Download 03/08 Sudden Death in Athlete

Noninvasive
Cardiovascular Evaluation
of the Competitive Athlete
Gregory Piazza, M.D.
Beth Israel Deaconess Medical Center
March 19, 2008
Beth Israel Deaconess
Medical Center
Harvard
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Death on the Soccer Field
• Antonio Puerta, a midfielder for Sevilla
FC, collapsed during a game on
August 25, 2007.
• He regained consciousness and was
walked to the locker room where he
collapsed again.
• He was resuscitated and brought to
the ICU of a nearby hospital.
• He suffered multiple prolonged cardiac
arrests over the next several hours
resulting in anoxic brain injury and
multisystem organ failure.
• He died 3 days after his initial collapse
at age 22.
• Work-up revealed arrhythmogenic
right ventricular cardiomyopathy
(ARVC).
Beth Israel Deaconess
Medical Center
Antonio Puerta (November
26, 1984 – August 28, 2007)
http://soccernet.espn.go.com/news/story?id=457723&cc=5901
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Overview
• Although rare, sudden cardiac deaths
(SCD) among young competitive athletes
have substantial emotional and social
impact upon the lay public and medical
community.
• Because competitive athletes are often
thought to exemplify health and
invulnerability, their sudden deaths seem
counterintuitive.
Beth Israel Deaconess
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N Engl J Med 2003;349:11
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Overview
• Even with widespread availability of
portable automated defibrillators at
sporting events, the mortality for athletes
after syncope or cardiac arrest remains
high.
• An improved understanding of conditions
that predispose to SCD among trained
athletes has lead to a great interest in preparticipation screening.
Beth Israel Deaconess
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N Engl J Med 2003;349:11
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Objectives
• Describe the physiological adaptations of
the cardiovascular system to athletic
training
• Highlight the epidemiology and causes of
SCD in competitive athletes
• Discuss the role of noninvasive testing in
the evaluation of competitive athletes
• Review the recommendations for preparticipation screening
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The Physiological Adaptations in
the Trained Athlete
• Athletic training for competitive endurance
(aerobic) or isometric (static or power) sports
results in characteristic changes in cardiac
structure and function.
• This physiological form of left ventricular (LV)
hypertrophy is known as the “athlete’s heart” and
must be distinguished from pathological
conditions that may predispose to SCD.
• Depending on the nature of the exercise training
benign increases in LV mass, wall thickness,
and cavity size as well as left atrial volume may
be observed in healthy athletes.
Beth Israel Deaconess
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N Engl J Med 2003;349:11
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The Physiological Adaptations in
the Trained Athlete
Endurance Training
•Increase in LV cavity size
•Minimal increase in LV wall
thickness
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Medical Center
Circulation 2000;101:336
Isometric Training
•Increase in LV wall
thickness out of
proportion to increase
in cavity size
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The Athlete’s Heart
Gray area of overlap between the “athlete’s heart” and
cardiomyopathies.
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N Engl J Med 2003;349:11
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The Athlete’s Heart
• The physiological changes of the athlete’s heart have
been evaluated by cardiac MRI and 3-D echo.
• In a study of 30 patients, members of a men’s
professional rowing team were compared with sedentary
untrained male subjects.
• Each patient underwent evaluation with 3-D echo and
cardiac MRI.
• While 2-D echo significantly underestimated
measurements, 3-D echo demonstrated good agreement
with cardiac MRI.
• Compared with sedentary subjects, athletes had
significantly increased LVEDV, LVESV, and LV mass.
• There were no differences in LVEF or the ratio of LV
mass to LVEDV (LV remodeling index).
Beth Israel Deaconess
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Heart 2006;92:975
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The Athlete’s Heart
• In another study, 23 male and 20 female
endurance athletes were compared with agematched controls using cardiac MRI.
• Male and female athletes demonstrated similar
increases in LV and RV volumes and mass
indices compared with controls.
• No gender-specific differences in the effect of
training on LV and RV volumes, mass indices,
ejection fractions, and LV to RV ratios of volume
and mass indices were noted.
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J Magn Reson Imaging 2006;24:297
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Competitive Sports
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Medical Center
Classification of sports based on peak static
and dynamic components achieved during
competition.
uptodateonline.com
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School
Extrinsic Risk Factors for SCD
• The risk of SCD in competitive sports increases
with “burst” exertion (rapid acceleration and
deceleration; common in basketball, tennis, and
soccer).
• Extreme environmental conditions (temperature,
humidity, and altitude) that affect blood volume
and electrolyte balance also contribute to the
risk.
• Progressive and systematic training to achieve
higher levels of conditioning and performance
may further increase the risk by resulting in a
total cardiovascular demand that often exceeds
that of competition.
Beth Israel Deaconess
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Circulation 2004;109:2807
J Am Coll Cardiol 2005;45:1364
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Other Extrinsic Risk Factors for
SCD
• Cocaine abuse
• Amphetamine abuse
• Performance enhancing drugs
(anabolic steroids)
• Dietary and nutritional supplements
(including ephedra-containing products)
Beth Israel Deaconess
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N Engl J Med 2001;345:351
J Am Coll Cardiol 2002;39:1083
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Epidemiology of Sudden Cardiac
Death
• Although likely underestimated, the incidence of
SCD among competitive athletes appears to be
low, ranging from 1 per 50,000 to 1 per 300,000.
• In a study of Minnesota high school athletes, the
incidence of SCD was 1 in 200,000.
• In a study of nearly 220,000 marathon runners,
SCD occurred in 4 individuals.
– None had any prior cardiac symptoms
– 2 had competed in several previous marathons
– 3 had coronary disease on autopsy
Beth Israel Deaconess
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JAMA 1996;276:1999
J Am Coll Cardiol 1998;32:1881
J Am Coll Cardiol 1996;28:428
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Causes of Sudden Cardiac Death
• Causes of SCD in athletes vary by age
and geographic location.
• Among young competitive athletes (< 35
years old) in the U.S., inherited or
congenital heart conditions (such as
hypertrophic cardiomyopathy) are the
most common etiologies.
• Among “masters” athletes (> 35 years old),
coronary artery disease (CAD) appears to
be the predominant cause of SCD.
Beth Israel Deaconess
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J Am Coll Cardiol 2003;41:974
Am J Cardiol 1980;45:1292
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Causes of Sudden Cardiac Death
in Young Athletes
• In a U.S. registry of 236 young competitive athletes with
SCD and structural heart disease on autopsy, the
following conditions were reported:
–
–
–
–
–
–
–
–
–
–
Hypertrophic cardiomyopathy (HCM)(36%)
Anomalous coronary artery (13%)
Myocarditis (7%)
Ruptured aortic aneurysm (4%)
ARVC (4%)
Myocardial bridging (4%)
Aortic stenosis (3%)
CAD (3%)
Idiopathic dilated cardiomyopathy (3%)
Mitral valve prolapse (MVP)(3%)
Beth Israel Deaconess
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J Am Coll Cardiol 2003;41:974
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Causes of Sudden Cardiac Death
in Young Athletes
Distribution of causes of SCD in 1435 young competitive athletes.
From the Minneapolis Heart Institute Foundation Registry, 1980 to 2005.
Beth Israel Deaconess
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Circulation 2007;115:1643
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Causes of Sudden Cardiac Death
in Young Athletes
• In an analysis of data from over 6 million
U.S. military recruits ≤ 35 years old, 64
exercise-related deaths were due to an
identifiable structural abnormality:
– Anomalous coronary artery (33%)
– Myocarditis (20%)
– CAD (16%)
– HCM (13%)
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Ann Intern Med 2004;141:829
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Causes of Sudden Cardiac Death
in Young Athletes
• In contrast, a series of 49 young athletes
with SCD from Northern Italy
demonstrated the following distribution:
– ARVC (22%)
– CAD (18%)
– Anomalous coronary artery (12%)
– MVP (10%)
– Myocarditis (6%)
– HCM (2%)
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N Engl J Med 1998;339:364
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Hypertrophic Cardiomyopathy
• Incidence is
approximately 1 in 500.
• It is a heterogeneous
genetic disorder resulting
in LV hypertrophy and
fibrosis.
• Sudden death is most
likely due to reentrant
ventricular
tachyarrhythmias.
• Most patients have an
abnormal ECG.
• May be diagnosed by
echo and cardiac MRI.
Beth Israel Deaconess
Medical Center
JAMA 2002;287:1308
Marked septal hypertrophy
with SAM
Late gadolinium
enhancement consistent
with myocardial fibrosis
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Anomalous Coronary Anatomy
• Incidence is likely underestimated.
• In SCD, most common anomaly is
a left main coronary artery
originating from the right sinus of
Valsalva.
• May be suggested by chest pain or
syncope with exercise but often
SCD is the first symptom.
• Mechanism of ischemia is likely
kinking or compression of the
anomalous artery between the
aorta and pulmonary trunk.
• ECG and echo are often normal.
• Best diagnosed by cardiac MRI,
CT, or catheterization.
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J Am Coll Cardiol 2000;35:1493
Two patients with left main
coronary arteries originating
from right sinus of Valsalva
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Myocarditis
• May be preceded by a viral illness.
• Clinical findings may include chest
pain and heart failure symptoms in
an otherwise healthy young person.
• ECG often demonstrates diffuse
repolarization changes.
• SCD is likely due to ventricular
arrhythmias or atrioventricular
conduction disease.
• May be suggested by LV systolic
dysfunction (as detected by echo,
cardiac MRI, or cath) in the absence
of CAD.
• Cardiac MRI may demonstrate
focally increased T2-signal
consistent with myocardial
inflammation and late gadolinium
enhancement suggestive of fibrosis.
Beth Israel Deaconess
Medical Center
Inferolateral and lateral hypokinesis
in a young patient with myocarditis
Late gadolinium enhancement of the
inferolateral and lateral wall in the
same patient
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Aortic Aneurysm and Dissection
• In young athletes, aortic aneurysm and dissection is
most often associated with aortopathy.
• Closely linked with inherited connective tissue
disorders (Marfan’s syndrome).
• Marfan’s is inherited in an autosomal dominant fashion
with an incidence of 1 in 10,000 to 20,000.
• Characteristic morphological findings (arachnodactyly,
hyperflexible joints) may be noted on examination.
• SCD occurs due to aortic aneurysm rupture or
dissection.
• Diagnosed on basis of clinical criteria.
• Echo is recommended to evaluate for aortic disease
(including AR).
• Cardiac MRI and CT also detect aortic pathology.
Beth Israel Deaconess
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J Am Coll Cardiol 2005;45:1340
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Arrhythmogenic Right
Ventricular Cardiomyopathy
• Characterized by fibrofatty infiltration of
the RV free wall (may affect the LV).
• Symptoms include exercise induced
palpitations, presyncope, or syncope.
• SCD is due to catecholamine-sensitive
ventricular arrhythmias.
• ECG findings include increased QRS
duration, epsilon waves in V1-2, and T
wave inversions in the right
precordium.
• Imaging may demonstrate RV
dilatation and aneurysms.
• Echo and cardiac MRI are the most
widely used noninvasive tests for
ARVC.
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J Am Coll Cardiol 2001;38:1773
Epsilon waves
Increased signal on T1weighted imaging in the RV
free wall (left) and decreased
signal on fat suppressed
Harvard
imaging (right)
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School
Myocardial Bridging
• Myocardial bridging occurs when
a portion of an epicardial
coronary artery “tunnels” into the
myocardium.
• Systolic vessel compression and
delayed diastolic relaxation impair
coronary blood flow in the
intramyocardial segment.
• Although usually of little clinical
consequence, myocardial
bridging may infrequently result in
exertional angina, infarction, and
SCD.
• Myocardial bridging may be
diagnosed on cardiac CT, MRI, or
catheterization.
Beth Israel Deaconess
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N Engl J Med 2003;349:1047
Contrast-enhanced EBCT image
revealing an intramyocardial
segment of the LAD
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Aortic Stenosis
• Aortic stenosis (AS) in young athletes is most often due
to congenital abnormalities of the aortic valve.
• Most common abnormality is a bicuspid aortic valve.
• More unusual etiologies include subvalvar and
supravalvar aortic stenoses.
• Nearly all adult patients with SCD and congenital AS
experience preceding symptoms.
• The majority of children may not have symptoms before
SCD.
• Echo is the test of choice (although cardiac CT or MRI
may be required to assess for concomitant aortic
pathology).
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Circulation 1993;87:I16
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Premature Coronary Artery
Disease
• CAD in young patients is frequently
asymptomatic.
• Therefore, its incidence is likely underestimated.
• In an autopsy study, advanced coronary
stenoses were noted in 20% of men and 8% of
women aged 30-34 years.
• 19% and 8% of men and women aged 30-34
years, respectively, had ≥ 40% stenosis of the
LAD.
• Coronary artery disease is the most common
cause of SCD among “masters” athletes (> 35
years old).
Beth Israel Deaconess
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Circulation 2000;102:374
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Idiopathic Dilated
Cardiomyopathy
• Idiopathic cardiomyopathy
is a relatively uncommon
cause of SCD in young
competitive athletes (3%).
• The mechanism of SCD is
most often reentrant
ventricular tachyarrhythmia
originating from areas of
abnormal myocardium.
• Bradyarrhythmia or
asystole may lead to SCD
if cardiomyopathic process
involves the conduction
system.
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Medical Center
Late gadolinium enhancement in a
patient with cardiomyopathy and
normal coronary arteries
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School
Mitral Valve Prolapse
• Although its relationship to
tachyarrhythmia has been
controversial, MVP is associated with
an increased risk of SCD.
• However, the increased risk of SCD
seems to correlate with the degree of
mitral valve pathology and MR.
• In one study, the annual SCD
mortality was significantly increased
(from 0.9% to 1.9%) in patients with
advanced mitral valve pathology
compared with patients with isolated
MVP (no MR) or the general
population.
• Late gadolinium enhancement of the
papillary muscles may be noted in
some patients with MVP suggesting
the presence of scarring or fibrosis.
Beth Israel Deaconess
Medical Center
Late gadolinium enhancement
of the anterolateral papillary
muscle in a patient with MVP
Am Heart J 1987;113:1298
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Other Congenital Heart Disease
• In addition to arrhythmic causes, cyanosis during
exercise in the setting of adult congenital heart
disease with right-to-left shunt may lead to syncope
and SCD.
• Cardiac arrest is an unusual first presentation of adult
congenital heart disease as most are symptomatic
and therefore diagnosed before SCD.
• Adult congenital heart disease may be diagnosed by
echo, cardiac CT, or MRI.
• Cardiac MRI currently offers the best definition of the
complex anatomy of repaired and unrepaired
congenital heart disease.
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Sudden Cardiac Death in the
Absence of Structural Heart Disease
• SCD in competitive athletes may also occur in
the absence of structural heart disease.
• Causes of SCD in structurally “normal” hearts
include inherited arrhythmia syndromes such as:
–
–
–
–
–
Long QT syndrome
Brugada syndrome
Catecholaminergic polymorphic VT
Wolf-Parkinson-White syndrome
Congenital short QT syndrome
• In addition, idiopathic VF and commotio cordis
may result in SCD among competitive athletes.
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Long QT Syndromes
Examples of long QT
syndromes
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• Often acquired, long QT syndrome can be
inherited.
• Long QT syndromes may result in polymorphic
VT (torsade de pointes) and SCD.
• Among inherited long QT syndromes,
precipitants and prognosis vary.
N Engl J Med 2008;113:1298
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Brugada Syndrome
• Autosomal dominant
disorder resulting in
increased risk of SCD.
• Multiple mutations in
the cardiac sodium
channel SCN5A have
been described.
• Characterized by
RBBB and ST
segment elevations in
V1-V3 on ECG.
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uptodateonline.com
Typical ECG pattern for Brugada
Syndrome
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Catecholaminergic Polymorphic
VT
• Also known as familial polymorphic VT,
catecholaminergic polymorphic VT typically
manifests itself in childhood or adolescence.
• SCD may occur in the setting of emotional or
physical stress.
• Like LQT1, SCD while swimming has been
described.
• Several mutations have been described
including in the cardiac ryanodine receptor and
calsequestrin 2 genes.
Beth Israel Deaconess
Medical Center
Circulation 2002;106:69
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Wolf-Parkinson-White
• WPW syndrome has
been associated with an
increased risk of SCD.
• The mechanism of SCD
is most often atrial
fibrillation or AVNRT that
degenerates to VF.
• In up to 25% of patients
with SCD due to WPW,
pre-excitation and
arrhythmias have been
previously undiagnosed.
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Medical Center
Typical pre-excitation pattern for
WPW
J Am Coll Cardiol 1991;18:1711
uptodateonline.com
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Congenital Short QT Syndrome
• Congenital short QT syndrome is a rare
autosomal dominant disorder associated with
SCD due to VF.
• Multiple genetic abnormalities have been
described including gain-of-function mutations in
potassium channel genes.
• Short QT is defined as a corrected QT interval
(QTc) ≤ 340 msec.
• Patients often develop atrial fibrillation at a
young age .
• Not all patients with short QTc carry an
increased risk of SCD.
Beth Israel Deaconess
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Circulation 2003;108:965
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Idiopathic VF
• Also called “primary electrical disease,”
idiopathic VF is diagnosed when SCD
occurs in a structurally normal heart and
other arrhythmic disorders are excluded.
• May account for up to 5% of SCD cases.
• Idiopathic VF is more common in men and
has a mean onset of 36 years.
• A history of syncope precedes SCD in up
to 25% of patients.
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Am Heart J 1990;120:661
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Commotio Cordis
• Commotio cordis describes SCD that occurs following
precordial trauma.
• A registry analysis revealed that 62% of cases occurred
during organized or recreational sporting activities
(baseball, hockey).
• In an animal model, low-energy impact to the chest wall
just before the peak of the T wave produced VF, while
impact during the QRS complex produced complete
heart block.
• Frequency of VF was related to the hardness of the
projectile and velocity of impact.
• In one series, only 16% of individuals survived an
arrhythmic event in the setting of commotio cordis.
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JAMA 2002;287:1142
N Engl J Med 1998; 338:1805
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Commotio Cordis
Fatal commotio cordis in a 14-year-old boy during a
karate match.
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N Engl J Med 2003;349:11
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Syncope in Competitive Athletes
• Syncope in competitive athletes without known
structural heart disease is most often due to
neurocardiogenic, or vasovagal, mechanisms.
• However, the diagnosis of neurocardiogenic
syncope in this patient population is a diagnosis
of exclusion.
• Careful evaluation warrants a detailed history,
physical examination, and ECG.
• Echocardiography, exercise treadmill testing,
cardiac MRI, and electrophysiological testing
may be required to exclude structural and
dysrhythmia-related causes of syncope.
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Cardiovascular Events in
Spectators
• The emotional stress of
watching competitive sports
may increase the risk of
cardiovascular events.
• A recent study demonstrated
an increased incidence of
cardiac emergencies among
German men and women on
days that the German team
was playing a 2006 World Cup
match compared to non-match
days (incidence ratio 2.66,
95% CI 2.33-3.04; p<0.001.
• The incidence of STEMI,
NSTEMI, and arrhythmia
increased by a factor of 2.5,
2.6, and 3.1, respectively,
during match days.
Beth Israel Deaconess
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Daily cardiovascular events from May 1
to July 31 in 2003, 2005, and 2006.
Numbers 1-7 correspond to German
soccer matches during the 2006 World
Cup (8 = Final, Italy v. France).
N Engl J Med 2008;358:475
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Screening
• Due to the devastating nature of SCD and the potential
to prevent such deaths by diagnosing associated
disorders noninvasively, clinicians have a strong
incentive to screen athletes.
• However, the following obstacles prevent widespread
screening with noninvasive testing:
– Large number of competitive athletes (8 million in the U.S.,
including high school, collegiate, professional)
– Low prevalence of underlying congenital heart disease
– Number of disorders to consider, each with different optimal
testing modalities
– Impact of false-positive studies (substantial when screening for
rare diseases; possible medicolegal implications)
– No randomized trials evaluating the impact of pre-participation
screening on the incidence of SCD
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N Engl J Med 2003;349:11
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Screening
• In an observational series from Italy, a
mandatory screening program including ECG
was associated with a decrease in the annual
incidence of SCD in athletes from 3.6 to 0.4 per
100,000 person-years from 1980 to 2004.
• AHA guidelines differ from those of the
European Society of Cardiology (ESC) and the
International Olympic Committee (IOC) such that
routine noninvasive testing (including ECG) is
not recommended.
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JAMA 2006;296:1593
Circulation 2007;115:1643
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AHA Screening
Recommendations
• Younger competitive athletes (<35)
– Complete personal/family history and physical exam
– Performed by physicians or certified non-physicians
– q2 years for high school and yearly for college/pro
• Masters athletes (>35)
– Complete personal/family history and physical exam
– Exercise testing for moderate-to-high risk patients
(men >40, women >50 with one or more CAD risk
factors; symptoms suggestive of CAD; ≥65 regardless
of risk factors/symptoms)
• Recreational athletes
– No explicit AHA guidelines; exercise testing
recommended in patients at high risk for CAD
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Circulation 2007;115:1643
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12-Element AHA Pre-Participation
Screening Recommendations
•
Personal history (confirmed by parent if minor)
–
–
–
–
–
•
Exertional chest discomfort
Unexplained syncope/presyncope
Excessive exertional fatigue/dyspnea
Prior heart murmur
Elevated blood pressure
Family history (confirmed by parent if minor)
– Premature death due to heart disease before age 50
– Disability due to heart disease in relative <50
– Specific knowledge of certain cardiac conditions (HCM, other CM, ion
channelopathy, Marfan’s, arrhythmias)
•
Physical examination
–
–
–
–
Cardiac exam (supine and standing)
Femoral pulses
Physical stigmata of Marfan’s
Bilateral blood pressure readings
*Positive finding of any 1 element warrants referral to cardiovascular specialist
+/- further testing
Beth Israel Deaconess
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Circulation 2007;115:1643
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Activity Restriction
Recommendations
• The 26th Bethesda Conference guidelines have
established clear recommendations for the athletic
eligibility and restriction of athletes with conditions
associated with SCD.
• The decision to remove athletes from eligibility may be
associated with complex social and medicolegal
ramifications.
• A U.S. appellate court has ruled that the Bethesda
Conference report can be used by clinicians to determine
an athlete’s eligibility.
• Guidelines such as the Bethesda Conference report have
been endorsed as a means for resolving medicolegal
disputes involving the eligibility of young athletes.
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N Engl J Med 2003;349:11
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Conclusions
• SCD in competitive athletes may result from a
variety of disorders that may be detected by
noninvasive testing.
• Noninvasive testing must be interpreted carefully
in order to distinguish the physiological effects of
exercise training from pathology.
• AHA guidelines do not endorse routine preparticipation screening with noninvasive testing.
• However, noninvasive testing plays a critical role
in the evaluation of competitive athletes with
positive findings on screening history and
physical examination.
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