The Pathophysiology of Trauma Induced Secondary Cardiac Injury (TISCI)


Cardiac dysfunction is a significant cause of mortality and morbidity in trauma patients. Complications related to the heart may occur months or years after discharge from hospital. This cardiac injury may develop in the absence of direct trauma to the heart and is not necessarily related to pre-existing coronary disease. This secondary cardiac injury has been verified in clinical studies and characterised by elevations in heart specific biomarkers.

Our previous pre-clinical studies revealed a trauma-induced secondary cardiac injury (TISCI) in an experimental model of trauma haemorrhage. The cellular changes seen in these studies were yet to be fully defined and the impact of changes within cardiomyocytes (terminally differentiated cardiac cells) upon cardiac function remains unclear. Our objectives with the TISCI study were to further characterise the cardiac injury resulting from a period of haemorrhagic shock related to trauma and to investigate the impact of this physiological insult on cardiac perfusion and performance.


We developed a resuscitation model from our existing small animal model of trauma haemorrhage. This model was used to assess the biochemical evidence for cardiac injury and correlated this with changes seen on the cellular level. Cardiac biomarkers including Troponin I and Fatty acid binding protein (FABP) were used as surrogate markers of cellular injury and the rise in these markers was correlated with disruption seen on histopathological analysis.

Cardiac imaging techniques including Single Photon Emission Computed Tomography (SPECT) and echocardiography were used to investigate cardiac perfusion and functional parameters after a period of trauma haemorrhage with subsequent resuscitation.


Results from these experiments are currently being analysed and will be available soon.

Trauma Associated Cardiac Injury and Dysfunction (TACID)


Trauma is the leading cause of death in the United Kingdom in those under the age of 40. Mortality in trauma mainly occurs in the acute phase, however, trauma patients have a sustained increase in mortality rates when compared to the normal population. It is thought that the cause of mortality in up to 25% of trauma patients can be attributed to cardiac complications.

The pathophysiology of cardiac dysfunction in trauma has not been fully explored despite the burden of cardiac disease in our population. It has been noted that there is a rise in markers of cardiac injury in trauma patients even in the absence of direct thoracic injury, alluding to the presence of trauma induced secondary cardiac injury.


TACID was an observational study which aimed to:

  • Ascertain the significance of cardiac injury in trauma patients and investigate whether it leads to cardiac dysfunction
  • Understand the pathophysiology of trauma induced cardiac injury  particularly in the absence of direct thoracic injury
  • Investigate the contribution of pre-morbid cardiovascular disease on short and long-term outcomes in trauma patients
  • Identify useful screening tools for post-traumatic secondary cardiac injury


Simpson R, Praditsuktavorn B, Wall J, Morales V, Thiemermann C, Tremoleda JL, Brohi K. Myocardial alterations following traumatic hemorrhagic injury. J Trauma Acute Care Surg. 2023 Oct 1;95(4):481-489. doi: 10.1097/TA.0000000000003987. Epub 2023 May 29. PMID: 37249511

Wall J, Naganathar S, Praditsuktavorn B, Bugg OF, McArthur S, Thiemermann C, Tremoleda JL, Brohi K. Modeling Cardiac Dysfunction Following Traumatic Hemorrhage Injury: Impact on Myocardial Integrity. Front Immunol. 2019 Dec 6;10:2774. doi: 10.3389/fimmu.2019.02774. PMID: 31866998; PMCID: PMC6908477

Additional Research

Wilson NM, Wall J, Naganathar V, Brohi K, De'Ath HD. Mechanisms Involved in Secondary Cardiac Dysfunction in Animal Models of Trauma and Hemorrhagic Shock. Shock. 2017 Oct;48(4):401-410. doi: 10.1097/SHK.0000000000000882. PMID: 28915215


Core Facilities Manager: Dr Jordi Lopez Tremoleda


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