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Case Study: Demand Ischemia

November 13, 2014

Case:  A 70 year old female multiple myeloma is admitted with rapid atrial fibrillation, substernal chest pressure and mild dyspnea. EKG shows non-specific changes. Hemoglobin is 7.5 gm/dl. Stool occult blood is negative. Atrial fib is converted with cardizem and 2 units of packed RBC transfused with relief of symptoms. Serial Troponin I levels are 0.01 / 0.04 / 0.08 / 0.05. Troponin I “normal” reference range in this lab is 0.0 to 0.04 mcg/L (99th percentile).   Diagnoses are rapid atrial fibrillation, severe anemia due to myeloma, and demand ischemia.

Based on the Troponin levels and a diagnosis of demand ischemia, should the physician be queried for a myocardial infarction?

Answer: The typical MI, STEMI or non-ST elevation MI (NSTEMI), is classified as a Type 1 MI involving decreased blood flow to the heart due primarily to coronary artery disease.

Demand ischemia is commonly used to describe cardiac ischemia primarily due to cardiac supply/demand mismatch rather than coronary artery disease. 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).

The use of the term “demand ischemia” is often ambiguous and inconsistent as physicians may not make the distinction between ischemia vs. infarction in the supply/demand setting. When supply/demand infarction is diagnosed, physicians often use the more familiar term “NSTEMI” rather than “Type 2 MI”.

The authoritative definition of supply/demand infarction (Type 2 MI) is a rise of Troponin above the 99th percentile of the reference range for the lab test in use; in this case the 90th percentile is 0.04.   Since the troponin level reached 0.08, well above the 99th percentile, it appears that this patient sustained a supply/demand infarction, or Type 2 MI. The ambiguity and inconsistency of “demand ischemia” in this case requires clarification.

It is essential to know what the 99th percentile reference range for your hospital is, because there are many different Troponin tests available with different reference ranges. Your lab director should be able to provide this information.

Finally, the management of Type 2 MI is directed primarily at the precipitating cause; in this case, rapid atrial fibrillation and severe anemia. The usual aggressive therapy for Type 1 MI due to coronary artery disease is rarely necessary. This should be documented in the record to avoid any potential deficiency in quality measures when Type 2 MI is diagnosed.

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