[SCD-FORUM] EXPERTS ASK, EXPERTS ANSWER

[SCD Symposium]

专家问答

巴拉圭的Luciano Pereira教授问
——在过去的几年里，心震荡的诊断明显增加。因为 
死亡率高且主要影响年轻男运动员，公立医院和私人 
诊所是不是为运动员们必备心脏除颤器和其它复苏的 
装置？

巴西的Andres Perez Riera教授回答
——亲爱的Luciano：我是巴西São Paulo的Andrés Ricardo  
Pérez Riera。由突发的局部非穿透性胸部损伤引起的心 
震荡（Cardiac concussion, commotio cordis）或非穿透性胸壁 
疼痛（胸壁外伤引起的VT/VF）理论上会引起传导系统 
的破坏导致猝死。心震荡可引起VF的急性发作导致心 
脏猝死。多相复极导致易损期的突然延长可以造成 
VF。详细的外在/内在的身体检查都没有提示心脏有结 
构、病理或组织学损伤的证据。心震荡是一种少见 
的、常常被忽略的猝死原因。这种类型的猝死多见于 
参加诸如投掷等碰撞发生相对较少的项目的年轻运动 
员，心震荡在临床、病理、化学方面都与心脏挫伤不 
同。
年轻运动员（< 35岁）猝死的主要原因是：

①    肥厚型心肌病（HCM）是年轻有竞争性的运动员 
猝死的最常见类型；

②    心律失常性右室发育不良（ARVD）；

③    异常的冠脉起源：White-Bland-Garlad综合症等；

④    马凡综合征；

⑤    过早的冠状动脉疾病；

⑥    结构正常的心脏（离子通道疾病）：年轻女性 
新兵在军事训练中最常见的死因是猝死伴心脏结构正 
常。而本质的原因有：先天性LQTS，SQTS，BrS和CPVT。这 
些疾病有不同的表型和病因，但有共同的途径导致猝 
死：以TDR的形式增加复极的离散时间；

⑦    炎症性心肌疾病：心肌炎；

⑧    心震荡。

分析正式拳击比赛与发生心肌损伤的关系。低能量的 
胸壁损伤就能引起SCD，例如心震荡，而拳击是创伤性 
运动，常常会出现胸部受击，研究正式比赛回合中心 
脏是否发生显著变化颇为有趣。Bianco等人研究了15个 
参加意大利冠军赛半决赛的业余拳击手。

在参赛前、比赛后即刻、比赛后1小时和12小时给每一 
个运动员做标准心电图并分析：

①    房室传导；

②    QRS电轴和时程；

③    心室的复极化。

在比赛前和比赛后的12小时海采集血样分析总肌酸磷 
酸激酶、肌红蛋白和T-肌钙蛋白。在比赛后的数据 
中，发现了以下有意义的改变：

①    QRS波群高电压；

②    侧壁导联中J点降低和ST段抬高；

③    ST段斜率升高；

④      T波达峰时间缩短；

⑤      QT间期缩短。

最后两个参数校正心率后QTc无查别，而T波达峰时间 
明显增加。所有这些改变持续到比赛后1小时，而且， 
3/15的拳击手（12%）在赛后出现了明显的心室复极异 
常，有一例持续了12小时。然而，赛后无一人出现心 
肌损伤的临床和激素水平异常。也就是说，在业余拳 
击比赛之后，没有临床和激素的指标提示心肌损伤， 
尽管20%的拳击手的心电图中发现了复极异常，这可能 
与对抗行为有关的交感系统的过度活化有关。



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.
徐怡琼译 王玲洁校
EXPERTS ASK, EXPERTS ANSWER
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