[SCD-FORUM] EXPERTS ASK, EXPERTS ANSWER
SCD Symposium
info at scd-symposium.org
Tue Oct 17 07:38:00 ART 2006
Dr. Luciano Pereira from Paraguay asks
- The Commotio Cordis is an entity increasingly being diagnosed over
the last few years. Since it is highly deadly and affects young
sportsmen in most cases, cardioverter defibrillators and other
reanimation devices availability should not be obligatory in public
and private institutions devoted to sports?
Dr. Andres Perez Riera from Brazil answers
- Dear Luciano: Here Andrés Ricardo Pérez Riera from São Paulo
Brazil. Cardiac concussion, commotio cordis, or nonpenetrating
chest wall impact (traumatic blow to the chest wall causing VT/VF) is
caused by a sudden, nonpenetrating, localized impact to the chest
that is theorized to result in almost simultaneous SD from a
disruption to the conductive system. Commotio cordis may lead to SCD
due to the acute initiation of VF. VF may result from sudden stretch
during a vulnerable window, which is determined by repolarization
inhomogeneity. The detailed external/internal forensic examination
of the body reveals no evidence of structural, pathologic, or
histologic signs of trauma to the heart. A cardiac concussion is a
rare and often overlooked cause of SD. This type of SD is typically
seen among younger individuals participating in sports involving
projectiles and, to a lesser degree, where collisions occur. Cardiac
concussions are clinically, pathologically, and chemically different
from a cardiac contusion1.
The main cause’s of SD among young athetes (<35 years old) are:
1) Hypertrophic cardiomyopathy (HCM) is the most common form of SD in
young competitive athletes;
2) Arrhythmogenic right ventricular dysplasia (ARVD);
3) Anomalous coronary origins: White-Bland-Garlad syndrome and others;
4) Marfan syndrome;
5) Premature coronary artery disease;
6) Structurally normal heart (ion channel disorders.): SD with a
structurally normal heart was the leading cause of death among female
young recruits during military training2. These main entities are:
congenital LQTS, the SQTS, BrS and CPVT. These are pathologies with
very different phenotypes and aetiologies, but which share a common
final pathway in causing SD: amplification of spatial dispersion of
repolarization in the form of TDR(3).
7) Inflammatory myocardial diseases: Myocarditis
8) Commotio cordis.
Analyze the presence of myocardial damage in relation to official
boxing matches. Low-energy chest wall impact could be responsible for
SCD h, i.e. commotio cordis. As boxing is a traumatic sport in which
thoracic hits usually occur, it seems interesting to know if there
are any significant cardiac changes during official bouts. Fifteen
amateur boxers, participating in the semifinals of the Italian
Championship were investigated by Bianco et al.
A standard ECG before, immediately after, 1 hour and 12 hours after
the match were obtained from each athlete to analyze:
1) Atrio-ventricular conduction;
2) QRS axis and duration;
3) Ventricular repolarization.
A blood sample was also obtained before and 12 hours after the match
for analysis of total-creatin-phosphokinase, myoglobin, and T-
troponin. After the fight, the following significant changes were
encountered:
1) Higher QRS voltages;
2) Lowering of J-point and ST segment in lateral leads;
3) Higher ST-slope;
4) Lower T-wave amplitude;
5) Shorter T-wave peak time, and
6) Shorter QT interval.
When the last 2 parameters were corrected for heart rate, no
differences were observed for QTc, while T-wave peak time
significantly increased. All these changes persisted until one hour
after the match. Moreover, 3/15 boxers (20 %) showed marked
ventricular repolarization anomalies in lateral leads after the
contest, persisting for 12 hours in one case. However, no athlete had
clinical and humoral signs of myocardial damage following the match.
It was concluded that no clinical and humoral signs of myocardial
damage were found after amateur boxing matches, although ventricular
repolarization abnormalities can be found on ECG in 20 % of boxers,
probably due to sympathetic hyper-activity related to the agonistic
event(4).
References
1) Koehler SA, Shakir A, Ladham S, et. al. Cardiac concussion:
definition, differential diagnosis, and cases presentation and the
legal ramification of a misdiagnosis. Am J Forensic Med Pathol.
2004;25:205-208.
2) Eckart RE, Scoville SL, Shry EA, Potter RN, Tedrow U. Causes of
sudden death in young female military recruits.Am J Cardiol. 2006;
97:1756-1758.
3) Antzelevich C, Oliva A. Amplificaion of spatial dispersion of
repolarization underlies sudden cardiac death associated with
catecholaminergic J Intern Med. 2006;259:48-58
4) Bianco M, Colella F, Pannozzo A, Oradei A, et al. Boxing and
"commotio cordis": ECG and humoral study. Int J Sports Med.
2005;26:151-157.
All the for all
Andrés Ricardo Pérez Riera MD
Chief of Electro-Vectocardiology Sector of the Discipline of
Cardiology,
ABC Faculty of Medicine (FMABC), Foundation of ABC (FUABC)
– Santo André – São Paulo – Brazil.
Sebastião Afonso 885 Jardim Miriam SP Brazil
Zip Code: 04417-100
riera at uol.com.br
--
Dr. Sergio Dubner
President of Scientific Committee
Dr. Edgardo Schapachnik
President of Steering Committee
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