1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.
While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.
If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.
2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.
This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
Why is it so important to get this diagnosis right?
Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.
Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.
- A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
- A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
- Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
- To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
- An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.
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