Treatment and outcomes of type 2 myocardial infarction and myocardial injury compared with type 1 myocardial infarction

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.

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Understanding cardiac troponin part 1: avoiding troponinitis

Emergency Medicine Journal ◽

10.1136/emermed-2017-206812 ◽

2017 ◽

Vol 35 (2) ◽

pp. 120-125 ◽

Cited By ~ 8

Author(s):

Richard Body ◽

Edward Carlton

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Supply And Demand ◽

Clinical Context ◽

Serial Sampling ◽

Artery Disease

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.

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Cardiac Troponin Thresholds and Kinetics to Differentiate Myocardial Injury and Myocardial Infarction

Circulation ◽

10.1161/circulationaha.121.054302 ◽

2021 ◽

Author(s):

Ryan Wereski ◽

Dorien M. Kimenai ◽

Caelan Taggart ◽

Dimitrios Doudesis ◽

Kuan Ken Lee ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Troponin I ◽

Controlled Trial ◽

Rate Of Change ◽

Coronary Syndrome ◽

Diagnostic Threshold

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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Different Causes of Death in Patients with Myocardial Infarction Type 1, Type 2, and Myocardial Injury

The American Journal of Medicine ◽

10.1016/j.amjmed.2017.11.043 ◽

2018 ◽

Vol 131 (5) ◽

pp. 548-554 ◽

Cited By ~ 28

Author(s):

Sascha Lambrecht ◽

Laura Sarkisian ◽

Lotte Saaby ◽

Tina S. Poulsen ◽

Oke Gerke ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury ◽

Causes Of Death

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P1578Outcomes in patients with renal impairment and myocardial injury or infarction identified by high-sensitivity cardiac troponin testing: a secondary analysis of the High-STEACS trial

European Heart Journal ◽

10.1093/eurheartj/ehz748.0338 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

P J Gallacher ◽

E Miller-Hodges ◽

A Shah ◽

A Anand ◽

K K Lee ◽

...

Keyword(s):

Myocardial Infarction ◽

Renal Function ◽

Renal Impairment ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Primary Outcome ◽

Secondary Analysis ◽

High Sensitivity

Abstract Background Patients with renal impairment are at increased risk of myocardial infarction (MI), but the interpretation of cardiac troponin is challenging in this setting. The use of high-sensitivity cardiac troponin (hs-cTn) assays increases the detection of myocardial injury, yet may contribute to uncertainty in the diagnosis of MI in those with renal impairment. Purpose To describe the diagnosis and outcomes of patients with myocardial injury or infarction identified using a hs-cTnI assay, stratified by renal function. Methods In a pre-specified secondary analysis of a stepped-wedge cluster-randomised controlled trial, we identified consecutive patients with a hs-cTnI concentration greater than the sex-specific 99th centile between June 2013 and March 2016. The diagnoses of type 1 or type 2 MI were adjudicated and classified according to the 4th Universal Definition of Myocardial Infarction. Renal impairment was defined as an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73m2.The primary outcome of type 1 or type 4b MI or cardiovascular death was compared in patients with and without renal impairment at 1 year. Results A measure of renal function was available in 47,334 (98.0%) patients, of whom 7,933 (16.8%) had renal impairment (mean age 76±12 years; 54% female). Plasma hs-cTnI concentrations were >99th centile in 47.9% (3,800/7,933) of patients with renal impairment and 16.3% (6,439/39,401) of patients with normal renal function. In those with and without renal impairment, the adjudicated diagnosis was type 1 MI in 35.2% (1,336/3,800) and 55.8% (3,596/6,439) of patients, and type 2 MI in 12.6% (480/3,800) and 9.7% (626/6,439) of patients, respectively (P<0.001 for both). In patients with hs-cTnI concentrations >99th centile, the primary outcome occurred in 24.9% (945/3,800) of patients with renal impairment, compared to 12.1% (779/6,439) of patients with normal renal function (P<0.001). In patients with type 1 MI, the primary outcome occurred in 32.6% (436/1,336) of those with renal impairment and 11.7% (419/3,596) of those without (P<0.001). In patients with type 2 MI, the primary outcome occurred in 20.4% (98/480) and 9.9% (62/626) of patients with and without renal impairment, respectively (P<0.001). Conclusion Almost half of all patients with suspected acute coronary syndrome and renal impairment have hs-cTnI concentrations greater than the sex-specific 99th centile. Whilst only one in three had a diagnosis of type 1 MI, an elevated troponin concentration was associated with a poorer prognosis in those with concomitant renal impairment compared to those without, irrespective of the index diagnosis. Acknowledgement/Funding British Heart Foundation

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Short-Term Prognosis of Myocardial Injury, Type 1, and Type 2 Myocardial Infarction in the Emergency Unit

The American Journal of Medicine ◽

10.1016/j.amjmed.2018.04.032 ◽

2018 ◽

Vol 131 (10) ◽

pp. 1209-1219 ◽

Cited By ~ 12

Author(s):

Alain Putot ◽

Sophie Buet Derrida ◽

Marianne Zeller ◽

Aurélie Avondo ◽

Patrick Ray ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury ◽

Emergency Unit ◽

Short Term ◽

Injury Type

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Assessment and Treatment of Patients With Type 2 Myocardial Infarction and Acute Nonischemic Myocardial Injury

Circulation ◽

10.1161/circulationaha.119.040631 ◽

2019 ◽

Vol 140 (20) ◽

pp. 1661-1678 ◽

Cited By ~ 28

Author(s):

Andrew P. DeFilippis ◽

Andrew R. Chapman ◽

Nicholas L. Mills ◽

James A. de Lemos ◽

Armin Arbab-Zadeh ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury ◽

Treatment Strategies ◽

Diagnostic Tools ◽

Acute Myocardial Injury ◽

Universal Definition ◽

New Research ◽

Acute Atherothrombosis

Although coronary thrombus overlying a disrupted atherosclerotic plaque has long been considered the hallmark and the primary therapeutic target for acute myocardial infarction (MI), multiple other mechanisms are now known to cause or contribute to MI. It is further recognized that an MI is just one of many types of acute myocardial injury. The Fourth Universal Definition of Myocardial Infarction provides a taxonomy for acute myocardial injury, including 5 subtypes of MI and nonischemic myocardial injury. The diagnosis of MI is reserved for patients with myocardial ischemia as the cause of myocardial injury, whether attributable to acute atherothrombosis (type 1 MI) or supply/demand mismatch without acute atherothrombosis (type 2 MI). Myocardial injury in the absence of ischemia is categorized as acute or chronic nonischemic myocardial injury. However, optimal evaluation and treatment strategies for these etiologically distinct diagnoses have yet to be defined. Herein, we review the epidemiology, risk factor associations, and diagnostic tools that may assist in differentiating between nonischemic myocardial injury, type 1 MI, and type 2 MI. We identify limitations, review new research, and propose a framework for the diagnostic and therapeutic approach for patients who have suspected MI or other causes of myocardial injury.

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Interphysician agreement on subclassification of myocardial infarction

Heart ◽

10.1136/heartjnl-2017-312409 ◽

2018 ◽

Vol 104 (15) ◽

pp. 1284-1291 ◽

Cited By ~ 14

Author(s):

Anton Gard ◽

Bertil Lindahl ◽

Gorav Batra ◽

Nermin Hadziosmanovic ◽

Marcus Hjort ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury ◽

Interobserver Agreement ◽

Plaque Rupture ◽

Protein Levels ◽

The Third ◽

Universal Definition ◽

Definition Of

ObjectiveThe universal definition of myocardial infarction (MI) differentiates MI due to oxygen supply/demand mismatch (type 2) from MI due to plaque rupture (type 1) as well as from myocardial injuries of non-ischaemic or multifactorial nature. The purpose of this study was to investigate how often physicians agree in this classification and what factors lead to agreement or disagreement.MethodsA total of 1328 patients diagnosed with MI at eight different Swedish hospitals 2011 were included. All patients were retrospectively reclassified into different MI or myocardial injury subtypes by two independent specially trained physicians, strictly adhering to the third universal definition of MI.ResultsOverall, there was a moderate interobserver agreement with a kappa coefficient (κ) of 0.55 in this classification. There was substantial agreement when distinguishing type 1 MI (κ: 0.61), compared with moderate agreement when distinguishing type 2 MI (κ: 0.54). In multivariate logistic regression analyses, ST elevation MI (P<0.001), performed coronary angiography (P<0.001) and larger changes in troponin levels (P=0.023) independently made the physicians agree significantly more often, while they disagreed more often with symptoms of dyspnoea (P<0.001), higher systolic blood pressure (P=0.001) and higher C reactive protein levels on admission (P=0.016).ConclusionDistinguishing MI types is challenging also for trained adjudicators. Although strictly adhering to the third universal definition of MI, differentiation between type 1 MI, type 2 MI and myocardial injury only gave a moderate rate of interobserver agreement. More precise and clinically applicable criteria for the current classification, particularly for type 2 MI diagnosis, are urgently needed.

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