[Pathologic changes of the cardiac conduction system in 12 patients with abnormal ECG].

OBJECTIVE: To investigate the relationship between abnormal ECG and pathologic changes in the cardiac conduction system (CCS). METHOD: Pathological changes of the CCS in 12 cases with abnormal ECG out of 16 pre-death ECG were observed. RESULTS: (1) Among 7 cases of sudden cardiac death, ECG monitoring recorded bradyarrhythmia in 6 cases, tachyarrhythmia 6 cases, bradycardia-tachycardia syndrome 2 cases, conduction block 6 cases, atrial premature beats 6 cases, ventricular premature beats 6 cases, and ST-T changes 4 cases. (2) The histopathological findings in the CCS were noted in all cases. Of these 12 cases, three had signs of fatty infiltration, and/or fibrous 4 cases, three of amyloidosis, one of chronic inflammatory changes, two of acute inflammatory changes, two of developmental anomalies, two of hemorrhages and one of LAD stenosis. (3) Acute inflammation changes in the CCS corresponded to tachyarrhythmia and multiple ventricular premature beats, whereas chronic inflammation and degenerative changes in the CCS were often related to bradyarrhythmia, bradycardia-tachycardia syndrome and conduction block. (4) The CCS changes alone could lead to ST-T changes in ECG. CONCLUSION: The pathological changes in the CCS are related to ECG changes, and attributed to the pathological bases of arrhythmia.

[Traumatic cerebral infarction: a histopathological study of 17 cases].

OBJECTIVE: To assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism. METHODS: Specimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations. RESULTS: (1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus. CONCLUSION: Brain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.

[Morphological changes of tissues after extensive soft tissue injury].

OBJECTIVE: To study the pathological morphological changes for diagnosing the cause of death of extensive soft tissue injury or crush syndrome. METHODS: The tissues were stained by HE and IHC. RESULTS: (1) The Mb positive rate was 60%, 75%, 95% respectively. (2) Both the HSP70 positive rate of hearts and brains were 90%. CONCLUSION: (1) The animal model of broad soft tissue injury was established. (2) Accumulated the pathological morphological data for diagnosing the cause of death of extensive soft tissue injury or crush syndrome.