Transcript 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
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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).
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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.
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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.
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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.
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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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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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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).
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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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Classification of sports based on peak static
and dynamic components achieved during
competition.
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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.
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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)
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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
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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.
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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:
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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%)
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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.
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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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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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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.
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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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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.
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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.
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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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Epsilon waves
Increased signal on T1weighted imaging in the RV
free wall (left) and decreased
signal on fat suppressed
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imaging (right)
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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.
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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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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).
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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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Late gadolinium enhancement in a
patient with cardiomyopathy and
normal coronary arteries
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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.
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Late gadolinium enhancement
of the anterolateral papillary
muscle in a patient with MVP
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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:
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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.
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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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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.
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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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Typical pre-excitation pattern for
WPW
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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.
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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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Commotio Cordis
Fatal commotio cordis in a 14-year-old boy during a
karate match.
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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.
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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).
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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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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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12-Element AHA Pre-Participation
Screening Recommendations
•
Personal history (confirmed by parent if minor)
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•
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
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–
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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
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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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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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