Case #1: A 66-year-old male is admitted with PAT and substernal chest pressure with ventricular rate of 180. Troponin = 0.01--0.03--0.02 (Ref Range 0.0−0.04). PAT and chest pain resolved with IV Cardizem. Physician diagnosis: (1) PAT and (2) Troponin leak due to supply/demand mismatch.
Answer: This clinically indicates demand ischemia since the troponins were in normal range, but with evidence of acute ischemia (chest pressure). The PAT created a myocardial oxygen demand that exceeded myocardial oxygen supply.
Demand ischemia describes myocardial ischemia primarily due to cardiac supply/demand mismatch rather than CAD. In other words, the supply of blood flow to the heart is not limited but is inadequate to match the increased oxygen demands of an increased workload on the heart. Supply/demand ischemia can be either “demand ischemia” (no infarction) or “Type 2 MI” (infarction due to supply/demand mismatch). Because the troponins were within the normal range, this would not be classified as a Type 2 myocardial infarction.
Case #2: A 62-year-old male with a personal medical history of CHF, myocardial infarction, CAD with three stents, ischemic cardiomyopathy, and CKD, is admitted for acutely decompensated chronic systolic CHF. He had no chest pain or other ischemic symptoms. The initial troponin level was 0.26 (URL <0.10) which slowly trended downward: 0.19, 0.15, 0.14. EKG reported ST and T-wave abnormality, consider inferolateral ischemia.
The attending physician spoke with Cardiology who believed the troponin elevation was likely due to a combination of CKD and “troponin leak” from cardiac strain due to CHF. The attending MD documented Troponin above reference range. No further testing was done.
Answer: This clinically indicates non-ischemic myocardial injury. Although there were positive troponins, they were relatively flat, and the cardiologist indicated that the troponin elevation is likely due to non-ischemic causes - a combination of CKD and “troponin leak” from cardiac strain due to CHF. CHF and CKD are common "non-ischemic" causes of elevated troponins, and there was no further testing or treatment for the patient's CAD. There is also nothing stated in the record to indicate symptoms of ischemia, the EKG report notwithstanding. Non-ischemic causes of troponin elevation may be cardiac or non-cardiac in origin.
Case #3: An 82-year-old male admitted with BP 250/135, neck and shoulder pain and shortness of breath. EKG reported NSTTW changes. Troponin = 0.08--1.5--1.8. (Ref Range 0.00−0.04). BP reduced to 160/90 with IV nitroglycerin. Also given aspirin, atenolol, ASA, and clopidogrel. Repeat EKG prior to discharge unchanged.
Discharge Diagnosis: (1) Hypertensive emergency, and (2) NSTEMI probably due to #1 – prob demand ischemia.
Answer: This clinically supports a Type 2 MI based on the elevated Troponins above the 99th percentile with a rise and/or fall, and evidence of acute ischemia with neck and shoulder pain and shortness of breath, as well as EKG changes. The cause was hypertensive emergency, and not CAD. A type 1 NSTEMI is due to CAD.
Based on discharge diagnosis, this must be coded as a Type 2 MI. According to official coding guidelines, a "NSTEMI probably due to demand ischemia" is assigned to code I21.A1, Myocardial infarction type 2 with the underlying cause coded first.
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