The injuries of the heart are classified into the penetrating and the nonpenetrating myocardial injuries with or without underlying heart disorders and they are clinically emergent. Generally, nonpenetrating myocardial injuries are combined with
the
other realtively emergent injuries of the lung, brain, skeleton, or abdominal organs. In these cases, sometimes, clinicians overlook the myocardial injuries due to externally serious symptoms of other injuries, in spite of life-threatening
myocardial
injury.
To save the patients with nonpenetrating myocardial injuries, close observation, severallaboratory tests, and intensive care with exact diagnosis are necessary. And in autopsy, clinical data must be reviewed, and the whole heart must be examined
grossly
and microscopically. However, in the cases combined with underlying heart disorder which could be the cause of sudden unexpected natrual death, minute trauma which is not valuable in the healty person and has no visible injuries in myocardium
grossly or
microscopically act as a triggering factor of sudden death. Nonpenetrating injuries of the heart are cardiac concussion, cardiac contussion, complete or partial rupture of atrium, ventricle, papillarymuscle, or corda tendinae, and delayed rupture
of
cardiac structures, myocardial infarct, cardiac tamponade, sudden or delayed onset of arrhythmia, and so on. All of these injuries are engaged in the sudden death, regardless to the underlying heart disease.
In autopsy reports, to decide the direct cause of sudden death such as trauma induced injury, underlying heart disorder, or both, the relationship between them must be clarified.
Experimental rats injured by blunt chest trauma with optimum kinetic energy reveal abnormal ECG findings such as increased amplitude of impulse, bradycardia, or arrhythmia in early stage of trauma, and ST segment elevation after 24 hours.
Microscopically the injured myocardium is replaced by mononuclear cells in posttraumatic 48 or 72 hours and pathophsyologically expected to be replaced by fibrosis after several days or weeks. From these results, experimental model may be useful
to
investigate about the pathophysiology, clinical course, and response to various treatment in posttranumatic myocardial injury.
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