Misclassification of Myocardial Injury as Myocardial Infarction: Implications for Assessing Outcomes in Value-Based Programs

Key Points

Question  To what extent are patients with myocardial injury being misclassified as having type 2 myocardial infarction (T2MI) and what are the possible implications for 30-day readmission and mortality rates?

Findings  This study used the new International Statistical Classification of Diseases and Related Health Problems, Tenth Revision code to identify 633 patients who were coded as having T2MI. After strict adjudication, only 57% of patients met the criteria for T2MI and 42% had myocardial injury; both groups had similar in-hospital mortality rates and 30-day mortality and readmission rates.

Meaning  A substantial proportion of patients who are coded as having T2MI actually have myocardial injury, which likely has implications for hospital reimbursement under current policy programs.

Importance  Similar to other patients with acute myocardial infarction, patients with type 2 myocardial infarction (T2MI) are included in several value-based programs, including the Hospital Readmissions Reduction Program and the Hospital Value-Based Purchasing Program. To our knowledge, whether nonischemic myocardial injury is being misclassified as T2MI is unknown and may have implications for these programs.

Objective  To determine whether patients with nonischemic myocardial injury are being miscoded as having T2MI and if this has implications for 30-day readmission and mortality rates.

Design, Settings, and Participants  Using the new International Statistical Classification of Diseases and Related Health Problems, Tenth Revision code, we identified patients who were coded as having T2MI between October 2017 and May 2018 at Massachusetts General Hospital. Strict adjudication using the fourth universal definition of MI was then applied.

Main outcome and Measures  Clinical adjudication of T2MI and 30-day readmission and mortality rates as a function of T2MI or nonischemic myocardial injury.

Results  Of 633 patients, 369 (58.3%) were men and 514 (81.2%) were white. After strict adjudication, 359 (56.7%) had T2MI, 265 (41.9%) had myocardial injury, 6 (0.9%) had type 1 MI, and 3 (0.5%) had unstable angina. Patients with T2MI had a higher prevalence of cardiovascular comorbidities than those with myocardial injury. Patients with T2MI and myocardial injury had high in-hospital mortality rates (10.6% and 8.7%, respectively; P = .50). Of those discharged alive (563 [88.9%]), 30-day readmission rates (22.7% vs 21.1%; P = .68) and mortality rates (4.4% vs 7.4%; P = .14) were comparable among patients with T2MI and myocardial injury.

Conclusions and Relevance  A substantial percentage of patients coded as having T2MI actually have myocardial injury. Both conditions have high 30-day readmission and mortality rates. Including patients with high-risk myocardial injury may have substantial implications for value-based programs.

With the widespread introduction of high-sensitivity troponin assays, the detection of myocardial injury in hospitalized patients has become more frequent; currently, the most common cause of troponin elevation may now be nonischemic myocardial injury rather than acute myocardial infarction (MI).¹ The detection of abnormal troponin concentrations in the absence of ischemia has led to confusion; this circumstance has frequently been labeled as “troponinemia,” “troponinitis,” or incorrectly as a type 2 MI (T2MI; for which coronary ischemia is a prerequisite). To address this confusion, the fourth universal definition of MI distinguishes the various subtypes of MI from myocardial injury.² Specifically, myocardial injury is defined by at least 1 cardiac troponin concentration above the 99th percentile upper reference limit.² Myocardial infarction is a form of myocardial injury but requires clinical evidence of acute myocardial ischemia. The most common subtypes are type 1 MI (T1MI; characterized by plaque rupture, ulceration, erosion, or dissection resulting in coronary thrombosis) and T2MI (infarction from myocardial oxygen supply-demand mismatch in the absence of atherothrombosis).²

Currently, as with other patients with acute MI, patients with T2MI are included in several value-based programs, such as the Hospital Readmission Reduction Program and the Hospital Value-Based Purchasing Program.³ To our knowledge, how often patients with myocardial injury are being misclassified as T2MI is unknown and may have implications for these programs. Since an International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) code for T2MI was introduced in October 2017, there is an opportunity to characterize patients who are coded as having T2MI.

We identified patients coded as having T2MI (ICD-10 code, I21.A1) between October 2017 and May 2018 at Massachusetts General Hospital. Strict adjudication with physician medical record reviewers using the fourth universal definition of MI was then applied to confirm the diagnosis.² To ensure consistency with the diagnoses, uncertain cases were rereviewed by one of us (C.M). Myocardial injury was defined by a cardiac troponin T concentration of 0.03 ng/mL or more (to convert to micrograms per liter, multiply by 1; 10% coefficient of variation) or a fifth-generation high-sensitivity troponin T concentration of 10 ng/L or more for women or 15 ng/L or more for men. An MI was defined as a rising or falling elevation in cardiac troponin (conventional or high sensitivity) more than the 99th percentile and at least 1 of the following: (1) symptoms of ischemia, (2) new electrocardiographic evidence of ischemia, (3) new pathological Q waves, (4) new regional wall motions on imaging in an ischemic territory, or (5) coronary thrombus on angiography. Type 2 MI was defined as an MI with an identifiable preceding imbalance between myocardial oxygen supply and demand not associated with coronary thrombus.

Baseline characteristics, diagnostic testing, and treatments were compared between patients with T2MI and patients with nonischemic myocardial injury who were misclassified as having T2MI. This study was approved by the Partners HealthCare institutional review board and as it was a retrospective study, the data reported are deidentified, and patient consent was not required. In-hospital outcomes and postdischarge 30-day mortality and readmission rates at Massachusetts General Hospital or outside institutions (identified by a medical record review of available records from outside institutions and data linked to our medical record system via Care Everywhere [EPIC]) were recorded. In-hospital outcomes and 30-day readmission and mortality rates were compared using the Fisher exact test. Time-to-postdischarge events were compared using log-rank tests. Statistical analyses were performed using Stata, version 14.1 (StataCorp) and statistical significance was set at P < .05.

Over the study period, we identified 633 patients who were coded as having T2MI. Following adjudication, 359 (56.7%) met criteria for T2MI, 265 (41.9%) had myocardial injury, 6 (0.9%) had T1MI, and 3 (0.5%) had unstable angina.

Patients with adjudicated T2MI had a higher prevalence of known coronary artery disease (50.6% vs 33.2%; P < .001), prior MI (21.8% vs 14.3%; P = .02), heart failure (52.4% vs 37.4%; P < .001), and peripheral arterial disease (23% vs 12.1%; P < .001) and a lower prevalence of malignancy (27.2% vs 19.8%; P = .03) than patients with myocardial injury (Table 1). Patients with adjudicated T2MI underwent more inpatient echocardiography (67.7% vs 55.5%; P = .002), stress testing (9.2% vs 4.5%; P = .03), and coronary angiography (12.3% vs 2.6%; P < .001) than patients with myocardial injury. Prescriptions of aspirin (69.1% vs 61.1%; P = .04) and clopidogrel (10.6% vs 5.7%; P = .03) were higher on discharge among patients with T2MI compared with those with myocardial injury (Table 2).

In-hospital outcomes were similar among patients with T2MI and myocardial injury, including all-cause mortality (10.6% vs 8.7%; P = .50), cardiovascular mortality (2.5% vs 0.8%; P = .18), recurrent MI (3.3% vs 1.1%; P = .11), stroke (1.1% vs 1.9%; P = .51), and median length of stay (6 days [interquartile range, 4.0-12.0] vs 7 days [interquartile range, 4.0-12.0]; P = .15). Of those discharged alive (n = 563), 30-day readmission rates (22.7% vs 21.1%; P = .68) and 30-day mortality rates (4.4% vs 7.4%; P = .14) were comparable among patients with T2MI and myocardial injury (Figure).

After the introduction of a new ICD-10 code for T2MI at a large tertiary care center, we observed several findings. Patients with nonischemic myocardial injury frequently receive incorrect diagnoses and are billed as having T2MI (approximately 265 patients [41%] coded as having T2MI actually had nonischemic myocardial injury). Patients with myocardial injury and T2MI face high in-hospital mortality (8%-10%), 30-day mortality (4%-7%), and 30-day readmission rates (21%-22%). These findings not only indicate the challenge of correctly distinguishing myocardial injury from infarction, but also demonstrate the high risk of patients with injury.

Miscoding myocardial injury as MI has substantial financial ramifications, as such events would be captured under readmission penalties and/or value-based programs. For instance, the Hospital Value-Based Purchasing Program creates an incentive payment fund by reducing inpatient Medicare payments by 2% and then distributes the fund to hospitals by applying a value-based adjustment factor that is determined by the hospital’s total performance score (which includes inpatient mortality rates for MI). Based on performance levels, some hospitals will earn less than the 2% back, resulting in a “penalty,” while other hospitals will earn more than 2% back and receive a “bonus.” Current inpatient mortality rates for acute MI based on national registry data in the United States are approximately 4.6%,⁴ almost half the inpatient mortality rate for nonischemic myocardial injury seen in this study (8.7%). Thirty-day readmission rates for myocardial injury in this study are higher than the national 30-day readmission rates for acute MI (21% vs 14.8%),⁵ and many patients with T2MI are included in Hospital Readmission Reduction Program penalties.⁶ Because the methods for these programs effectively compare hospitals against one another, hospitals that include high-risk patients with myocardial injury as having T2MI may perform more poorly in value-based payment programs. Alternatively, because patients with myocardial injury may have more comorbidities than the general MI population, including patients with myocardial injury patients could conceivably reduce risk-standardized mortality and readmission rates.

This single-center observational study has certain limitations. The observed misdiagnosis rates of T2MI may not be generalizable to other health systems. Furthermore, physician coding practices may change as they have more experience with the new billing code. Finally, from this analysis we cannot determine how these results may differentially affect hospitals with different populations of patients. Further analyses, including simulations with risk-adjustment, would be required to assess the likely association with hospital reimbursement.

A substantial percentage of patients with myocardial injury may be miscoded as having T2MI. Both conditions have high 30-day readmission and mortality rates. This may have substantial implications for hospital reimbursement under value-based programs.

Accepted for Publication: February 1, 2019.

Corresponding Author: Jason H. Wasfy, MD, MPhil, Cardiology Division/GRB 804, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114 (jwasfy@mgh.harvard.edu).

Published Online: March 17, 2019. doi:10.1001/jamacardio.2019.0716

Author Contributions: Dr McCarthy had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: McCarthy, Cohen, Vaduganathan, Januzzi Jr, Wasfy.

Acquisition, analysis, or interpretation of data: McCarthy, Murphy, Cohen, Rehman, Jones-O'Connor, Olshan, Singh, Wasfy.

Drafting of the manuscript: McCarthy, Cohen, Rehman, Jones-O'Connor, Januzzi Jr, Wasfy.

Critical revision of the manuscript for important intellectual content: Murphy, Cohen, Olshan, Singh, Vaduganathan, Januzzi Jr, Wasfy.

Statistical analysis: McCarthy, Cohen, Jones-O'Connor, Singh, Wasfy.

Obtained funding: Wasfy.

Administrative, technical, or material support: Murphy, Cohen, Rehman.

Supervision: Januzzi Jr, Wasfy.

Conflict of Interest Disclosures: Dr Vaduganathan reported grant support from a KL2/Catalyst Medical Research Investigator Training award from Harvard Catalyst funded by the National Institutes of Health/National Center for Advancing Translational Sciences and serves on advisory boards for AstraZeneca, Bayer AG, and Baxter Healthcare. Dr Januzzi Jr reported grants and personal fees from Roche, Siemens, and Abbott. Dr Wasfy reported grants from the American Heart Association, National Institutes of Health, and Harvard Catalyst during the conduct of the study. No other disclosures were reported.

Meeting Presentation: This study was presented at the American College of Cardiology 2019 Annual Meeting; March 17, 2019; New Orleans, Louisiana.