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dc.contributor.authorDe’Ath, Henry D. I.
dc.date.accessioned2015-09-07T14:04:34Z
dc.date.available2015-09-07T14:04:34Z
dc.date.issued2013
dc.identifier.citationDe’Ath. D.I. 2013. Trauma Associated Cardiac Injury & Dysfunction. Queen Mary University of London.en_US
dc.identifier.urihttp://qmro.qmul.ac.uk/jspui/handle/123456789/8466
dc.descriptionPhDen_US
dc.description.abstractThe existence of a trauma induced secondary cardiac injury (TISCI) remains in doubt. The risk factors and pathological processes that lead to its development are not known, whilst the effects of TISCI on injured patient outcome are uncertain. Concurrently, the incidence of coronary heart disease (CHD) in a trauma population and its influence on mortality are inconclusive. The aim of this research project was to address these specific areas of uncertainty. Critically injured patients (n=135) were retrospectively investigated for the incidence and nature of adverse cardiac events (ACEs), and levels of the cardiac specific biomarkers Troponin I, B-type Natriuretic Peptide and Heart-type Fatty Acid Binding Protein were measured. Biomarkers and cardiac events were evaluated against outcome. Thereafter, the relationship of pro-inflammatory cytokines with TISCI was explored. A prospective cohort study of 199 trauma patients followed, to confirm the existence of TISCI and describe its clinical features, risk factors and outcomes. Finally, coronary artery calcium, as a marker of CHD, was evaluated on 432 CT scans of the chest of trauma patients aged 45 years or over, and its association with survival after injury was established. ACEs and early biomarker rises occurred in trauma patients and both were unrelated to the severity of chest injury. Each was associated with higher mortality, and confirmed the existence of TISCI. Risk factors for the development of the condition included increasing age, worsening tissue injury and shock. A relationship with cytokines was demonstrated, and implicated acute inflammation in the pathogenesis of TISCI. Calcification on CT scans revealed the incidence of CHD in an injured cohort approached 70%, although its presence did not impact survival. There exists a trauma induced secondary cardiac injury which was related to poorer outcome. The condition was associated with inflammation. CHD was widespread in older trauma patients but was not associated with increased in-hospital mortality.en_US
dc.language.isoenen_US
dc.publisherQueen Mary University of Londonen_US
dc.subjectMedicineen_US
dc.subjectTraumaen_US
dc.subjectCoronary heart diseaseen_US
dc.titleTrauma Associated Cardiac Injury & Dysfunctionen_US
dc.typeThesisen_US
dc.rights.holderThe copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without the prior written consent of the author


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