Clinical Progress Notes: Updates from the 4th Universal Definition of Myocardial Infarction
© 2019 Society of Hospital
CLINICAL PRACTICE UPDATE
Proper distinction between infarction or injury without infarction is central to proper evaluation, treatment, and eventual documentation in patients with elevated troponin levels. In the case of T2MI and NIMI, identifying what underlying illness is causing the troponin elevation is essential for acute management.
Evaluation
Troponin elevation is associated with an elevated risk for major adverse cardiovascular events, regardless of etiology.4 While patients with suspected T1MI are most often evaluated by coronary angiography, this may not be necessary for patients with T2MI or NIMI. Developing an evaluation strategy for patients with T2MI or NIMI requires understanding the underlying etiology of myocardial injury. In patients with septic shock for example, there are many potential mechanisms for cardiac myocyte injury, many of which are nonischemic (eg, cytokine-mediated).5 Prompt evaluation and treatment of septic shock, therefore, often leads to resolution of cardiac dysfunction, and ischemic evaluation may not be necessary.6 In many cases of T2MI or NIMI, waiting for an acute underlying illness to resolve is necessary before deciding whether ischemic evaluation is appropriate. It is important that this decision is deferred but not forgotten though as patients with T2MI or NIMI may benefit from further cardiac evaluation. There are no society recommendations and minimal evidence to guide this evaluation, but clinical trials testing different evaluation strategies are underway.7 Until an optimal evidence-based evaluation strategy becomes clear, clinicians should focus on two key principles: first, determine and treat the underlying etiology; second, identify patients with traditional risk factors for CAD and consider further evaluation with either coronary angiography or cardiac imaging. Referral to a cardiologist for assistance with the latter issue, especially for challenging or equivocal cases, is encouraged.
Treatment
While T1MI therapies have a strong evidence base with high rates of appropriate treatment, there are relatively few evidence-based therapies for T2MI and NIMI. The benefits of traditional T1MI therapies should be considered in terms of each therapy’s risk-benefit profile. Among patients with T2MI or NIMI in whom atherosclerotic plaque rupture is unlikely, or in whom bleeding risk is high, antithrombotic agents such as unfractionated heparin and dual antiplatelet therapy represent low value and potentially harmful therapies.8 Conversely, patients with multiple risk factors for CAD may benefit from low-risk guideline directed medical therapies such as HMGCoA reductase inhibitors (ie, “statins”). Recent data suggest that lipid-lowering therapies may even be beneficial for preventing T2MI.9
Given the lack of evidence for therapies to treat patients with T2MI or NIMI, clinical judgment remains central to creating an optimal management plan. Clinicians should consider consultation with a cardiologist any time there is ambiguity in whether the diagnosis is T1MI or T2MI. For example, postoperative patients represent a particularly challenging clinical scenario due to the difficulty of assessing ischemic signs and symptoms in the operating room. In this setting, early evaluation by a cardiologist has been shown to improve outcomes.10
Documentation
Documentation of non-ST elevation MI (NSTEMI) for every case of elevated troponin, rather than using the more specific T1MI, T2MI, or NIMI terminology, can have adverse consequences for health systems. From a coding perspective, the terms STEMI and NSTEMI mean T1MI, and the ICD-10 codes used to identify T1MI patients for value-focused programs frequently include patients with T2MI and NIMI due to imprecise documentation.11 When T2MI and NIMI are imprecisely documented as NSTEMI, health systems and clinicians are held to the T1MI care standards. This can negatively skew the performance of a health system or individual clinician because T2MI and NIMI patients have worse outcomes than T1MI patients.4 Inaccurate categorization of patients can lead to inaccurate quality and registry reporting, which may hinder the ability of health systems to monitor and implement quality improvement programs for MI patients. The distinction between T1MI and T2MI in documentation is all the more important now that a new ICD-10 code exists for T2MI (I21.A1), which allows clinicians to more precisely identify these patients, both clinically and administratively, as distinct from T1MI patients.12 While there is no similarly specific ICD-10 code for NIMI, using the appropriate terminology in documentation should prompt coding personnel to use a code for “other abnormal findings of blood chemistry,” reflecting cardiac biomarker elevation (R79.89), rather than using one of the T1MI codes. Clinicians may not be able to determine the etiology of troponin elevation in the initial phase of a hospitalization, but a definitive diagnosis should be documented in the discharge summary.
