Complicated coding of type 2 myocardial infarctions.

Advancing technology often leads to evolution of medicine. As our laboratory studies become more sensitive, we need to evaluate what the clinical significance of a positive test is. Such is the case with troponin.

In October 2012, the Third Universal Definition of Myocardial Infarction (TUDMI) was published by the American Heart Association, redefining myocardial infarction (MI). The classification of MI went from transmural/subendocardial to ST-elevation myocardial infarction (STEMI/NSTEMI), and is now categorized as Types 1 through 5. I strongly recommend reading this sentinel paper. I’m going to try to parse it for you now.

Acute myocardial infarction (MI) is the term for myocardial necrosis, or cell death, in a clinical setting, consistent with myocardial ischemia. “Ischemia” implies insufficient blood perfusion, and prolonged ischemia results in cell death. Other disease processes (e.g., myocarditis, cardiac contusion, etc.) can also result in cell death, and these often manifest low-level troponin elevations. This is an example of myocardial injury. I refer you to TUDMI Table 1 for a more extensive list.

Myocardial infarction is a specific subset of myocardial injury. The definition of MI includes a rise and/or fall (depending on when the patient is encountered in the evolution of the MI) of a cardiac biomarker signifying cell death, with at least one value above the 99th percentile upper reference limit (URL), plus some evidence of myocardial ischemia (be it symptoms, EKG or imaging evidence, or demonstration of a thrombus).

Current troponin blood tests are very sensitive (i.e., they pick up low levels) and very specific (i.e., they home in on release resulting from cardiac tissue damage). The release of cardiac biomarkers indicates myocardial injury. A significant trending of troponin indicates myocardial infarction.

Typical signs and symptoms suggestive of ischemia are chest, jaw, or arm pain, dyspnea, and diaphoresis, but other symptoms may predominate, such as fatigue, nausea, or syncope. TUDMI also acknowledges that MI may occur even without symptoms in women, the elderly, diabetics, postoperative patients, and critically ill patients.

Type 1 MI is due to atherosclerotic plaque and rupture or thrombosis causing mechanical coronary artery obstruction, with necrosis developing downstream in an anatomic distribution (e.g., anterior or inferior wall MI). STEMIs and NSTEMIs are subtypes of Type 1 MI.

Type 2 MI arises on the basis of something other than coronary artery disease (CAD) and is due solely to “supply-demand mismatch.” There is either an increase in demand, such as tachycardia or hypertension, or a decrease in supply, such as hypotension or severe anemia (see Figure 2 in TUDMI). There is always an underlying etiology. The implication of a Type 2 MI is that it portends a worse prognosis for the causative condition. There is also higher resource utilization with ICU placement, cardiology consult, repeat EKGs, and troponin levels. Type 2 MI is a genuine diagnosis.


In the inpatient hospital setting, one may also see:

  • Type 3 MI, which is cardiac death with symptoms of myocardial ischemia and suggestive EKG changes, but demise occurs before any biomarker trending can be demonstrated;
  • Type 4a MI, which is related to percutaneous coronary intervention;
  • Type 4b MI, related to stent thrombosis;
  • Type 4c MI, associated with percutaneous coronary intervention restenosis or >50 percent stenosis on coronary angiography; or
  • Type 5 MI, related to coronary artery bypass grafting.

If the troponin is elevated but it does not constitute a Type 2 MI, there are numerous ways to refer to it, such as troponinemia, troponin leak, and non-zero troponin. The ICD-10-CM code that signifies this is R79.89, Other specified abnormal findings of blood chemistry. If it establishes the DRG, it goes into MS-DRGs 948/947, Signs and symptoms. These are relatively low-weighted DRGs (0.7726; 1.1739). If used as a secondary diagnosis, R79.89 has no risk-adjustment implications.

One of the problems providers have had with diagnosing Type 2 MI was that there was no unique code for a Type 2 MI until October 2017. This meant that every time a Type 2 MI was diagnosed, the patient was marked as having atherosclerotic heart disease, and the core measures were initiated. Last October, the code I21.A1, Myocardial infarction, Type 2, was added to ICD-10-CM.

So now all we have to do is to rehabilitate all the bad documentation habits our clinicians fell into. To avoid triggering core measures, they resorted to diagnosing, “demand ischemia,” and “supply-demand mismatch.” Some of the aliases are not codable, but “demand ischemia” goes to I24.8, Other forms of acute ischemic heart disease. The DRG this goes to, if PDx, is MS-DRG 311, Angina pectoris, with a relative weight of 0.6793. If it is a secondary diagnosis, it is a comorbid condition or complication (CC).

There is always an underlying condition, but a Type 2 MI may be sequenced first if it was the diagnosis that, after study, occasioned the admission. If this were the case, the DRG falls into the Acute Myocardial Infarction sets (MS-DRGs 280-285) with higher weights than MS-DRG 311. All myocardial infarctions are major CCs (MCCs).


Here are my suggestions for clinicians:

  1. Order troponins when you are concerned about MI, not routinely or as a stab in the dark. Consider whether you are ruling in/out a Type 1 MI based on CAD or a Type 2 MI based on supply-demand mismatch. This will inform your action, depending on the results.
  2. When you have a first elevated troponin, make an uncertain diagnosis:

    e.g., Elevated troponin, suspect Type 2 MI

  3. Analyze additional troponins for a trend.
  1. If there is a significant rise and/or fall, and there is a level which exceeds the 99th percentile URL, strongly consider Type 2 MI and link to the underlying etiology. As the encounter unfolds, evolve your diagnosis from uncertainty to definitive Type 2 MI. Document that core measures are not indicated for Type 2 MI. Treat the underlying condition. 

    e.g., Troponins consistent with Type 2 MI due to hypertensive emergency.

  2. If the patient has EKG changes or known CAD, it may be appropriate to diagnose NSTEMI or STEMI instead of Type 2 MI. If you do so, be sure to attend to core measures.
  3. If there is no significant rise and/or fall, make an alternate diagnosis. Explicitly document that you have ruled out Type 2 MI (to save yourself a potential query):e.g., Troponin has remained constant at 0.2-0.3. Do not believe this is Type 2 MI. Suspect troponinemia due to CKD Stage 4.
  4. If Type 2 MI is ruled out, do not propagate it in subsequent progress notes. Remove it from your list.
  5. Please try to avoid documenting “NSTEMI Type 2.” Although Coding Clinics have given coders permission to extract and code Type 2 MI, this offends my sensibilities as oxymoronic.

Here are my observations/suggestions for clinical documentation integrity purposes:

  1.  There are still lots of providers who do not know what a Type 2 MI is. You may need to offer education.
  2. If you note an abnormal troponin early and you are interacting with a provider verbally and concurrently, bring it to their attention. It is optimal to consider Type 2 MI early, and to diagnose or rule out subsequently. I would not formally query unless and until the condition declares itself.
  3. If troponins stay relatively constant and are not significantly elevated (by significantly, I mean exceeding the 99th percentile URL), and your provider doesn’t remark on it, don’t query. It isn’t a Type 2 MI and you will just irritate.
  4. If troponins trend up or down, are substantially elevated, and/or there is an underlying condition that could be causing a supply-demand mismatch, query for Type 2 MI.
  5. If a patient dies with an elevated troponin prior to being able to demonstrate a trend, it is appropriate to query for an uncertain diagnosis of myocardial infarction. In this case, the diagnosis should really be Type 3 MI, but good luck getting that documented!

My loyal listeners know that my philosophy is to take excellent care of patients and to document well to get credit for having done so. We want the patient to look as sick and complex in the medical record as they look in real life. I do not believe this is padding the coffers. Patients with Type 2 MIs are sicker than patients with the same underlying condition without a Type 2 MI. We need to get this right.



Erica E. Remer, MD, CCDS

Erica Remer, MD, FACEP, CCDS, has a unique perspective as a practicing emergency physician for 25 years, with extensive coding, CDI, and ICD-10 expertise. As physician advisor for University Hospitals Health System in Cleveland, Ohio for four years, she trained 2,700 providers in ICD-10, closed hundreds of queries, fought numerous DRG clinical determination and medical necessity denials, and educated CDI specialists and healthcare providers with engaging, case-based presentations. She transitioned to independent consulting in July 2016. Dr. Remer is a member of the ICD10monitor editorial board and is the co-host on the popular Talk Ten Tuesdays weekly, live Internet radio broadcasts.

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