ICD-10-CM supports this new classification system.

Four major cardiology associations have once again collaborated to update the universal standard definition of myocardial infarction (MI), and this effort was more ambitious than any prior effort.

In a document published simultaneously by the American College of Cardiology (ACC), the American Heart Association (AHA), the European Society of Cardiology (ESC), and the World Heart Federation (WHF), the organizations furthered the framework of the five-category MI definition. Also, for the first time since the publishing of the universal definitions, ICD-10-CM currently supports this classification system.

For those who may not be familiar with the history of MI definitions, the first universal definition was put forth by the ACC and ESC in 2000. This definition called for a rise/fall in cardiac troponin (cTn) or CK-MB associated with ischemic symptoms, development of pathologic Q waves or ST segment elevation or depression on ECG, or the need for coronary artery intervention. The second universal definition, put forth in 2007, first introduced the five-category MI definition.

The five types of MI introduced (that are still used today) are the following:

  • Type 1 – spontaneous MI due to a primary coronary event such as plaque rupture or erosion
  • Type 2 – MI due to either increased oxygen demand or decreased supply
  • Type 3 – MI resulting in death before cardiac enzymes can be obtained
  • Type 4 – MI associated with percutaneous coronary intervention (PCI) or stent thrombosis
  • Type 5 – MI associated with CABG procedure

The third universal definition, published in 2012, further refined these categories of MI in light of more sensitive biomarker tests, and introduced the idea of myocardial injury as a distinct clinical entity from myocardial infarction.

Since the introduction of the concept of MI types 2-5 in 2007, much debate has been published both supporting and criticizing the new categories – especially of Type 2 MI.

The clinical literature has supported the heightened risk faced by patients who suffer Type 2 MIs, with even higher mortality rates than Type 1 MIs being recorded in some studies. However, providers over the years have been reluctant to diagnose a Type 2 MI because there was not a separate ICD code for it, and those patients would be thrown into cardiology registries intended for “Type 1 MIs.” Apparent quality would suffer because those Type 2 MI patients didn’t receive statin drugs or aspirin or cardiac rehab referrals. In addition, many providers considered “demand ischemia” a more proper diagnosis, which coded to a non-MI code, and wouldn’t be considered an MI for insurance or pilot license purposes. There were rumblings of a fourth universal MI definition in the works; would it totally rework the MI definition and scrap the five-category framework?

We now have our answer, and it is a resounding “no.” The five types of MI are alive and well, with the four major cardiology societies doubling down on this classification system as the proper basis for clinical care, research, and epidemiologic MI classification for years to come. Like the third universal definition did for the second, the fourth universal definition adds clarity on how newer and more sensitive tests, such as high-sensitivity cardiac troponin (hs-cTn) and late gadolinium enhanced cardiac magnetic resonance (LGE-CMR), fit into the classification scheme first introduced in 2007. If you haven’t learned the classification system yet, it’s about time you did, as it ain’t going anywhere.

So let’s dive in.

The diagnosis of a Type 1 or Type 2 MI is dependent on having a rise and/or fall in cardiac troponin (cTn), with at least one value above the 99th percentile upper reference limit (URL) and clinical evidence of acute myocardial ischemia. Thus, it is a two-part definition, and you must have evidence of  both. Clinical evidence of myocardial ischemia is explicitly stated as at least one of the following:

  • Symptoms (what the patient reports) of myocardial ischemia
  • New ischemic ECG changes
  • Development of pathological Q waves (also a type of ECG change)
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
  • Identification of a coronary thrombus by angiography or autopsy (for Type 1 only)

Depending on the specific assay used, and whether it is a

hs-cTn or regular cTn test, the 99th percentile URL will change, but will be listed by the manufacturer of that assay. However, all can be used in conjunction with the MI definition.

The fourth universal definition does state that the epidemiologic incidence of MI will rise as providers use more and more sensitive cTn tests, but the definition is remaining the same, because these small and early rises detected by

hs-cTn are clinically meaningful, with abnormal values being predictive of poorer outcomes.

The fourth universal definition further clarifies Types 4b and 4c MIs, using the same definition as for Type 1 MIs. Type 4b MI is related to stent thrombosis, and is now divided into four time periods relative to the stent insertion. 0-24 hours is acute, 1-30 days is subacute, 30 days to one year is late, and more than one year is very late. Type 4c MI is an MI related to focal or diffuse restenosis of a prior stent or angioplasty site.

The concept of myocardial injury, introduced in the third universal definition, received much greater emphasis in the fourth universal definition. Simply defined, myocardial injury is the detection of any cardiac troponin level above the 99th percentile URL.

If there is a rise and/or fall of cTn, then the myocardial injury is acute. If there is not, then the myocardial injury is chronic. Myocardial injury is thus half of the definition of Type 1 or Type 2 MI. The other half, of course, is whether evidence of acute myocardial ischemia is present. Thus, if acute myocardial injury is coming from heart cells not getting enough oxygen, then it is an MI. If the acute myocardial injury is coming from viral inflammation, chest trauma, or myocardial stretch, then the proper diagnosis is acute myocardial injury and not an MI. Myocardial injury codes to the S26.- “injury of heart” family of ICD-10-CM codes, rather than the I21.- “acute MI” family of codes.

The other types of MI, Types 3, 4a, and 5, are specified in greater detail than in the prior universal definitions, but the concept is unchanged. Type 3 represents an MI in which cardiac enzymes were not able to be obtained, usually due to death occurring but potentially also due to lack of laboratory resources in some countries.

Type 4a is an MI that occurs around the time of percutaneous coronary intervention. Type 5 is an MI that occurs around the time of coronary artery bypass grafting (CABG). The time period for these two types of MI is now within 48 hours of the procedure. The degree of troponin elevation alone is not sufficient to diagnose a Type 4a or 5 MI; another specified objective finding (such as new wall motion abnormality) must also be met. Also, because the rise in troponin could be due to the event (like a Type 1 MI) that led to the PCI or CABG, in order to diagnose a Type 4a or 5 MI, the baseline troponin level must be normal, stable, or falling before the criteria are applied.

The fourth universal definition also devotes significant airtime to certain common clinical situations in which the diagnosis of MI may be particularly difficult. Patients with chronic renal failure are known to often have chronically elevated cTn levels. The new definition is still applicable to these patients. A rise and/or fall in troponin, together with clinical evidence of myocardial ischemia, should still be used to diagnose an MI in this patient population.

Patients with heart failure also frequently have elevated cTn levels, and they also have shortness of breath. The new definition recommends caution in labeling shortness of breath as the clinical evidence of myocardial ischemia resulting in an MI diagnosis. However, a significant rise and/or fall of cTn, with a compatible history suggesting myocardial ischemia, should lead to a high suspicion for a Type 1 MI. Cardiac imaging can assist in helping to clarify the proper diagnosis.

Patients with tachycardia syndromes that resolve may experience “cardiac memory,” which is an electrical remodeling phenomenon that can lead to EKG changes that alone may not represent myocardial ischemia. A changing pattern of cTn, careful history taking, and myocardial imaging may assist in differentiating an MI from “cardiac memory.”

There are also new sections in the fourth definition that describe other sometimes-encountered situations, such as Takotsubo Syndrome and MI with non-obstructive coronary arteries (MINOCA). Newer cardiac imaging modalities are also described, as well as their potential usage in diagnosing MIs.

In summary, the fourth universal definition of MI really didn’t retract anything from the second and third universal definitions. What it does do, however, is provide much greater clarity on how to approach diagnostic dilemma situations, and how to use the newer and more sensitive troponin assays and imaging modalities to help clarify the diagnosis.

As much as this article is your “user’s guide” to the fourth universal definition, the new definition itself is designed as a “user’s guide” to diagnosing MI with the tools now at clinicians’ disposal in 2018.

The full text article of the Fourth Universal Definition of Myocardial Infarction (2018) may be accessed here.

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Edward Hu, MD CHCQM-PHYADV is a board-certified internist and is the current president of the American College of Physician Advisors (ACPA). Dr. Hu is executive director of Inpatient Physician Advisor Services for the University of North Carolina Health Care System. Opinions expressed are his own and not representative of ACPA or UNC.

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