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

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.

Download Full-text

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.

Download Full-text

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

Coronary Artery Disease ◽

10.1097/mca.0000000000000545 ◽

2018 ◽

Vol 29 (1) ◽

pp. 46-52 ◽

Cited By ~ 9

Author(s):

Nathaniel R. Smilowitz ◽

Pritha Subramanyam ◽

Eugenia Gianos ◽

Harmony R. Reynolds ◽

Binita Shah ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury

Download Full-text

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

Download Full-text

Comparison of in-hospital outcomes and 30-days readmissions between type 1 and type 2 myocardial infarction patients: a study of the nationwide readmissions database

European Heart Journal ◽

10.1093/eurheartj/ehab724.1144 ◽

2021 ◽

Vol 42 (Supplement_1) ◽

Author(s):

L Wu ◽

D D Song ◽

J A Daibes ◽

S Das ◽

M K Pena ◽

...

Keyword(s):

Myocardial Infarction ◽

Length Of Stay ◽

Early Mortality ◽

St Elevation Myocardial Infarction ◽

Index Admission ◽

Short Term ◽

Readmission Rates ◽

St Elevation

Abstract Introduction Traditionally Type- 1 myocardial infarction (T1-MI) results from a plaque erosion, rupture, or fissure. In contrast, Type- 2 myocardial infarction (T2-MI) is a consequence of severe supply and demand mismatch. Despite the different mechanisms, both T1-MI and T2-MI can be associated with severe morbidity and mortality. Yet there is sparse data analyzing in-hospital outcomes and readmission rates comparing patients who present with T1-MI and T2-MI. Purpose We aimed to compare the outcome data of patients with T1-MI and T2-MI derived from the Nationwide Readmissions Database, a large national database of hospital readmissions. Method We utilized the 2018 Nationwide Readmissions Database to identify all index hospital admissions with a primary diagnosis of “acute MI” (AMI) using ICD-10 diagnosis codes. All AMI admissions were further categorized into ST-elevation myocardial infarction (STEMI), no-ST-elevation myocardial infarction (NSTEMI), or T2-MI. Primary outcomes analyzed included 30-days major adverse cardiovascular events (MACE) (defined as re-infarction, repeat revascularization and death within 30 days of admission), short term mortality and readmission rates. Results Among 556,816 total admissions for AMI, 28,250 (5.1%) were T2-MI. Table 1 compares baseline variables and short-term outcomes for patients with T1-MI vs T2-MI. Compared to patients with T1-MI patients with T2-MI were older, more likely to be female, and had a higher burden of comorbidities. Additionally, T2-MI patients were less likely to receive coronary revascularization during the index admission. The mean length of stay for T2-MI patients was 4.7±0.6 days, which is longer than the length of stay for STEMI patient (4.1±0.4 days) but slightly shorter than NSTEMI patient (4.9±0.4 days). T2-MI patients had a higher rate of all-cause 30-days readmissions but a lower rate of 30-days MACE. Early mortality rate (within 30 days of index admission) in T2-MI patients was comparable to NSTEMI patients but was lower than STEMI patients. Cox proportional-hazards model adjusting for age, sex, comorbidities and type of hospital setting demonstrated that T2-MI was associated with a lower 30-day MACE risk (T2-MI vs STEMI: [HR 0.33 (95% CI 0.31–0.36)]; T2-MI vs NSTEMI [HR 0.70 (95% CI 0.64–0.75)]) and a lower risk of early mortality (T2-MI vs STEMI: [HR 0.29 (95% CI 0.26–0.32)]; T2-MI vs NSTEMI [HR 0.71 (95% CI 0.65–0.79)]). The adjusted HR for 30-days all-cause readmissions was higher with T2-MI, (T2-MI vs STEMI: [HR 1.16 (95% CI 1.10–1.23)]; T2-MI vs NSTEMI: [HR 1.11 (95% CI 1.06–1.16)]). Conclusion T2-MI patients are older and have a higher burden of comorbidities. After adjusting for baseline comorbidities, all-cause readmission risk is higher in T2-MI but short-term MACE and mortality is lower with T2-MI. FUNDunding Acknowledgement Type of funding sources: None.

Download Full-text

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

Download Full-text

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

Download Full-text

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.

Download Full-text

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.

Download Full-text

P852Frequency and prognosis of type 2 myocardial infarction vs non ischemic myocardial injury: large observational study from an emergency department

European Heart Journal ◽

10.1093/eurheartj/ehz747.0450 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

A Putot ◽

S Buet-Derrida ◽

A Avondo ◽

P Ray ◽

M Maza ◽

...

Keyword(s):

Risk Factors ◽

Myocardial Infarction ◽

Emergency Department ◽

Hospital Mortality ◽

Myocardial Injury ◽

Biological Data ◽

University Hospital ◽

Emergency Unit ◽

L 14

Abstract Background Type 2 Myocardial Infarction (T2MI), due to myocardial oxygen supply-demand mismatch in the absence of atherothrombosis and non-ischemic myocardial injury (NIMI), corresponding to troponin elevation without overt ischemia, are emerging concepts which are suspected to be common in patients hospitalized. However, their respective frequencies, risk profiles and short term prognosis in current routine clinical practice of emergency unit remains to be investigated. Methods Among the medical records of all the patients admitted from January 2014 to December 2016 in a university hospital emergency unit (n=82 543), patients with elevated troponin Ic (≥0.10μg/L) (n=4568) were systematically adjudicated as T2MI in the presence of symptoms or signs of myocardial ischemia (typical chest pain and/or ECG changes), or as NIMI without such signs. Patients with missing biological data on admission (n=112) or T1MI diagnosis (n=2467) were excluded. Results Among the 1989 patients included, 539 (27%) were classified as T2MI and 1450 (73%) as NIMI. When compared with patients with NIMI, T2MI had higher troponin levels (0.27 (0.14–0.71) vs 0.22 (0.13–0.54) μg/L, p=0.008, respectively). NIMI and T2MI had similar risk factors (age (84 (74–90) vs 84 (75–91) y, p=0.3), male sex (43 vs 48%, p=0.07), hypertension (67 vs 71%, p=0.133), diabetes (25 vs 25%, p=0.9), prior CAD (24 vs 26%, p=0.342), systemic inflammatory response syndrome (SIRS, 47 vs 49%, p=0.3), and systolic blood pressure (SBP) (130 (111–153) vs 132 (112–153) mmHg, p=0.545). Biological data on admission were also similar (hyperglycemia (glucose ≥11 mmol/L), 14 vs 13%, p=0.37, creatinine (96 (72–148) vs 94 (72–141) μmole/L, p=0.598), anemia (Hemoglobin rate ≤10g/dL, 13 vs 14%, p=0.5), C-reactive protein elevation (CRP ≥3 mg/L, 88 vs 89%, p=0.7)). Moreover, in-hospital mortality was high and similar for both groups (15 vs 18%, p=0.2). In multivariate analysis, age, troponin rate, SIRS, anemia, SBP, hyperglycemia, creatinine and CRP elevation were independent factors associated with hospital mortality, but not T2MI (vs NIMI) (OR: 0.88 (0.66–1.17)). Older age and hyperglycemia were specific covariates associated with increased risk of mortality in T2MI, but not in NIMI. Conclusions This large real-life study of non-T1MI inpatients with elevated troponins from emergency department shows that myocardial injury without necrosis and T2MI share the same risk factors, characterized by a high rate of infections and anemia and a high risk of hospital mortality. Acknowledgement/Funding University Hospital Center Dijon Bourgogne, France

Download Full-text