Troponin elevation reflects myocardial injury in carbon monoxide poisoning.

We describe the case of a 48-year-old white man, who was admitted to the emergency department with neurologic deficits and high suspicion of carbon monoxide (CO) poisoning. Blood carboxyhemoglobin (COHb) level was foundsubstantially increased (i.e., 18%). Clinical symptoms of myocardial infarction were lacking and the medical history was negative for major risk factors of coronary heart disease. However, electrocardiogram and troponin value were both suggestive for an acute coronary syndrome (i.e., a highly-sensitive troponin T value of 0.12 μg/L), while the echocardiogram showed hypokinesia of left ventricular apical lateral wall. The coronary angiogram performed one week after admission did not reveal the presence of coronary obstructions. It is hence assumed that high levels of COHb in blood, such as after CO exposure, may trigger myocardial injury by severe generalized tissue hypoxia (i.e.,impaired oxygen delivery) and a direct toxic effect on myocardium. Contributing factors that also decrease myocardial oxygenation include inadequate myocardial perfusion and prothrombotic state. This case report suggests that increased troponin values, especially when measured with highly-sensitive immunoassays, may be observed in patients with CO poisoning, and mirror the presence of myocardial injury. Therefore, although the measurement of cardiac biomarkers may be advisable in the presence of CO toxicity to identify cardiac involvement, aution should be used when troubleshooting the underlying source of troponin elevations in order to preven t overdiagnosis or misdiagnosis of acute coronary syndrome