Cardiac troponin I: a marker for post-burn cardiac injury

Abstract

SUMMARY. 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

ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations

“…In small series, modest cardiac troponin I elevations have been found in almost all patients with significant (Ͼ15% total body surface area) burn injuries, with peak levels higher and earlier with more severe/extensive burns (238,239). Troponin elevation in the setting of severe burns appears to be related to systemic stress (wound infection, tachycardia, and systemic inflammation) but exclusive of findings of ACS or myocardial ischemia.…”

Cardiac troponin I release in non-ischemic reversible myocardial injury from parvovirus B19 myocarditis

“…Cardiac troponin I release was initially reported with myocardial infarction, but subsequently, such release has been reported with reversible ischemic myocardial injury such as in unstable angina and pulmonary embolism; reversible or irreversible non-ischemic myocardial injury such as in myocarditis, cardiac contusion, and chemotherapyinduced or sepsis-induced myocardial injury; and in noncardiac diseases such as in renal failure [5][6][7][8][9][10][11][12]. The changes in myocyte membrane related to reversible injury could be enough for the release of cardiac troponin I from the free cytosolic pool of the myocytes, whereas in the case of myocardial necrosis the source of troponin release is from the structural damage to the myocytes.…”