CardioNerds (Amit Goyal & Daniel Ambinder) join University of Washington cardiology fellows (Shannon McConnaughey, Betty Ashinne and Andrew Perry - host of the AP Cardiology podcast) for some tacos and beer at the water and discuss a puzzling case of recurrent troponin elevation. Dr. Kelly Branch provides the E-CPR and program director, Dr. Rosario Freeman, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Eunice Dugan with mentorship from University of Maryland cardiology fellow Karan Desai.
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Episode graphic by Dr. Carine Hamo
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Patient Summary
A female is her late 50s with past medical history of alcohol use disorder and intravenous drug use complicated by hepatitis C presented with generalized weakness and was found to have lower extremity fractures. Cardiology was consulted for pre-operative management. When obtaining a cardiac history, she reported rare, intermittent, and non-anginal chest pain. She had no current chest pain or dyspnea. On chart review, she had multiple presentations over the past 3 years for various complaints - some were chest pain - during which she was found to have elevated troponin I values. Most of the elevations were in the 0.5 to 1 ng/mL range, but one time, her peak troponin was 32 ng/mL. At one of those presentations, she had a TTE that showed septal wall motion abnormalities. She underwent coronary angiography on two occasions, which both showed proximal and mid-LAD calcifications, but no significant stenosis and she was managed medically.
At the current presentation, her vitals were within normal limits and her exam did not show any cardiopulmonary abnormalities. Labs were notable for troponin I of 10 ng/mL but CK-MB was normal. Interestingly, alkaline phosphatase was 3 times the upper limit of normal, and rheumatoid factor was 1156 IU/mL compared to 70 previously (normal range 0-20 IU/mL). EKG was without ischemic changes. TTE showed no wall motion abnormalities, normal LVEF, and no significant valvular disease. Cardiac catherization was deferred, and the patient was not interested in cardiac MRI. Due to an incongruent troponin elevation with the clinical presentation, there was concern for interference with the troponin assay due to the elevated rheumatoid factor and alkaline phosphatase levels. Upon further investigation, dilution of the troponin yielded results lower than factor of dilution or undetectable results. Mayo testing of the sample showed troponin-T of 0.024 ng/mL (normal < 0.01 ng/mL), and troponin I of 0.02 ng/mL (normal < 0.04 ng/mL). Although there were still some aspects of her previous presentations including rising troponin pattern and previous wall motion abnormalities that are unexplained at this time, her troponin elevation at this presentation was attributed to assay interference.
Case Media
ABCClick to Enlarge
A. ECG from MayB. Coronary angiography form MayC. ECG August (same year)
TTE 1 (May)
TTE 2 (May)
TEE 3 (May)
TTE 4 (May)
TTE 1 (August)
TTE 2 (August)
TTE 3 (August)
TTE 4 (August)
Episode Schematics & Teaching
Coming soon!
The CardioNerds 5! – 5 major takeaways from the #CNCR case
What is the universal definition of myocardial infarction?
· As per the current 4th universal definition, myocardial infarction is defined as an elevation in cardiac troponin (cTn) above the 99th percentile in high sensitivity assays in the setting of acute myocardial ischemia. It is considered acute if there is a characteristic rise/fall pattern in cTn.
