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[Heart injury caused by air shock wave trauma]
K Leksowski1, R Dancewicz, J Sapiezko
1Kliniki Chirurgicznej Instytutu Chirurgii WAM w Lodzi.
Insights
Air shock wave trauma causes significant heart muscle damage, indicated by ECG changes and elevated cardiac enzyme levels. These effects manifest as multifocal myocardial injury, with enzyme levels peaking 120 hours post-trauma.
Area of Science:
- Cardiovascular Physiology
- Trauma Medicine
- Biochemistry
Context:
- Air shock wave trauma presents a unique challenge to cardiovascular health.
- Understanding the cardiac response to such trauma is crucial for developing effective treatments.
- Previous research has not fully elucidated the temporal dynamics of myocardial injury following air shock wave exposure.
Purpose:
- To estimate the extent and nature of heart muscle injury following air shock wave trauma.
- To analyze the temporal changes in cardiac biomarkers and electrocardiographic patterns post-trauma.
- To correlate biochemical and morphological findings of cardiac damage.
Summary:
- Animals exposed to air shock wave trauma were assessed at 3, 24, 48, and 120 hours.
- Electrocardiograms (ECG) and plasma levels of creatinine kinase (CK), CK-MB, lactate dehydrogenase (LDH), LDH1-2, and alpha hydroxybutyrate dehydrogenase (HBDH) were measured.
- Morphological examination, including histology and coronarography, revealed multifocal heart muscle injury, with significant increases in plasma enzyme activities observed 120 hours post-trauma and early ECG disturbances.
Impact:
- This study provides critical insights into the cardiac pathophysiology of air shock wave trauma.
- Findings can inform clinical management strategies for individuals exposed to blast injuries.
- Establishes a temporal profile of cardiac biomarker elevation and ECG abnormalities, aiding in diagnosis and prognosis.
Abstract:
The aim of the study was the estimation of heart muscle in response to air shock wave trauma. The animals were divided into four groups according to the time between trauma and the examination (3, 24, 48 and 120 hours). In all groups of animals ecg was performed and plasma level of creatinine kinase (CK), cardiac isoenzymes (CK-MB), lactic dehydrogenase (LDH) and its isoenzymes (LDH1-2) and alpha hydroxybutyrate dehydrogenase (HBDH) were determined. CK-MB activity as a percent of CK activity and rate of LDH isoenzymes activity were calculated. Morphologic estimation of heart injury based on macroscopic observation, histology and coronarography of heart specimens was performed. It was revealed that pathologic changes in ecg indicating intracardial conduction disturbances occur most intensively in first ten minutes after trauma. Plasma CPK, LDH and LDH1-2 activity increased significantly after 120 hrs following trauma. Morphologic manifestation of heart damage was multifocal injury of heart muscle.