Feature | Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians
The Fourth Universal Definition of Myocardial Infarction presents a long-awaited update on how myocardial infarction (MI) is clinically defined.1 Among the many key takeaways, the document emphasizes the critical concept of how to differentiate among type 1 MI, type 2 MI and non-MI causes of troponin elevation (e.g., myocardial injury without infarction).
This guidance is essential given the a) increasing accountability for high-quality MI care; b) ongoing implementation of high-sensitivity cardiac troponin assays in the U.S.; and c) increasing number of medical conditions other than MI associated with elevated troponin levels.
The Fourth Universal Definition of MI also recognizes there are multiple stakeholders who rely on the accurate diagnosis of MI and non-MI troponin elevation, including patients, clinicians, hospitals/health systems and insurers.
Beyond the pathophysiologic mechanisms and general diagnostic considerations of different MI types, a separate group of physicians, clinical documentation specialists, coding experts and health policy experts from the ACC and American Heart Association (AHA) has focused on educating clinicians about the importance of accurately documenting MI and non-MI causes of troponin elevation in the medical record.1
This group has specifically worked with members of the 10th Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the Centers for Medicare and Medicaid Services (CMS) to more closely align MI documentation and coding practices with clinical practice guidelines.
This is critical because clinician documentation not only influences payment of hospital claims but may also unintentionally contribute to penalties, such as those associated with CMS’ Hospital Readmissions Reduction Program.2
To mirror the Key Points to Remember from the Fourth Universal Definition of MI document published on ACC.org,3 here we present a complementary document summarizing 10 key points clinicians must remember when documenting the type of MI or non-MI causes of troponin elevation.
Avoid reflexively documenting an MI whenever troponin levels are elevated.
Clinicians should avoid documenting an MI as a “default” diagnosis in patients with elevated troponin levels. To document an MI, troponin elevations must be accompanied by clear clinical evidence of active myocardial ischemia. Such evidence includes: 1) Overt clinical symptoms attributable to myocardial ischemia that are not readily explained by other presenting conditions (dyspnea in particular is a nonspecific symptom commonly attributed to ischemia but may be due to other active conditions); 2) New or dynamic ischemic ECG changes or pathological Q waves that are not explained by pre-existing conditions (such as left ventricular hypertrophy); or 3) New perfusion abnormalities or segmental wall motion abnormalities on noninvasive imaging in a pattern consistent with an ischemic etiology.4
Documentation of MI type requires identification of etiology (Figure).
Documentation of a type 1 MI (acute STEMI and NSTEMI) is supported by the presence of acute coronary thrombus (STEMI) or plaque rupture/erosion (NSTEMI) on coronary angiography,4 or a strong suspicion for acute thrombus or plaque rupture when angiography is unavailable or contraindicated. Type 1 MI (STEMI and NSTEMI) is generally a primary reason for a patient’s presentation to a hospital, and accordingly should be documented as the principal diagnosis in the discharge summary. In contrast, a type 2 MI results from imbalance between myocardial oxygen supply and demand that is unrelated to acute coronary thrombosis or plaque rupture.4 In general, treatment of a type 2 MI does not include antithrombotic therapy or urgent coronary angiography (as these may cause bleeding in medically complex patients), but rather should focus on resolving the underlying cause(s) of supply-demand mismatch. Accordingly, a type 2 MI should always be documented as a secondary diagnosis in the discharge summary, as it stems from an underlying (primary) cause (Figure).1
Terminology updates of MI types.
Historically, clinicians have documented “NSTEMI” as a “catch all” term to describe both type 1 NSTEMI and type 2 MI patients alike. However, since October 1, 2017, ICD-10 and CMS have implemented a new ICD-10 diagnosis code for type 2 MI (I21.A1), distinct from the ICD-10 diagnosis code for NSTEMI (I21.4).1 As such, now the term “NSTEMI” should only be used when referring to a type 1 MI. When referring to MI due to supply-demand mismatch, the term “type 2 MI” should be used. The term “type 2 NSTEMI” is no longer valid and should be eliminated from clinical documentation. For completeness, type 3 MI (suspected MI as a cause of sudden cardiac death), type 4 MI (PCI-related MI) and type 5 MI (CABG-related MI) are expected to be documented on an infrequent basis and would be coded under the common ICD-10 diagnosis code of I21.A9 (other MI types).
Documentation of the term “non-MI troponin elevation” (Figure).
In patients with elevated troponin levels without clear ischemic symptoms, ECG changes, and/or imaging or angiographic findings of acute myocardial ischemia, we recommend documenting “non-MI troponin elevation due to [underlying cause].” The term “non-MI troponin elevation” is appropriately used in the following clinical contexts:
- When referring to myocardial injury without infarction,4 of which there are myriad cardiac and systemic etiologies (Figure). Common examples include non-MI troponin elevations in patients with acute pericarditis, acute pulmonary embolism, or following cardiopulmonary resuscitation.
- In patients with advanced chronic kidney disease (e.g., one would document “non-MI troponin elevation due to end-stage renal disease”).
- When there is a suspicion of heterophile antibodies that can cause a falsely abnormal troponin assay (occurs in up to 3 percent of general population).5, 6
It is worth noting that the Fourth Universal Definition of MI document uses the terminology “myocardial injury without infarction” from a pathophysiologic standpoint. We are advocating the slightly different terminology of “non-MI troponin elevation” for clinical documentation purposes.
This is because there is no specific ICD-10 diagnosis code for “non-MI myocardial injury,” and thus documentation of “injury” creates uncertainty for professional coders regarding which diagnosis code to assign to the injury.
This uncertainty can lead to burdensome queries for clarification to the clinical team, errors in the assignment of diagnosis codes, and potentially poorer performance in quality metrics and value-based care programs (such as CMS’ Hospital Readmissions Reduction Program2) that rely on accurate assignment of diagnosis codes.
In contrast, documentation of “non-MI troponin elevation” will code to an “abnormal troponin” or “abnormal chemistry” code (ICD-10 code R79.89) and avoid this uncertainty. Therefore, until a separate diagnosis code for myocardial injury without infarction is established, we recommend the term “non-MI troponin elevation” be used for clinical documentation purposes.
Degree and pattern of troponin elevation.
A common clinical error is to assume that a markedly elevated troponin level must mean that a type 1 MI (STEMI or NSTEMI) has occurred. However, markedly elevated troponin levels have been observed in several non-MI conditions, including myocarditis, pericarditis, spontaneous implantable defibrillator shocks without acute ischemia, and even critically ill patients with sepsis.7,8
Another assumption is that a characteristic rise and fall in cardiac troponin seals the diagnosis of an acute MI, but such a “rise-and-fall” troponin pattern is also seen in many non-MI causes of troponin elevation (once again, the presence of ischemic symptoms, ECG findings, and/or findings on imaging or angiography is what differentiates an MI from a non-MI troponin elevation).
Troponin elevation in patients with heart failure exacerbation.
In the majority of patients with acute systolic or diastolic heart failure, an elevated troponin level is unrelated to type 1 MI.9
In acute heart failure, elevated troponin levels are commonly due to nonischemic mechanisms (e.g., apoptosis, autophagy and direct cellular toxicity of circulating neurohormones)4, 9 and are most appropriately documented as a non-MI troponin elevation due to acute heart failure.
In some cases of acute heart failure, the rise in troponin may be related to supply-demand mismatch due to increased transmural pressure, endothelial dysfunction, hypoxia or hypotension; in such cases, documenting a type 2 MI secondary to acute heart failure would be appropriate as long as there are also objective ischemic findings on ECG or on imaging.
In heart failure patients, the interpretation of dyspnea as an ischemic equivalent may be unreliable, and more emphasis should be placed on objective (ECG, imaging, angiographic) findings to distinguish heart failure associated with MI vs. without MI.
Troponin elevation in hypertensive emergency.
Troponin elevation is common in hypertensive emergency patients.10 The mechanisms of troponin elevation in patients with hypertensive emergency are multifactorial10 and may be ischemic (subendocardial ischemia) or nonischemic in nature.
Documentation of a type 2 MI secondary to hypertensive emergency is justified only when the patient has clear ischemic symptoms (again, caution must be exercised when interpreting the significance of isolated dyspnea) and/or ischemic findings on ECG, imaging and/or angiography.
Hypertensive emergency in patients with left ventricular hypertrophy may be associated with ST-T changes on ECG that are chronic, therefore in these patients dynamic ST-T changes are critical to distinguish hypertensive emergency with ischemia vs. without ischemia. When ischemic symptoms and objective findings of ischemia are lacking, it is more appropriate to document a non-MI troponin elevation in the setting of hypertensive emergency.
Troponin elevation in patients with tachyarrhythmias.
Elevated troponin levels in the setting of tachyarrhythmias, e.g., atrial fibrillation with rapid ventricular response (AFRVR) may represent a type 2 MI or a non-MI troponin elevation. While new ST depressions on ECG can generally be used to support a diagnosis of MI in patients with elevated troponin levels, this is not the case in patients with tachyarrhythmias.
In AFRVR in particular, the ECG may show diffuse ST depressions on ECG that mimic myocardial ischemia but in fact are nonischemic in nature and represents repolarization changes (termed “cardiac memory”).4
Once the acute tachyarrhythmia episode has resolved, provocative stress testing can be useful in diagnostically challenging cases to help distinguish a type 2 MI from a non-MI troponin elevation.11-13
Critically ill patients and perioperative patients.
Troponin elevations in critically ill patients and in perioperative patients may represent a type 1 MI, a type 2 MI or a non-MI troponin elevation.4 As always, conclusive documentation of either type 1 or type 2 MI requires objective evidence of ischemia on ECG, imaging, and/or angiography.
However, advanced cardiac testing is commonly deferred in critically ill patients or perioperative patients until they become more stable or even until after hospital discharge.
When cardiac testing is deferred to the outpatient setting, inpatient clinicians should use their best judgment when documenting the etiology of the troponin elevation, or should document that the cause of the troponin elevation remains uncertain at the time of discharge and may be investigated further as an outpatient.
Documenting uncertainty during the diagnostic workup.
It is permissible for clinicians to document uncertainty regarding the etiology of the elevated troponin level cut during the hospitalization, with subsequent refinement of the diagnosis before hospital discharge. For example, it is common (and acceptable) to not know the cause of a presenting patient’s troponin elevation and to document “rule out NSTEMI.” However, if the results of further inpatient testing and clinical observation suggest against the diagnosis of type 1 NSTEMI, clinicians must document “type 1 NSTEMI has been ruled out.”
- Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new icd-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation 2017;136:1180-2.
- McCarthy CP, Vaduganathan M, Singh A, et al. Type 2 myocardial infarction and the hospital readmission reduction program. J Am Coll Cardiol 2018;72:1166-70.
- Fourth Universal Definition of MI: Key Points. Available here. Accessed September 7, 2018.
- Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol 2018;Aug 25:[Epub ahead of print].
- Zaidi A, Cowell R. False positive cardiac troponin elevation due to heterophile antibodies: more common than we recognise? BMJ Case Rep 2010;2010. doi: 10.1136/bcr.11.2009.2477.
- Fleming SM, O’Byrne L, Finn J, Grimes H, Daly KM. False-positive cardiac troponin I in a routine clinical population. Am J Cardiol 2002;89:1212-5.
- Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest 2004;125:1877-84.
- Hasdemir C, Shah N, Rao AP, et al. Analysis of troponin I levels after spontaneous implantable cardioverter defibrillator shocks. J Cardiovasc Electrophysiol 2002;13:144-50.
- Januzzi JL Jr., Filippatos G, Nieminen M, Gheorghiade M. Troponin elevation in patients with heart failure: on behalf of the third Universal Definition of Myocardial Infarction Global Task Force: Heart Failure Section. Eur Heart J 2012;33:2265-71.
- Afonso L, Bandaru H, Rathod A, et al. Prevalence, determinants, and clinical significance of cardiac troponin-I elevation in individuals admitted for a hypertensive emergency. J Clin Hypertens 2011;13:551-6.
- Berger M, Emir M, Brünnler T, Rockmann F, Lehmann R. Non-coronary predictors of elevated high-sensitive cardiac troponin T (hs-cTnT) levels in an unselected emergency patient cohort. Clin Cardiol 2018;41:1055-61.
- Cediel G, Gonzalez-Del-Hoyo M, Carrasquer A, et al. Outcomes with type 2 myocardial infarction compared with non-ischaemic myocardial injury. Heart 2017;103:616-22.
- Smilowitz NR, Weiss MC, Mauricio R, et al. Provoking conditions, management and outcomes of type 2 myocardial infarction and myocardial necrosis. Int J Cardiol 2016;218:196-201.
Clinical Topics: Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Pericardial Disease, Stable Ischemic Heart Disease, Atherosclerotic Disease (CAD/PAD), Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Novel Agents, Acute Heart Failure, Chronic Heart Failure, Interventions and Coronary Artery Disease, Interventions and Imaging, Interventions and Vascular Medicine, Angiography, Nuclear Imaging
Keywords: ACC Publications, Cardiology Interventions, American Heart Association, Angiography, Coronary Angiography, Antibodies, Heterophile, Apoptosis, Atrial Fibrillation, Autophagy, Cardiopulmonary Resuscitation, Centers for Medicare and Medicaid Services (U.S.), Coronary Artery Disease, Coronary Thrombosis, Critical Illness, Death, Sudden, Cardiac, Defibrillators, Implantable, Depression, Depression, Diabetes Mellitus, Type 2, Documentation, Dyspnea, Electrocardiography, Fibrinolytic Agents, Health Policy, Heart Failure, Heart Failure, Diastolic, Hypertrophy, Left Ventricular, Hospitalization, Hypotension, Infarction, Inpatients, Insurance Carriers, International Classification of Diseases, Kidney Failure, Chronic, Medical Records, Medicare, Myocardial Infarction, Myocardial Ischemia, Myocarditis, Neurotransmitter Agents, Outpatients, Oxygen, Patient Readmission, Percutaneous Coronary Intervention, Pericarditis, Preexisting Condition Coverage, Pulmonary Embolism, Renal Insufficiency, Chronic, Sepsis, Specialization, Tachycardia, Troponin
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