A 21-year-old male with no past medical history presented to the Emergency Department (ED) with intermittent severe substernal chest pain beginning 40 hours earlier. The chest pain began at 1:30 am on the day before admission, shortly after he awoke, was retrosternal, pressure-like, 4/10 in severity, slightly aggravated by inspiration, and lasted approximately four hours. The chest pain was preceded by dizziness. It was not severe enough to interrupt plans to go meet friends at 2:00 am. The pain resolved spontaneously; however he had a second episode the following morning at 6:00 am, this time waking him from sleep and with radiation to the base of his neck and right arm, was more severe (7/10) and aggravated both by inspiration and by lying on his right or left side. The patient's chest pain resolved spontaneously after three hours so he decided not to go to the ED. After a third severe episode occurred, he decided to go to the ED.
The patient denied any recent viral illnesses or illicit drug use. He works at a meat smoking company where he cleans the meat smoking generators. He had never experienced this type of pain before. In the ER, the patient's vitals were within normal limits: 127/75 mmHg, 90 bpm, RR 18, temp 99.4 C. His ECG was normal without dynamic ischemic changes. Initial troponin was 29 ng/mL. The patient was chest pain-free throughout his two-day hospitalization and had no abnormalities on telemetry monitoring.
Past Medical History: none Social History: (+) tobacco use, 2 cigarettes per month (-) drug or alcohol use/abuse Medications: none
CBC and Chem-7 were within normal.
LDL 75mg/dL HDL 34mg/dL. HbA1c: 5.7 TSH normal.
ESR/CRP just slightly above upper limit of normal. HIV nonreactive.
Inpatient Diagnostic Testing: CT Thorax with contrast: negative for PE, dissection or other abnormality Cardiac Catheterization: non-obstructive 30% stenosis in mid LAD, otherwise no coronary artery disease Echocardiogram: normal LV and RV function without valvular or other abnormalities Cardiac MRI: normal LV and RV function without regional wall motion abnormality, absence of abnormal T2 signal, no first pass or delayed gadolinium enhancement abnormality
What is the most likely explanation for the troponin-I elevation?
The correct answer is: D) Carbon monoxide cardiotoxicity
A number of substances (fibrin or microclots,1 endogenous antibodies such as heterophile antibodies) can interfere with current troponin assays, leading to either spuriously elevated or decreased troponin values. This should be suspected in a patient in whom the clinical scenario does not appear consistent with ACS. When one suspects interference with the troponin assay, measuring CK-MB may be helpful, as these will be elevated in true ACS but likely not in the case of interference with the troponin assay. In this case, we doubt assay interference as the absorption interference studies did not confirm the presence of interfering antibodies, the CK was elevated, and the outpatient troponin-I was normal.
To establish the underlying cause for the troponin-I elevation, cardiovascular magnetic resonance (CMR) non-invasively identifies areas of in-vivo inflammation and replacement fibrosis with a high spatial resolution.2 T2 enhancement on MRI imaging represents inflammation and edema as might be seen with acute myocarditis. First pass gadolinium enhancement represents perfusion abnormality seen in coronary occlusion. Late gadolinium enhancement represents tissue necrosis and fibrosis seen after myocardial infarction, and has a high sensivity for identifying even small amounts of myocardial necrosis. While myocarditis can present with chest pain and elevated troponin as in this patient, the normal echocardiogram and CMR here make myocarditis unlikely. The normal CMR also makes recent vasospasm and embolic myocardial infarction sufficient to produce such troponin elevation very unlikely.
Meat smoking is a way of preserving meat. Smoke contains chemical compounds that retard the growth of harmful bacteria. More than three hundred components of smoke have been identified. Carbonyl compounds in smoke contribute to the distinctive flavor and aroma of smoked meat, while the carbon dioxide and carbon monoxide help produce the bright red pigment. Carbon monoxide has been associated with troponin release3 via a direct effect on mitochondrial oxygen metabolism via competitive inhibition of cytochrome c oxidase and myoglobin-mediated oxidative phosphorylation. Autopsy studies show carbon monoxide to induce diffusely distributed focal myocardial injury and necrosis, focal leukocyte infiltration, and punctuate hemorrhages.4 Such diffuse, homogeneous injury, one may speculate, may not be detected on CMR especially in less severe carbon monoxide poisoning. A prospective study of carbon monoxide poisoning in Swiss soldiers shows that dizziness, a common symptom of carbon monoxide toxicity, tends to precede chest pain which is also common and rarely lasts more than two days.5 This is what happened in our patient.
Overall, we believe that the significant troponin-I elevation in a young patient with occupational exposure to carbon monoxide, an initial symptom compatible with carbon monoxide toxicity (dizziness), and normal diagnostic imaging results make carbon monoxide toxicity the most likely diagnosis. We welcome alternate diagnoses!
Johannes Mair. Tissue release of cardiac markers. Clin Chem Lab Med 1999; 37(11/12):1077-1084
Assomull RG, Lyne JC, Keenan N, et al. The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries. Eur Heart J 2007;28:1242-9
Satran D et al. Cardiovascular Manifestations of Moderate to Severe Carbon Monoxide Poisoning. J Am Coll Cardiol 2005;45:1513-6
Anderson RF, Allensworth DC, DeGroot WJ. Myocardial Toxicity from Carbon Monoxide Poisoning. Ann Int Med 1967, 67:1172-82
Henz S, Maeder M. Prospective Study of accidental carbon monoxide poisoning in 38 Swiss soldiers. Swiss Med Wkly 2005;135:398-408