Doppler-derived LV diastolic filling or
relaxation indices
-By the existence of a family member with HCM.

 Magnetic resonance imaging has value in resolving the
HCM-versus–athlete’s heart differential diagnosis in
selected athletes by virtue of its superiority over
echocardiography in identifying segmental LV
hypertrophy in the antero lateral free wall or apex.

Critical evaluation of cardiac
morphology measurement
Echocardiographic imaging
 Large methodological error range in measuring LVID, LVWT
Magnetic resonance imaging (MRI)
 Highly accurate and reproducible technique for determining
LVM and cardiac dimensions
 Drawback- expensive,limited availibility
MRI x Echocardiography (DeCastro, 2006)
 18 male, elite-level rowers,12 untrained sedentary subjects
 Echocardiography – underestimation LVIDd and LVM relative
to MRI

 Rapid commercial laboratory testing is now available
for both HCM and cardiac ion channel mutations with
the potential for achieving a DNA-based diagnosis.
 If a proband is positive for one of the known disease-causing
mutant genes in the panel, the result is
definitive.

 Marked LV cavity enlargement in an athlete, even in
the absence of cardiac symptoms, may intuitively raise
the differential diagnosis between physiological
hypertrophy and pathological cardiomyopathies,
particularly when ejection fraction is judged to be at
the lower range of normal or mildly depressed.
 This difficult clinical situation can often be resolved
by surveillance with serial testing of ejection fraction
at rest and with exercise, after disqualification from
sports.

 Complex and frequent ventricular tachyarrhythmias
evident on ambulatory Holter ECG in trained athletes
without cardiovascular abnormalities can raise the
possibility of disease states such as myocarditis, for
which a high index of clinical suspicion is required.
 Periods of forced deconditioning may not be useful in
resolving such differential diagnoses, because
detraining is associated with reduction of ventricular
tachyarrhythmias in athletes both without and with
underlying pathological substrates.

Long-Term Consequences of
Athlete’s Heart
 Extreme LV remodeling evident in some highly trained
athletes has intuitively raised a concern of whether
such exercise-related morphological adaptations are
always innocent.
 15% of highly trained athletes show striking LV cavity
enlargement, with end-diastolic dimensions 60 mm,
similar in magnitude to that evident in pathological
forms of dilated cardiomyopathy.

 One longitudinal echocardiographic study reported
incomplete reversal of extreme LV cavity dilatation .
 With deconditioning substantial chamber
enlargement persisted in 20% of retired and
deconditioned former elite athletes after 5 years.

 There is no evidence at present showing that athlete’s
heart remodeling leads to long-term disease
progression,cardiovascular disability, or sudden
cardiac death.
 The possibility that persistence of extreme remodeling
after prolonged and intensive conditioning will
ultimately convey deleterious cardiovascular
consequences to some athletes is perhaps unlikely but
at this time cannot be excluded with certainty.

THANK YOU

Athletes heart a short review

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