implementation of the preparticipation screening...
TRANSCRIPT
Implementation of the
preparticipation screening
and IOC Recommendation is
the goal for sport physicians
Antonio Pelliccia, MD
SD
per
100,0
00 a
thle
te-y
ears
Annual incidence of SCD in screened athletes vs. unscreened non-athletes
Corrado et al. JAMA 2006;296:1593-601
3.6
0.4
0.7 0.8
The PPS is efficient to reduce SCD in young athletes
Comparison of Italian and US sudden deaths rates
Corrado et al. JAMA 2006; 296: 1593-601
Maron et al. Am J Cardiol 2009; in press
Incidence of SCD in NCAA Athletes
Harmon et al. Circulation 2011
Case identification (2003-2008):
NCAA Resolutions List (87%)
Media Reports (56%)
Catastrophic insurance claims (20%)
VF/Asystole
EXERCISE:
Deydratation
Electrolyte
imbalance
Adrenergic
output
Ischemia
Unstable Electrophysiological Substrate
The mechanisms for reduced
mortality in athletes with CV diseases
disqualified from competitive sports
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40
60
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2000
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10000
12000
14000
16000
18000 NSVTPVBs
Detraining Re-trainingPeak-training
Impact of detraining and resumed training on VAs:
In athletes with structural CV disease
intensive training and competition increases
the incidence and severity of arrhythmias at
risk for SD.
On the contrary, detraning reduces the risk
and may have life-saving impact.
In conclusion, scientific evidence shows that:
ECG abnormalities in up to 95%:
ST-T wave changes
Deep Q waves
Left axis deviation
Exceedingly high QRS voltages
P wave changes
(LAenlargement)
ECG abnormalities in > 80%:
Inverted T waves in anterior
precordial leads (beyond V1)
RV conduction delay
Epsilon wave
PVBs with LBBB morphology
HCM
RVLV
RA
LA
ARVC
The rationale for including the 12-lead ECG:
Diagnosis of HCM in young athletes
Adolescence Adulthood
Genotype
anomaliesAbnormal ECG
LV Hypertrophy
Ab
norm
al
fin
din
gs
Sudden death can occur at any time !
Long-term follow-up of athletes with abnormal ECG (Pelliccia et al. New Engl J Med 2008; 358: 152-63)
5
70
6Cardiomyopathies
(HCM3; ARVC1; DCM1)Other CV disease (Hpt 3, CAD 1, myoc 1, SVT 1)
No symptoms,
no CV disease
1, sudden death
1, cardiac arrest
81Study group
9-year follow-up
Probability to identify cardiac diseases at risk for SCD
by ECG or by Hx+PE:
ECG Hx+PE
Hypertrophic cardiomyopathy up to 90% < 10%
Arrhythmogenic right ventricular
cardiomyopathy 60-80% < 10%
Dilated cardiomyopathy 30-60% < 10%
Myocarditis 30-60% < 10%
Marfan’s syndrome < 10% > 90%
Valvular Disease < 10% > 90%
Long QT and Short QT syndrome > 80% zero
Brugada syndrome > 90% zero
Pre-excitation syndrome (WPW) > 90% zero
Congenital Coronary Artery Anomalies < 10% < 10%
510Study
Population
Mean age: 19 years
White 67% (Black 10%)
Gender: Males 61%
College athletes
Matriculated Harvard Univ.
11
387
110
Echocardiography;
History, PE and 12-lead ECG
Relevant
Cardiac
Findings
Normal
Heart
Physiologic
Remodeling
(from A. Baggish et al. Ann Intern Med 2010; 152: 269)
CV Screening in 510 Bostonian College Athletes
by A. Baggish et al. Ann Int Med 2010; 152: 269
1, Bicuspid aortic valve Murmur None None
2, Bicuspid aortic valve Murmur/Click None None
3, MVP Murmur None None
4, MVP Murmur None None
5, MVP None None None
6, Pulm. stenosis Murmur None Pul. St.
7, LV hypertrophy None QRS volt/LAE None
8, LV hypertrophy None QRS volt/T neg HCM
9, LV dilation None LBBB None
10, LV dilation None LBBB Myocarditis
11, RV dilation None RBBB None
Cardiac morphology His. + PE ECG Diagnosis
31,864 athletes evaluated in 19 National Medical
Centers across all Italy
Normal ECGs
28.108
(88.2%)
Abnormal ECGs
3.756(11.8%)
Early repolarization;
incomplete RBBB; mildly
increased R/S wave voltages
(59%)
Inverted T waves
(20%)
LAFB
(4%)LVH
(7%)
WPW
(1%) Prolonged QT interval (0.03%)
RBBB
(9%)
ECG abnormalities found at PPS
42,386Athletes screened
in Padua,
1982-2004
38,472
(91%)
Normal findings
3,914 (9%)
“Positive” findings
From Corrado et al.
JAMA 2006
879
(2%)Cardiac
abnormalities
91
(0.2%)Cardiac
disease at risk
True
Positives
7% False
Positives
Witout CV diseases(i.e., true negatives)
4,438
(>99%)Structural CVAbnormalities
(i.e., false negatives)
12(<1%)
(Pelliccia et al. Eur Heart J. 2006)
4,450 athletes judged free of CV diseasesat CV preparticipation screening
ECHOCARDIOGRAPHY
Aortic valve
disease
MVP
Myocarditis
Marfan’s ARVC
(n = 2)
(n = 2) (n = 1)
(n = 3)
(n = 4)
Athletes with Structural CV Abnormalities
No HCM was found !
(Pelliccia et al. Eur Heart J. 2006)
Novel ECG Interpretation in athletes:
“Normal”
Common and
Physiologic
Training-related
ECG alteration
“Abnormal”
Uncommon and
Pathologic
Training-unrelated
Need for further
work-up
510Study
Population
Mean age: 19 years
White 67% (Black 10%)
Gender: Males 61%
College athletes
Matriculated Harvard Univ.
Echocardiography;
History, PE and 12-lead ECG
(from A. Baggish et al. Personal communication)
Old ECG criteria New ECG criteria
16% ECG considered
abnormal
9% ECG considered
abnormal
Sensitivity 90%;
Specificity 83%
Sensitivity 91%;
Specificity 89%
Limitations of the PPS The Center for Coronary Artery
Anomalies (CCAA) at the Texas
Heart Institute launched in 2010 a
research program that involves
voluntary screenings of 10,000
middle school students for CCAA.
The study includes: 1) history
(personal and familial); 2) ECG
and, 3) a simplified program of
CMR.
1. The 12-lead ECG is efficient to identify (or raise
suspicion for) most CMPc and channelopathies, but
not for CCAA;
2. The prevalence of abnormal findings (ECG+PE+Hx) is
about 10% in large athlete populations; most are false
positive findings;
3. Routine echocardiography does not significantly
increase sensitivity of the ECG-screening for CMPs;
4. Disqualifying athletes with CV disease from competitive
sport may be life-saving;
In conclusion,
the Italian experience shows that:
Sudden Death in Athletes
“The fragility of life”
Dedicated to Marc-Vivien Foe
Antonio Pelliccia, MD
Institute of Sport Medicine and Science. Rome.