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Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction
Birte Weber1, Ina Lackner1, Florian Gebhard1
1Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, 86081 Ulm, Germany.
Insights
Trauma significantly impacts cardiac function, leading to poor outcomes. This review explores inflammation and complement activation as key mechanisms driving post-traumatic cardiac dysfunction.
Area of Science:
- Cardiology
- Trauma Surgery
- Immunology
Background:
- Trauma is a leading cause of mortality, with blunt cardiac trauma affecting thousands annually in the US.
- Cardiac damage is a significant predictor of poor outcomes, prolonged hospitalization, and reduced survival in trauma patients.
- Clinical manifestations of cardiac trauma include dysrhythmias and wall motion disorders, necessitating early consideration in hypotensive patients.
Purpose of the Study:
- To review cardiac damage following trauma.
- To elucidate the mechanisms of post-traumatic cardiac dysfunction, focusing on inflammation and complement activation.
- To illustrate the causal links between various trauma types and cardiac dysfunction, and discuss therapeutic options.
Main Methods:
- Review of existing literature on post-traumatic cardiac dysfunction.
- Focus on mechanisms involving inflammation and complement activation.
- Analysis of relationships between traumatic brain injury, blunt chest trauma, multiple trauma, burn injury, psychosocial stress, fracture, hemorrhagic shock, and cardiac dysfunction.
Main Results:
- Systemic elevation of cardiac troponins correlates with survival, injury severity, and catecholamine consumption.
- Echocardiography and troponin measurements are crucial for diagnosing cardiac dysfunction after trauma.
- Inflammation and complement activation play critical roles in the development of post-traumatic cardiac dysfunction.
Conclusions:
- Cardiac dysfunction is a critical complication of various trauma types.
- Understanding the inflammatory and complement-mediated mechanisms is key to managing post-traumatic cardiac dysfunction.
- Further research into therapeutic strategies targeting these mechanisms is warranted.
Abstract:
Trauma remains a leading global cause of mortality, particularly in the young population. In the United States, approximately 30,000 patients with blunt cardiac trauma were recorded annually. Cardiac damage is a predictor for poor outcome after multiple trauma, with a poor prognosis and prolonged in-hospitalization. Systemic elevation of cardiac troponins was correlated with survival, injury severity score, and catecholamine consumption of patients after multiple trauma. The clinical features of the so-called "commotio cordis" are dysrhythmias, including ventricular fibrillation and sudden cardiac arrest as well as wall motion disorders. In trauma patients with inappropriate hypotension and inadequate response to fluid resuscitation, cardiac injury should be considered. Therefore, a combination of echocardiography (ECG) measurements, echocardiography, and systemic appearance of cardiomyocyte damage markers such as troponin appears to be an appropriate diagnostic approach to detect cardiac dysfunction after trauma. However, the mechanisms of post-traumatic cardiac dysfunction are still actively being investigated. This review aims to discuss cardiac damage following trauma, focusing on mechanisms of post-traumatic cardiac dysfunction associated with inflammation and complement activation. Herein, a causal relationship of cardiac dysfunction to traumatic brain injury, blunt chest trauma, multiple trauma, burn injury, psychosocial stress, fracture, and hemorrhagic shock are illustrated and therapeutic options are discussed.
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