ICD-10 Coding of Type 2 Myocardial Infarction and Myocardial Injury as It Relates to US Centers for Medicare & Medicaid Services Value-Based Payment Programs—Reply

2019 ◽  
Vol 4 (10) ◽  
pp. 1051
Author(s):  
Cian P. McCarthy ◽  
Sean T. McWalters ◽  
Jason H. Wasfy
2019 ◽  
Vol 208 ◽  
pp. 11-20 ◽  
Author(s):  
Kristina Lambrakis ◽  
John K. French ◽  
Ian A. Scott ◽  
Tom Briffa ◽  
David Brieger ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Laura Sarkisian ◽  
Lotte Saaby ◽  
Tina S Poulsen ◽  
Oke Gerke ◽  
Axel C Diederichsen ◽  
...  

Introduction: Troponin elevations occur in a myriad of clinical conditions other than myocardial infarction (MI) and imply a poor prognosis. So far, data comparing the short-term outcome in patients with myocardial injury vs. patients with type 1 or type 2 MI are not available. Methods: Over a 1-year period we prospectively studied hospitalized patients having cardiac troponin I (cTnI) measured on clinical indication. The diagnosis of type 1 and type 2 MI was according to the universal definition involving a rising and/or falling pattern of cTnI values above the decision limit of 30 ng/L. cTnI elevations above this limit in patients without overt myocardial ischemia were defined as myocardial injury. A 1-month follow-up was done with mortality as endpoint. Results: The study covered 1577 consecutive patients with cTnI values >30 ng/L, of whom 360 had a type 1 MI, 119 a type 2 MI and 1089 had myocardial injury. Type 1 MI patients were younger with a median age of 70 (IQR 61-81) yrs, whereas the median ages in type 2 MI and myocardial injury were higher but comparable : 78 (IQR 67-84) vs. 77 (IQR 67-85) yrs. Peak cTnI values, however, were highest in type 1 MI: 3820 (530-19030) ng/L, lower in type 2 MI: 850 (390-3270) ng/L, and smallest in patients with myocardial injury: 90 (50-270) ng/L (p=0.0001). At one-month follow-up 285 patients had died. Mortality in the different subgroups was: 9% (33/360) in type 1 MI, 24% (28/119) in type 2 MI, and 21% (224/1089) in patients with myocardial injury. The results are depicted in the figure (Kaplan-Meier curves, log-rank-test; p-value <0.0001). Multivariate COX regression analysis revealed a Hazard Ratio (95%) of 2.1 (1.2-3.7) for type 2 MI and 1.4 (0.9-2.1) for myocardial injury. Conclusion: The short-term mortality in patients with myocardial injury and type 2 MI is almost identical but higher than in patients with type 1 MI. These prognostic findings imply that the clinical distinction between myocardial injury and type 2 MI may be somewhat artificial.


2017 ◽  
Vol 35 (2) ◽  
pp. 120-125 ◽  
Author(s):  
Richard Body ◽  
Edward Carlton

Cardiac troponin (cTn) is a highly specific biomarker of myocardial injury and is central to the diagnosis of acute myocardial infarction (AMI). By itself, however, cTn cannot identify the cause of myocardial injury. ‘Troponinitis’ is the condition that leads clinicians to falsely assign a diagnosis of AMI based only on the fact that a patient has an elevated cTn concentration. There are many causes of myocardial injury other than AMI. Clinicians are required to differentiate myocardial injury caused by AMI from other causes.In part 1 of this series on cTn, we provide a structured overview to help practising clinicians to interpret ‘positive’ cTn results appropriately. There are three core principles. First, when reviewing a cTn result, clinicians must carefully consider the clinical context. Only this can distinguish primary (termed type 1) AMI caused by coronary artery disease from secondary (termed type 2) AMI caused by another condition with an imbalance in the supply and demand of oxygen to the myocardium. Second, clinicians must consider the patient’s baseline condition in order to determine the presence or absence of factors that may predict a chronic cTn elevation. Third, clinicians should routinely use serial sampling to detect a change of cTn that is expected in patients with acute (rather than chronic) myocardial injury. Using these simple principles, clinicians can avoid underdiagnosis and overdiagnosis of AMI.


2021 ◽  
Vol 78 (4) ◽  
pp. 415-416
Author(s):  
Claire E. Raphael ◽  
Véronique L. Roger ◽  
Yader Sandoval ◽  
Matthew Johnson ◽  
Allan Jaffe ◽  
...  

2018 ◽  
Vol 29 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Nathaniel R. Smilowitz ◽  
Pritha Subramanyam ◽  
Eugenia Gianos ◽  
Harmony R. Reynolds ◽  
Binita Shah ◽  
...  

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
R.W Ariss ◽  
A.M Minhas ◽  
S Nazir ◽  
C Meenakshisundaram ◽  
M.M Ali ◽  
...  

Abstract Background Patients with atrial fibrillation (AF) are often elderly and have higher rates of comorbidities which may predispose them to an increased risk of myocardial oxygen demand-supply mismatch. Scarce data exist on the prognostic impact of type 2 myocardial infarction (MI) in AF. Purpose To examine the association of type 2 MI with outcomes and resource utilization in primary AF hospitalizations. Methods We utilized the Nationwide Readmission Database 2018 to identify primary AF hospitalizations with and without type 2 MI. The International Classification of Diseases, Tenth Revision (ICD-10) diagnosis codes I48.0, I48.1, I48.2, I48.91 were utilized to identify primary AF hospitalizations within the United States. Of these, AF hospitalizations complicated by type 2 MI were identified using ICD-10 code I21.A1. Comorbidities and outcomes were identified using the corresponding ICD-10 codes. Complex samples multivariable logistic and linear regression models were used to determine the association between type 2 MI and outcomes (in-hospital mortality, index length of stay [LOS], hospital costs, discharge to nursing facility, and 30-day all-cause readmissions). Predictors of in-hospital mortality in AF with type 2 MI were also determined. Results Of 382,896 primary AF hospitalizations included in this study, 7,375 (1.9%) had type 2 MI. Compared to AF hospitalization without type 2 MI, those with type 2 MI are older (74.5 vs. 70.7-years-old) and have higher prevalence of chronic pulmonary disease, dyslipidemia, diabetes mellitus, hypertension, heart failure, peripheral vascular disease, chronic kidney disease, neurological disorders, deficiency anemia, coagulopathy, valvular disease, prior myocardial infarction, prior coronary artery bypass grafting, prior percutaneous coronary intervention, and prior cerebrovascular accident (P for all &lt;0.001). AF with type 2 MI is associated with significantly higher in-hospital mortality (1.3% vs. 0.5%; P&lt;0.001), LOS (4.1 vs. 3.3 days; P&lt;0.001), hospital costs ($10,293.6 vs. $8,820.3; P&lt;0.001), discharges to nursing facility (18.1% vs. 10.2%; P&lt;0.001), and 30-day all-cause readmissions (18.5% vs. 13.5%; P=0.001) compared to AF hospitalizations without type 2 MI (Table 1). Heart failure, chronic kidney disease, neurological disorders, and age (per year) were identified as independent predictors of in-hospital mortality among AF patients with type 2 MI (Figure 1). Conclusion In this large nationwide analysis, type 2 MI in the setting of AF hospitalization is associated with higher in-hospital mortality and increased resource utilization compared to AF hospitalizations without type 2 MI. FUNDunding Acknowledgement Type of funding sources: None. Figure 1


2019 ◽  
Vol 132 (2) ◽  
pp. 217-226 ◽  
Author(s):  
German Cediel ◽  
Yader Sandoval ◽  
Anne Sexter ◽  
Anna Carrasquer ◽  
Maribel González-del-Hoyo ◽  
...  

Author(s):  
rui xu ◽  
yan zhang ◽  
Yanping Bi ◽  
yan wang

A 60-years-old patient with sustained chest pain was referred to hypertension.The tertiary Troponin-I concentrations,namely the biomarker of myocardial injury,were 0.19ng per milliliter,1.288ng per milliliterand 16.698ng per milliliter,respectively.Electrocardiogram showed ST-segment and T wave dynamic changes.Type 2 MI was confirmed.


Author(s):  
Ryan Wereski ◽  
Dorien M. Kimenai ◽  
Caelan Taggart ◽  
Dimitrios Doudesis ◽  
Kuan Ken Lee ◽  
...  

Background: Whilst the 99th percentile is the recommended diagnostic threshold for myocardial infarction, some guidelines also advocate the use of higher troponin thresholds to rule-in myocardial infarction at presentation. It is unclear whether the magnitude or change in troponin concentration can differentiate causes of myocardial injury and infarction in practice. Methods: In a secondary analysis of a multi-centre randomized controlled trial, we identified 46,092 consecutive patients presenting with suspected acute coronary syndrome without ST-segment elevation myocardial infarction. High-sensitivity cardiac troponin I concentrations at presentation and on serial testing were compared between patients with myocardial injury and infarction. The positive predictive value (PPV) and specificity were determined at the sex-specific 99th percentile upper reference limit (URL), and rule-in thresholds of 64 ng/L and 5-fold of the URL for a diagnosis of type 1 myocardial infarction. Results: Troponin was above the 99th percentile in 8,188 (18%) patients. The diagnosis was type 1 or type 2 myocardial infarction in 50% and 14%, and acute or chronic myocardial injury in 20% and 16%, respectively. Troponin concentrations were similar at presentation in type 1 (median [25th percentile - 75th percentile] 91 [30-493] ng/L) and type 2 (50 [22-147] ng/L) myocardial infarction, and in acute (50 [26-134] ng/L) and chronic (51 [31-130] ng/L) myocardial injury. The 99th percentile and rule-in thresholds of 64 ng/L and 5-fold URL gave a PPV of 57% (95% confidence interval [CI] 56-58%), 59% (58-61%) and 62% (60-64%), and a specificity of 96% (96-96%), 96% (96-96%) and 98% (97-98%), respectively. The absolute, relative and rate of change in troponin concentration was highest in patients with type 1 myocardial infarction (P<0.001 for all). Discrimination improved when troponin concentration and change in troponin were combined compared to troponin concentration at presentation alone (area under curve, 0.661 [0.642-0.680] versus 0.613 [0.594-0.633]). Conclusions: Although we observed important differences in the kinetics, cardiac troponin concentrations at presentation are insufficient to distinguish type 1 myocardial infarction from other causes of myocardial injury or infarction in practice and should not guide management decisions in isolation. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01852123


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