Clinical and biomarker profile of trauma-induced secondary cardiac injury

Secondary cardiac injury has been demonstrated in critical illness and is associated with worse outcomes. The aim of this study was to establish the existence of trauma-induced secondary cardiac injury, and investigate its impact on outcomes in injured patients.

Injured adult patients eligible for enrolment in the Activation of Coagulation and Inflammation in Trauma 2 study, and admitted to the intensive care unit between January 2008 and January 2010, were selected retrospectively for the study. Markers of cardiac injury (brain natriuretic peptide (BNP), heart-type fatty acid binding protein (H-FABP) and troponin I) were measured on admission, and after 24 and 72 h in blood samples from injured patients. Individual records were reviewed for adverse cardiac events and death.

During the study period, 135 patients were enrolled (106 male, 78·5 per cent) with a median age of 40 (range 16-89) years. Eighteen patients (13·3 per cent) had an adverse cardiac event during admission and these events were not associated with direct thoracic injury. The in-hospital mortality rate was higher among the adverse cardiac event cohort: 44 per cent (8 of 18) versus 17·1 per cent (20 of 117) (P = 0·008). Raised levels of H-FABP and BNP at 0, 24 and 72 h, and troponin I at 24 and 72 h, were associated with increased adverse cardiac events. BNP levels were higher in non-survivors on admission (median 550 versus 403 fmol/ml; P = 0·022), after 24 h (794 versus 567 fmol/ml; P = 0·033) and after 72 h (1043 versus 753 fmol/ml; P = 0·036), as were admission troponin I levels.

Clinical and cardiac biomarker characteristics support the existence of trauma-induced secondary cardiac injury, which is associated with death, and unrelated to direct thoracic injury.