Evaluation of troponin-I as an indicator of cardiac dysfunction after thermal injury

Biochemical serum markers commonly used to assess human cardiac injury (creatinine phosphokinase, creatine phosphokinase-MB) have been shown to have diminished specificity for detection of cardiac injury in the setting of burn-related soft-tissue and skeletal muscle injury. Laboratory studies have demonstrated that severe cutaneous thermal injury is associated with cardiac contractile dysfunction and a corresponding elevation in serum cardiac troponin-I (cTn-I) in several species.

Twenty-three patients admitted to a tertiary care burn referral center were evaluated. Patients were monitored with pulmonary artery catheters, and creatinine phosphokinase, creatine phosphokinase-MB, and cTn-I levels were determined for 24 hours. Using a database, 6,722 burn patients were reviewed to determine the incidence of preexisting cardiac disease and postburn cardiac complications.

All patients had persistent sinus tachycardia (>115 beats per minute) without obvious electrical anomalies. All patients centrally monitored with a pulmonary artery catheter (n=20) maintained a cardiac index of greater than 3.0 L x min(-1) x m(-2) x cTn-I was present (>0.3 ng/mL) within 3.0 hours and elevated (>0.55 ng/mL) at 24 hours for all burns of more than 18% total body surface area. Historically, although only 5% of all admissions manifest acute postburn cardiac complications, 94% of these patients presented with preexisting heart disease.

Severe thermal injury was associated with a mild elevation in serum troponin-I; however, this did not correlate with overt cardiac morbidity or mortality. Postburn elevation of cTn-I suggested that a subtle degree of cardiac injury was present after a severe thermal injury despite hyperdynamic cardiac function during resuscitation.