Cardiac Troponin I: A Marker for Post-Burn Cardiac Injury

Abstract

Cardiac troponin I (cTnI) was measured by chemiluminescent immunoassay following burn injury. Thirty patients [total body surface area (TBSA) of burn 15-98%] were included in this study and each had four to six blood samples collected at 2-day intervals between the 5th and 14th days post-burn. All patients were found to have increased cTnI on two or more occasions. The mean cTnI concentration was significantly higher in patients with TBSA of burn > 30% (0'34 jlg/L compared with 0·09 jlg/L, P<O·OOI) and in those with obvious burn wound exudation (O·32jlg/L compared with 0·12jlg/L, P<O·OI). cTnI concentrations peaked at the time when there was obvious burn wound exudation or spontaneous separation of eschar, then decreased after surgical excision. Two patients with persistently high cTnI concentrations developed tachycardia. We conclude that burned patients have varying degrees ofnon-ischaemic cardiac injury, manifesting as leakage of cTnI from myocytes into the circulation.Thermal injury and sepsis initiate a systemic inflammatory cascade that causes multiple organ failure. t -3 Transient cardiac contractile dysfunction is believed to be a result of myocyte damage following thermal injury.v" These findings emphasize the need for a specific cardiac marker after burn injury. Creatine kinase (CK) and its MB isoenzyme (CK-MB) are recognized to be incompletely cardiac-specific.P Cardiac troponin I (cTnI) is a contractile protein exclusively present in cardiac muscle.v!' and elevation of serum cTnI concentration is only found in the presence of cardiac injury. [13][14][15][16] The sensitivity of cTnI for ischaemic cardiac damage is similar to that of CK_MB,J6-18 and the specificity and sensitivity of cTnI in detecting non-ischaemic heart disease have been shown to be better than those of CK_MB. 3.J8-20 Further to our recent report that cTnI detected myocyte damage in acute heart failure (non-ischaemic cardiac damage not indicated by CK-MB),21 we carried out a prospective study to explore the possibility of using cTnI as a specific cardiac marker for burned patients. In our initial experiment, we found that some patients had trace amounts of

Combination of ketamine and xylazine exacerbates cardiac dysfunction in severely scalded rats during the shock stage

“…These data indicate that there is likely to be a definite change in cTnI levels. The cTnI level 24 h after burns has been reported to be significantly higher in patients with burns covering >30% TBSA and cTnI has been regarded as a marker for post-burn cardiac injury (38). Therefore, we measured the changes in cTnI levels to assess the impact of anesthetics on burn injury.…”

Cats with thermal burn injuries from California wildfires show echocardiographic evidence of myocardial thickening and intracardiac thrombi

“…The lack of widespread cTnI elevation is suspected to be a function of the short half-life of cTnI and time of sample collection. Cardiac troponin I has a reported half-life of approximately 2 hours 30 and animal burn models have demonstrated that peak cTnI levels occur around 24 hours post-burn 31,36 . Given the timeline of patient presentation, active myocarditis and/or myocardial damage may have resolved by the time of evaluation.…”

“…Human burn patients with no pre-existing cardiac conditions had fluctuating elevations in cTnI following burn injury with elevations as early as 10 hours and peak cTnI concentrations at day 7-13 following injury. Normalization of cTnI occurred after excision of eschar formation and administration of cardiovascular support 31 . A separate retrospective evaluation demonstrated an increased risk of death associated with a high cTnI result 28 .…”