| Abstrakt: |
Subendocardial hemorrhages (SEH) occur after cardiac injuries and resuscitation as well as secondary to noncardiac injuries comprising head injuries, infectious diseases, intoxications, hemorrhagic diathesis, abdominal trauma, asthma, and hypovolemic shock. In particular, the common incidence of SEH in intracranial lesions led to the suggestion that the phenomenon is mediated by the autonomic nervous system via hypersecretion of catecholamines. Other modes of SEH induction are also discussed, especially a sudden hypotension followed by subendocardial myocardial cell necrosis. Furthermore, animal experiments with adult miniature swine led to the suggestion that high-impact accelerations could provoke the formation of SEH. Human experiments, however, point out that humans do not appear to have catecholamine levels (cardiac or systemic) as high as those observed in miniature swine during high-impact acceleration exposure and it is widely accepted that the lesions in miniature swine develop as a consequence of a somewhat unique form of the porcine stress syndrome. SEH are located in the upper part of the interventricular septum, the opposing papillary muscles, and adjacent trabeculae carneae of the free wall of the left ventricle. A part of the conducting system is located in the subendocardium, and the left branches of the atrioventricular bundle are localized in the region in which SEH are most commonly seen at autopsy. Therefore, the predisposition of the subendocardium to ischemia may suggest a mechanism for the explanation of ventricular arrhythmia and sudden death. Additionally, ischemic lesions of the papillary muscles of the left ventricle can cause mitral insufficiency, thus contributing to heart failure. [ABSTRACT FROM AUTHOR] |
