International Journal of Cardiology 186 (2015) 54–56
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Accuracy of acute myocardial infarction clinical diagnosis and its implications David M. Lofthus a, Houman Khalili a, Vijay N. Raja a, Christopher J. Regan b, Jay Y. Gadgil a, Demetrio Castillo a, Kazeen N. Abdullah c, Colby R. Ayers a, James A. de Lemos a, Sandeep R. Das a,⁎ a b c
Cardiology Division, University of Texas Southwestern Medical Center, Dallas, TX, United States Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, United States Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States
a r t i c l e
i n f o
Article history: Received 5 March 2015 Accepted 19 March 2015 Available online 20 March 2015 Keywords: Acute myocardial infarction type Diagnosis Coding Documentation
Myocardial infarction (MI) represents a spectrum of clinical entities as outlined by the Universal Definition of MI [1]. Type 1 MI, consisting of ST elevation MI (STEMI) and type 1 non-ST elevation MI (NSTEMI), occurs in the setting of spontaneous plaque rupture, ulceration, or dissection, with platelet activation and intraluminal thrombus formation [1], whereas type 2 MI is caused by myocardial oxygen supply–demand mismatch without spontaneous plaque rupture [2]. The majority of clinical trial evidence and guideline-based therapies are directed at type 1 events [3,4], while treatment for type 2 MI lacks a universal standard and is aimed at the underlying precipitant of supply–demand mismatch. Importantly, the International Classification of Diseases, Revisions 9 (ICD-9) and 10 (ICD-10) coding systems do not provide separate diagnosis codes to distinguish type 1 MI from other MI subtypes. Since quality metrics and performance measures are based on evidence-based therapies for type 1 MI, hospitals may therefore be held accountable for applying these quality standards to patients with type 2 MI even though these therapies are unproven and could even cause harm in such patients [5]. Given limited data evaluating the concordance between coded diagnoses of MI and adjudicated MI subtypes, we evaluated inpatient encounters at our institutions with a primary coded diagnosis of MI to determine the appropriate clinical MI subtype, and ⁎ Corresponding author at: Cardiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-8830, United States. E-mail address: [email protected] (S.R. Das).
http://dx.doi.org/10.1016/j.ijcard.2015.03.271 0167-5273/© 2015 Published by Elsevier Ireland Ltd.
examined the associations between MI subtype and treatment with guideline-based therapies. We retrospectively examined every inpatient encounter during calendar year 2013 with a final primary coded diagnosis of acute MI (ICD-9 codes 410–410.92) at our two affiliated hospitals — Parkland Memorial Hospital (PMH), a 968-bed teaching hospital that serves as the safetynet hospital for Dallas County, and St. Paul University Hospital (SPUH), a 300-bed private teaching hospital and quaternary referral center in Dallas, TX. There were 289 and 139 patient encounters at each hospital, respectively. Each case was adjudicated by two independent investigators with subspecialty cardiology training utilizing all available medical records, and classified using the Universal MI Definition [1] as STEMI; type 1 NSTEMI; type 2 NSTEMI either in the presence or absence of known coronary artery disease (CAD); periprocedural MI; or no MI. In the event of disagreement between the two initial adjudicators, the final classification was determined by committee review and majority vote. Evidence-based therapies were extracted from the electronic medical record (EMR), including discharge prescription for aspirin, P2Y12-inhibitors, statins, beta-blockers, and revascularization status. Patients were excluded from the denominator for a particular therapy if there was a documented contraindication. Readmission within 30 days of discharge and mortality within 30 days of index hospitalization were determined by EMR review, with data combined for PMH and SPUH due to low numbers of events. Quality metrics and outcomes were compared between patients adjudicated to type 1 MI versus all other diagnosis categories. A weighted kappa statistic was used to determine inter-rater agreement for MI classification. Summary statistics for categorical variables are reported as percentages, with Pearson's chi-squared test used to determine significance. Statistical analyses were performed using SAS version 9.2 (SAS Institute, Cary, NC). The independent reviewers agreed upon the MI classification in 83% of cases, with kappa statistic 0.76. At PMH, 76.7% of MI cases were adjudicated as type 1 MI, with 20.9% STEMI, 55.8% type 1 NSTEMI, 12.0% type 2 NSTEMI with underlying CAD, 3.1% type 2 NSTEMI without underlying CAD, and 6.9% as non-MI cases (Fig. 1, panel A). A similar distribution was seen for encounters at SPUH (Fig. 1, panel B). At both PMH and SPUH, rates of discharge aspirin, P2Y12-inhibitor, and revascularization were all significantly higher among patients with versus without type
D.M. Lofthus et al. / International Journal of Cardiology 186 (2015) 54–56
55
Fig. 1. Frequencies of adjudicated diagnoses at Parkland Memorial Hospital (A) and St. Paul University Hospital (B). STEMI indicates ST elevation myocardial infarction; NSTEMI, non-ST elevation myocardial infarction; CAD, coronary artery disease; MI, myocardial infarction.
1 MI, as was statin use at PMH. No difference was seen with betablocker use at either hospital or statin use at SPUH (Table 1). Rates of death (4.6% vs 4.3%, p = 0.86) and readmission (19.1% vs 18.2%, p = 0.82) at 30 days were not significantly different between patients with versus without type 1 MI. This analysis demonstrates that approximately 25% of patient encounters at our institutions with a primary coded diagnosis of acute MI did not represent type 1 MI events. Encounters not adjudicated as type 1 MI were significantly less likely to have received guidelinerecommended MI therapies, with marked differences seen in use of P2Y12-inhibitors and revascularization and more modest differences in use of aspirin and statins. The most common diagnosis after type 1 MI was type 2 NSTEMI. Previous studies of acute MI databases have shown variable proportions of type 2 MI ranging from 1.6% to 29.6% [6–8], likely reflective of heterogeneous underlying pathophysiology, differences in patient populations, and possibly inclusion of non-MI causes of troponin elevations [5]. Table 1 Rates of therapies at time of discharge. PMH Therapy (%)
a
Aspirin P2Y12-inhibitor Statin Beta-blocker Revascularization
SPUH
Type 1 MI
Other diagnoses
p value
Type 1 MI
Other diagnoses
p value
100 99.5 98.6 98.6 96.4
95.2 67.9 93.9 97.0 51.4
0.001 b0.0001 0.032 0.392 b0.0001
100 75.8 97.1 97.9 94.4
93.1 52.2 93.1 96.4 57.9
0.007 0.024 0.321 0.646 b0.0001
PMH = Parkland Memorial Hospital; SPUH = St. Paul University Hospital; MI = myocardial infarction. a Excluding patients with documented contraindication to therapy.
Collectively this may explain why no treatment standard exists for type 2 MI, and supports the inaccuracy of applying type 1 MI treatment standards to these diagnoses. An important issue highlighted by this study is a discord that can occur between clinician documentation, which is focused on patient care, and coder interpretation, which is bound by strict abstraction protocols as well as by restrictions inherent to coding systems like ICD-9. While a clinician may clearly describe a type 2 NSTEMI due to myocardial oxygen supply–demand mismatch as distinct from a plateletmediated arterial thrombotic event, ‘NSTEMI’ is coded the same for both MI subtypes. This is relevant because hospitals are graded and compared by their performance on guideline-based quality metrics for patients with coded diagnoses of acute MI [9]. Our data suggest important differences in treatments based on clinical understanding of distinct pathophysiology of MI subtypes, which may be appropriate on clinical grounds. The clustering of all MI subtypes together in current billing codes therefore serves to confound the assessment of MI process and outcome measures, with implications on pay-for-performance incentives and quality reporting. Our study has several limitations, including restriction to two hospitals, small numbers of mortality events, and 30-day follow-up information that was limited to our two institutions. However, we believe our findings raise important issues regarding the accuracy of acute MI documentation and coding, the implications of which merit further investigation. Conflict of interest Dr. de Lemos has received grant support from Abbott Diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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D.M. Lofthus et al. / International Journal of Cardiology 186 (2015) 54–56
Acknowledgments None.
References [1] K. Thygesen, J.S. Alpert, A.S. Jaffe, M.L. Simoons, B.R. Chaitman, H.D. White, Third universal definition of myocardial infarction, Circulation 126 (2012) 2020–2035. [2] J.S. Alpert, K.A. Thygesen, H.D. White, A.S. Jaffe, Diagnostic and therapeutic implications of type 2 myocardial infarction: review and commentary, Am. J. Med. 127 (2014) 105–108. [3] E.A. Amsterdam, N.K. Wenger, R.G. Brindis, D.E. Casey Jr., T.G. Ganiats, D.R. Holmes Jr., et al., 2014 AHA/ACC guideline for the management of patients with non-STelevation acute coronary syndromes, J. Am. Coll. Cardiol. 64 (2014) e139–228.
[4] P.T. O'Gara, F.G. Kushner, D.D. Ascheim, D.E. Casey Jr., M.K. Chung, J.A. de Lemos, et al., 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction, Circulation 127 (2013) e362–425. [5] J.A. de Lemos, Increasingly sensitive assays for cardiac troponins: a review, JAMA 309 (2013) 2262–2269. [6] L. Saaby, T.S. Poulsen, A.C. Diederichsen, S. Hosbond, T.B. Larsen, H. Schmidt, et al., Classification of myocardial infarction: frequency and features of type 2 myocardial infarction, Am. J. Med. 126 (2013) 789–797. [7] T. Baron, K. Hambraeus, J. Sundström, D. Erlinge, T. Jernberg, B. Lindahl, Type 2 myocardial infarction in clinical practice, Heart 101 (2015) 101–106. [8] T. Melberg, R. Burman, K. Dickstein, The impact of the 2007 ESC-ACC-AHA-WHF universal definition on the incidence and classification of acute myocardial infarction: a retrospective cohort study, Int. J. Cardiol. 139 (2010) 228–233. [9] Y. Sandoval, S.W. Smith, S.E. Thordsen, F.S. Apple, Supply/demand type 2 myocardial infarction: should we be paying more attention? J. Am. Coll. Cardiol. 63 (2014) 2079–2087.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Accuracy of acute myocardial infarction clinical diagnosis and its implications David M. Lofthus a, Houman Khalili a, Vijay N. Raja a, Christopher J. Regan b, Jay Y. Gadgil a, Demetrio Castillo a, Kazeen N. Abdullah c, Colby R. Ayers a, James A. de Lemos a, Sandeep R. Das a,⁎ a b c
Cardiology Division, University of Texas Southwestern Medical Center, Dallas, TX, United States Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, United States Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States
a r t i c l e
i n f o
Article history: Received 5 March 2015 Accepted 19 March 2015 Available online 20 March 2015 Keywords: Acute myocardial infarction type Diagnosis Coding Documentation
Myocardial infarction (MI) represents a spectrum of clinical entities as outlined by the Universal Definition of MI [1]. Type 1 MI, consisting of ST elevation MI (STEMI) and type 1 non-ST elevation MI (NSTEMI), occurs in the setting of spontaneous plaque rupture, ulceration, or dissection, with platelet activation and intraluminal thrombus formation [1], whereas type 2 MI is caused by myocardial oxygen supply–demand mismatch without spontaneous plaque rupture [2]. The majority of clinical trial evidence and guideline-based therapies are directed at type 1 events [3,4], while treatment for type 2 MI lacks a universal standard and is aimed at the underlying precipitant of supply–demand mismatch. Importantly, the International Classification of Diseases, Revisions 9 (ICD-9) and 10 (ICD-10) coding systems do not provide separate diagnosis codes to distinguish type 1 MI from other MI subtypes. Since quality metrics and performance measures are based on evidence-based therapies for type 1 MI, hospitals may therefore be held accountable for applying these quality standards to patients with type 2 MI even though these therapies are unproven and could even cause harm in such patients [5]. Given limited data evaluating the concordance between coded diagnoses of MI and adjudicated MI subtypes, we evaluated inpatient encounters at our institutions with a primary coded diagnosis of MI to determine the appropriate clinical MI subtype, and ⁎ Corresponding author at: Cardiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-8830, United States. E-mail address: [email protected] (S.R. Das).
http://dx.doi.org/10.1016/j.ijcard.2015.03.271 0167-5273/© 2015 Published by Elsevier Ireland Ltd.
examined the associations between MI subtype and treatment with guideline-based therapies. We retrospectively examined every inpatient encounter during calendar year 2013 with a final primary coded diagnosis of acute MI (ICD-9 codes 410–410.92) at our two affiliated hospitals — Parkland Memorial Hospital (PMH), a 968-bed teaching hospital that serves as the safetynet hospital for Dallas County, and St. Paul University Hospital (SPUH), a 300-bed private teaching hospital and quaternary referral center in Dallas, TX. There were 289 and 139 patient encounters at each hospital, respectively. Each case was adjudicated by two independent investigators with subspecialty cardiology training utilizing all available medical records, and classified using the Universal MI Definition [1] as STEMI; type 1 NSTEMI; type 2 NSTEMI either in the presence or absence of known coronary artery disease (CAD); periprocedural MI; or no MI. In the event of disagreement between the two initial adjudicators, the final classification was determined by committee review and majority vote. Evidence-based therapies were extracted from the electronic medical record (EMR), including discharge prescription for aspirin, P2Y12-inhibitors, statins, beta-blockers, and revascularization status. Patients were excluded from the denominator for a particular therapy if there was a documented contraindication. Readmission within 30 days of discharge and mortality within 30 days of index hospitalization were determined by EMR review, with data combined for PMH and SPUH due to low numbers of events. Quality metrics and outcomes were compared between patients adjudicated to type 1 MI versus all other diagnosis categories. A weighted kappa statistic was used to determine inter-rater agreement for MI classification. Summary statistics for categorical variables are reported as percentages, with Pearson's chi-squared test used to determine significance. Statistical analyses were performed using SAS version 9.2 (SAS Institute, Cary, NC). The independent reviewers agreed upon the MI classification in 83% of cases, with kappa statistic 0.76. At PMH, 76.7% of MI cases were adjudicated as type 1 MI, with 20.9% STEMI, 55.8% type 1 NSTEMI, 12.0% type 2 NSTEMI with underlying CAD, 3.1% type 2 NSTEMI without underlying CAD, and 6.9% as non-MI cases (Fig. 1, panel A). A similar distribution was seen for encounters at SPUH (Fig. 1, panel B). At both PMH and SPUH, rates of discharge aspirin, P2Y12-inhibitor, and revascularization were all significantly higher among patients with versus without type
D.M. Lofthus et al. / International Journal of Cardiology 186 (2015) 54–56
55
Fig. 1. Frequencies of adjudicated diagnoses at Parkland Memorial Hospital (A) and St. Paul University Hospital (B). STEMI indicates ST elevation myocardial infarction; NSTEMI, non-ST elevation myocardial infarction; CAD, coronary artery disease; MI, myocardial infarction.
1 MI, as was statin use at PMH. No difference was seen with betablocker use at either hospital or statin use at SPUH (Table 1). Rates of death (4.6% vs 4.3%, p = 0.86) and readmission (19.1% vs 18.2%, p = 0.82) at 30 days were not significantly different between patients with versus without type 1 MI. This analysis demonstrates that approximately 25% of patient encounters at our institutions with a primary coded diagnosis of acute MI did not represent type 1 MI events. Encounters not adjudicated as type 1 MI were significantly less likely to have received guidelinerecommended MI therapies, with marked differences seen in use of P2Y12-inhibitors and revascularization and more modest differences in use of aspirin and statins. The most common diagnosis after type 1 MI was type 2 NSTEMI. Previous studies of acute MI databases have shown variable proportions of type 2 MI ranging from 1.6% to 29.6% [6–8], likely reflective of heterogeneous underlying pathophysiology, differences in patient populations, and possibly inclusion of non-MI causes of troponin elevations [5]. Table 1 Rates of therapies at time of discharge. PMH Therapy (%)
a
Aspirin P2Y12-inhibitor Statin Beta-blocker Revascularization
SPUH
Type 1 MI
Other diagnoses
p value
Type 1 MI
Other diagnoses
p value
100 99.5 98.6 98.6 96.4
95.2 67.9 93.9 97.0 51.4
0.001 b0.0001 0.032 0.392 b0.0001
100 75.8 97.1 97.9 94.4
93.1 52.2 93.1 96.4 57.9
0.007 0.024 0.321 0.646 b0.0001
PMH = Parkland Memorial Hospital; SPUH = St. Paul University Hospital; MI = myocardial infarction. a Excluding patients with documented contraindication to therapy.
Collectively this may explain why no treatment standard exists for type 2 MI, and supports the inaccuracy of applying type 1 MI treatment standards to these diagnoses. An important issue highlighted by this study is a discord that can occur between clinician documentation, which is focused on patient care, and coder interpretation, which is bound by strict abstraction protocols as well as by restrictions inherent to coding systems like ICD-9. While a clinician may clearly describe a type 2 NSTEMI due to myocardial oxygen supply–demand mismatch as distinct from a plateletmediated arterial thrombotic event, ‘NSTEMI’ is coded the same for both MI subtypes. This is relevant because hospitals are graded and compared by their performance on guideline-based quality metrics for patients with coded diagnoses of acute MI [9]. Our data suggest important differences in treatments based on clinical understanding of distinct pathophysiology of MI subtypes, which may be appropriate on clinical grounds. The clustering of all MI subtypes together in current billing codes therefore serves to confound the assessment of MI process and outcome measures, with implications on pay-for-performance incentives and quality reporting. Our study has several limitations, including restriction to two hospitals, small numbers of mortality events, and 30-day follow-up information that was limited to our two institutions. However, we believe our findings raise important issues regarding the accuracy of acute MI documentation and coding, the implications of which merit further investigation. Conflict of interest Dr. de Lemos has received grant support from Abbott Diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
56
D.M. Lofthus et al. / International Journal of Cardiology 186 (2015) 54–56
Acknowledgments None.
References [1] K. Thygesen, J.S. Alpert, A.S. Jaffe, M.L. Simoons, B.R. Chaitman, H.D. White, Third universal definition of myocardial infarction, Circulation 126 (2012) 2020–2035. [2] J.S. Alpert, K.A. Thygesen, H.D. White, A.S. Jaffe, Diagnostic and therapeutic implications of type 2 myocardial infarction: review and commentary, Am. J. Med. 127 (2014) 105–108. [3] E.A. Amsterdam, N.K. Wenger, R.G. Brindis, D.E. Casey Jr., T.G. Ganiats, D.R. Holmes Jr., et al., 2014 AHA/ACC guideline for the management of patients with non-STelevation acute coronary syndromes, J. Am. Coll. Cardiol. 64 (2014) e139–228.
[4] P.T. O'Gara, F.G. Kushner, D.D. Ascheim, D.E. Casey Jr., M.K. Chung, J.A. de Lemos, et al., 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction, Circulation 127 (2013) e362–425. [5] J.A. de Lemos, Increasingly sensitive assays for cardiac troponins: a review, JAMA 309 (2013) 2262–2269. [6] L. Saaby, T.S. Poulsen, A.C. Diederichsen, S. Hosbond, T.B. Larsen, H. Schmidt, et al., Classification of myocardial infarction: frequency and features of type 2 myocardial infarction, Am. J. Med. 126 (2013) 789–797. [7] T. Baron, K. Hambraeus, J. Sundström, D. Erlinge, T. Jernberg, B. Lindahl, Type 2 myocardial infarction in clinical practice, Heart 101 (2015) 101–106. [8] T. Melberg, R. Burman, K. Dickstein, The impact of the 2007 ESC-ACC-AHA-WHF universal definition on the incidence and classification of acute myocardial infarction: a retrospective cohort study, Int. J. Cardiol. 139 (2010) 228–233. [9] Y. Sandoval, S.W. Smith, S.E. Thordsen, F.S. Apple, Supply/demand type 2 myocardial infarction: should we be paying more attention? J. Am. Coll. Cardiol. 63 (2014) 2079–2087.
