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PII: S0002-9343(17)30716-7
DOI: http://dx.doi.org/doi: 10.1016/j.amjmed.2017.05.049
Reference: AJM 14183
Please cite this article as: Yader Sandoval, Stephen W. Smith, Anne Sexter, Sarah E. Thordsen,
Charles A. Bruen, Michelle D. Carlson, Kenneth W. Dodd, Brian E. Driver, Yan Hu, Katherine
Jacoby, Benjamin K. Johnson, Sara A. Love, Johanna C. Moore, Karen Schulz, Nathaniel L.
Scott, Fred S. Apple, Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical
Transition to High-Sensitivity Cardiac Troponin I, The American Journal of Medicine (2017),
http://dx.doi.org/doi: 10.1016/j.amjmed.2017.05.049.
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Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to
Authors: Yader Sandoval1, MD, Stephen W. Smith2-3, MD, Anne Sexter, MPH, Sarah E.
Thordsen1, MD, Charles A. Bruen2,4, MD, Michelle D. Carlson1, MD, Kenneth W. Dodd2,4, MD,
Brian E. Driver2, MD, Yan Hu5, PhD Katherine Jacoby2,4, MD, Benjamin K. Johnson1, MD, Sara
A. Love6, PhD, Johanna C. Moore2, MD, Karen Schulz5, DC, Nathaniel L. Scott2,4, MD, Fred S.
Apple5,6, PhD
Affiliations:
1. Division of Cardiology, Hennepin County Medical Center and Minneapolis Heart Institute,
Minnesota, USA.
6. Department of Laboratory Medicine and Pathology, Hennepin County Medical Center and
Total word count: 2,996 (limit 3000, including abstract, text, acknowledgements).
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Funding source: UTROPIA study (NCT02060760); partially funded through a grant
from a) Abbott Diagnostics, who had no role in the design and conduction of the study;
including data collection, management, analysis, and interpretation of the data; and
preparation, review, or approval of the final manuscript; and b) the Minneapolis Medical
Research Foundation.
Biokit, Hytest Ltd., Instrumentation Laboratory; Other: Editorial Board Journal of Applied
Davita, Amgen; Other: Associate Editor Clinical Chemistry. All other authors have
nothing to disclose.
All authors had access to the data and a role in writing the manuscript.
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CLINICAL SIGNIFICANCE
myocardial injury have worse short-term outcomes, with mortality rates >20% at
2 years.
troponin I assay does not lead to more cases of myocardial injury or myocardial
infarction.
ABSTRACT
myocardial injury, including the impact of using high-sensitivity (hs) cardiac troponin
mortality and major adverse cardiac events, including 2-year follow-up for those with
myonecrosis.
Results: Among 1,640 patients, using a contemporary cTnI assay, 30% (n=497) had 1
cTnI >99th percentile; with 4.7% (n=77), 8.5% (n=140) and 17% (n=280) classified as
for type 2 myocardial infarction (4% vs. 13%, p<0.0001) (adjusted HR 2.7, 95% CI 1.6-
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4.8, p=0.0005) and myocardial injury (4% vs. 11%, p<0.0001) (adjusted HR 1.8, 95% CI
1.1-3.0, p=0.02), both with mortality >20% at 2-years. Predictors of 2-year mortality for
type 2 myocardial infarction included age, congestive heart failure, and beta-blockers.
Relative to the contemporary cTnI assay, hs-cTnI had less myonecrosis (30% vs. 26%,
p=0.003) and acute myocardial infarction (13.2% vs. 10.8%, p=0.032), including fewer
type 2 myocardial infarctions (8.5% vs. 6.3, p=0.01) with no difference in myocardial
myonecrosis, type 2 myocardial infarction and myocardial injury have worse short-term
outcomes, with mortality rates >20% at 2 years. hs-cTnI assay does not lead to more
Cardiac troponin (cTn) measurements are central for ruling in and out acute myocardial
infarction1. With improved analytical sensitivity of cTn assays, clinicians are often
challenged with determining whether cTn increases are due to acute myocardial
infarction or myocardial injury2-11. Among those with myocardial infarction, type 1 and 2
myocardial infarction have received the most attention due to their incidence and
or absence of atherothrombosis4-11.
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The goals of the present study were three-fold. First, we describe the incidence,
clinical features, management, and outcomes of patients with type 1 and 2 myocardial
for type 2 myocardial infarction and myocardial injury. Third, we determined the impact
METHODS
serial cTnI measurements at 0, 3, 6 and 9 hours (h), were ordered on clinical indication
at Hennepin County Medical Center (Minneapolis, MN, USA) to rule-in and rule-out
presentation and at least one additional cTnI within 24h of presentation before
discharge, and at least one 12-lead electrocardiogram (ECG). Exclusion criteria were:
<18 years old, pregnancy, trauma, declined to participate, did not present through the
emergency department, or transferred from an outside hospital. For patients with more
than one presentation during the study period, we included only the first. Management
and outcomes analyses are based on the contemporary cTnI results as such were used
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Fresh ethylenediaminetetraacetic acid plasma samples were measured with both the
contemporary cTnI (clinically used) and hs-cTnI (investigational) assays on the Abbott
ARCHITECT i1000SR or i2000SR analyzers. For cTnI, the 99th percentile was 0.030 g/L.
The coefficient of variation was 18.5% at 0.028 g/L. For hs-cTnI, sex-specific 99th
percentiles were: women 16 ng/L and men 34 ng/L. The coefficient of variation was
Event Adjudication
All cases with at least one cTnI value >99th percentile were adjudicated according to the
results and clinical presentation. Cases with an adjudication discrepancy were reviewed
and adjudicated by a third senior clinician. All cases were adjudicated twice,
independently using cTnI and hs-cTnI results separately, with adjudicators blinded to
the other adjudication process and alternate cTnI results. Using the contemporary cTnI,
a rise and/or fall in cTnI with at least one value >99th percentile was used to support the
used to guide the adjudication using the contemporary cTnI assay. To guide
ensure that changes within biological variation were not deemed abnormal 10. If the initial
hs-cTnI was <99th percentile, then a rise >69% and/or fall of >41% on serial sampling
were used to suggest a significant change. Conversely, if the initial hs-cTnI was >99th
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The term myocardial necrosis is used as follows: a) without myocardial necrosis
(serial measurements 99th percentile) or b) with myocardial necrosis (at least one
measurement >99th percentile). For the diagnosis of acute myocardial infarction, a rise
and/or fall with at least one value >99th percentile occurring in appropriate clinical
circumstances consistent with acute myocardial ischemia was required, plus at least
one additional myocardial infarction criteria1. Type 1 myocardial infarction was defined
myocardial oxygen supply and/or demand not due to atherothrombosis, and was
Outcomes
the index hospitalization) and major adverse cardiac events defined as post-discharge:
congestive heart failure. For those with myonecrosis, 2-year mortality follow-up was
performed.
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Statistical Analyses
Categorical variables were compared using Pearsons chi-square and Fishers exact
test where 50% of cells were less than 5. Continuous variables were compared using
the F-test. Cumulative survival curves were plotted using the Kaplan-Meier method and
compared between groups using the log-rank test. A multivariate Cox proportional
hazards model adjusted for age, congestive heart failure and estimated glomerular
filtration rate (eGFR > or < 60 mL/min/1.73m2) was used to determine the independent
long-term mortality for type 2 myocardial infarction and myocardial injury were
analyses were utilized to determine the impact on 2-year mortality in participants with
type 2 myocardial infarction and myocardial injury. Variables that were independent
predictors of 2-year mortality at the 0.1 significance level for type 2 myocardial infarction
or myocardial injury were included in a multivariate adjusted Cox regression model and
plotted on a Forest plot. Hazard ratios (HRs) with their respective 95% confidence
intervals (CI) are presented. Concordance between the hs-cTnI and cTnI assays was
evaluated using kappa statistics with respective 95% CIs. All tests were 2-sided and
RESULTS
1,640 patients were included. Using the contemporary cTnI assay, 30% (n=497) of
patients had 1 cTnI >99th percentile; with 17% (n=280) classified as myocardial injury,
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4.7% (n=77) as type 1 myocardial infarction, and 8.5% (n=140) as type 2 myocardial
infarction.
Patients with type 1 myocardial infarction presented more often with chest discomfort
than patients with type 2 myocardial infarction. They were also more likely to have
percutaneous coronary intervention, and had significantly higher baseline and maximum
than type 2 myocardial infarction (Supplemental Table 2). Among those undergoing
coronary angiography, type 1 myocardial infarction had higher rates of coronary artery
disease (91% vs. 54%, p<0.0001), with such patients more likely to undergo
infarction, patients with type 1 myocardial infarction were more likely to receive aspirin,
Table 4). During the initial 24h, compared to type 2 myocardial infarction, patients with
type 1 myocardial infarction were also more likely to receive aspirin, heparin and
used in both type 2 myocardial infarction and myocardial injury (Supplemental Table 5).
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The most common determinants leading to type 2 myocardial infarction were:
The most common etiologies for myocardial injury were: renal failure, congestive heart
Outcomes
At 180-days, all-cause mortality was 4%, 8%, 13% and 11% for patients without
type 2 myocardial infarction (4% vs. 13%, p<0.0001) (adjusted HR 2.7, 95% CI: 1.6-4.8,
p=0.0005) and myocardial injury (4% vs. 11%, p<0.0001) (adjusted HR 1.8, 95% CI:
1.1-3.0, p=0.02) had a higher mortality at 180-days (Figures 1 and 2). No difference was
observed compared to type 1 myocardial infarction (4% vs. 8%, p=0.12). Similarly,
compared to patients without myonecrosis, type 2 myocardial infarction (5% vs. 16%,
p<0.0001) (adjusted HR 2.2, 95% CI 1.4-3.7, p=0.001) and myocardial injury (5% vs.
19%, p<0.0001) (adjusted HR 2.2, 95% CI 1.4-3.2, p=0.0002) had a higher post
discharge major adverse cardiac events rate, with no difference observed compared to
discharge major adverse cardiac events between type 1 myocardial infarction and type
(Supplemental Table 8). At 2-years, all-cause mortality for type 1 myocardial infarction,
type 2 myocardial infarction and myocardial injury was 16%, 22% and 26%, respectively
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(Figure 3), with no differences observed between type 1 and 2 myocardial infarction
years included age (HR 1.04, 95% CI: 1.01-1.078, p=0.004), congestive heart failure
(HR 3.32, 95% CI: 1.49-7.41, p=0.003) and beta-blockers (HR 0.334, 95% CI: 0.15-
0.73, p=0.006) (Figure 4, Supplemental Table 9). For myocardial injury, predictors of
mortality at 2-years included: age (HR 1.034, 95% CI: 1.02-1.06, p<0.0001), maximum
cTnI (HR 1.74, 95% CI 1.18-2.55, p=0.005), congestive heart failure (HR 2.04, 95% CI:
1.19-3.51, p=0.01), and ACEI (HR 0.42, 95% CI 0.23-0.78, p=0.006) (Figure 5,
The incidence of patients with 1 cTnI >99th percentile, type 1 myocardial infarction,
type 2 myocardial infarction and myocardial injury using a contemporary vs. hs-cTnI
contemporary and hs-cTnI assays is shown in Table 2. Discordant diagnoses were due
to either a) a different test result, in which case most were classified as myocardial
injury with either assay; or b) differences in adjudication, in which case most were
30% of patients had 1 cTnI >99th percentile using contemporary cTnI, while 26%
lower incidence of acute myocardial infarction was observed using hs-cTnI (10.8% vs.
13.2%, p=0.032). A lower rate of acute myocardial infarction was seen in men (cTnI
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13.7% vs. hs-cTnI 9.8%, p=0.009), with no difference observed in women (cTnI 12.6%
The incidence of type 1 myocardial infarction did not change between assays
(cTnI 4.7% vs. hs-cTnI 4.5%, p=0.8). No differences were observed in type 1 myocardial
infarction rates for both men (cTnI 5.0% vs. hs-cTnI 4.5%, p=0.58) and women (cTnI
4.3% vs. hs-cTnI 4.6%, p=0.79). The incidence of type 2 myocardial infarction
decreased using hs-cTnI (8.5% vs. 6.3%, p=0.01), with a reduction seen in men (cTnI
8.7% vs. hs-cTnI 5.3%, p=0.0047) and no difference seen in women (cTnI 8.3% vs. hs-
The rate of myocardial injury was similar using either assay (cTnI 17% vs. hs-
cTnI 15%, p=0.1). For men, compared to cTnI, a lower rate of myocardial injury was
seen using hs-cTnI (18.3% vs. 12.4%, p=0.0005), whereas for women, no difference
DISCUSSION
Our study provides several unique observations. First, we demonstrate that type 2
associated with poor short- and long-term outcomes. Moreover, compared to patients
without myonecrosis, patients with type 2 myocardial infarction have significantly higher
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mortality and post discharge major adverse cardiac events rates within 180-days, with
wide range in frequency7. Contrary to studies performed outside the United States (US)
or assessing more select populations, our findings are aligned with the results of our
reported that 35% of cTnI increases or 57% of all myocardial infarctions were due type
observations emphasize that while studies performed outside the US often report lower
incidence rates4,6, studies in the US have higher rates of type 2 myocardial infarction.
have made in recent years demonstrating that compared to patients without myocardial
necrosis, patients with type 2 myocardial infarction have worse outcomes, independent
infarction7,9. Conversely, patients with type 1 myocardial infarction benefit from robust,
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cardiology consultants, as well as less likely to undergo additional studies compared to
type 1 myocardial infarction. Further, our study informs about predictors of long-term
practice, with only 15% of cTnI increases being due to due to type 1 myocardial
that patients with myocardial injury also have poor short- and long-term outcomes.
Compared to patients without myonecrosis, patients with myocardial injury had higher
rates of all-cause mortality and post-discharge major adverse cardiac events at 180-
days. Our findings are consistent with recent studies3,4,16 and demonstrate that patients
with myocardial injury are at high-risk, independent of covariates, and have mortality
etiologies leading to myocardial injury; with the most common causes in the current
study being renal failure, congestive heart failure and neurological conditions. These
Lastly, contrary to the perception that the adoption of hs-cTn assays will
uniformly be associated with more myocardial injury and infarction, we have shown that
the number of patients with concentrations >99th percentile, as well as the incidence of
acute myocardial infarction is actually significantly lower using hs-cTnI. These results
are of unique importance, particularly in the US, where hs-cTn assays have not been
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yet implemented into clinical practice and concern exists about adopting hs-assays due
to an expected increase in myocardial injury and infarction. Our findings, based Abbott
analytical perspective, our results are supported by our recent analytical studies
showing that compared to contemporary cTnI assay, the hs-cTnI assay has a) improved
our results underscore how the local contemporary assay used before transitioning to a
Our study has limitations. First, our findings related to the benefit of beta-blockers
are hypothesis-generating. Second, debate exists surrounding how to define both type 2
myocardial infarction and myocardial injury, with further guidance expected in the Fourth
Universal Definition of Myocardial Infarction. Our study illustrates the need for guidance
and potential for misclassification, based on results showing that discordant diagnoses
and myocardial injury. Third, the number of events at 180-days limited our analytical
CONCLUSIONS
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type 2 myocardial infarction and myocardial injury worse short-term outcomes, with
mortality rates >20% at 2 years. Further, the use of hs-cTnI does lead to more acute
REFERENCES
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EM, Antman EM, Wallentin LC, Armstrong PW, Simoons ML; Trials & Registries
Robertson RM, Weaver D, Tendera M, Bove AA, Parkhomenko AN, Vasilieva EJ,
Mendis S; ESC Committee for Practice Guidelines (CPG), Bax JJ, Baumgartner
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E, Anand A, Fersia O, Joshi NV, Walker S, Jaffe AS, Fox KA, Newby DE, Mills
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Apple FS. Cardiac troponin changes to distinguish type 1 and type 2 myocardial
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8. Alpert JS, Thygesen KA, White HD, Jaffe AS. Diagnostic and therapeutic
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cardiac troponin I assay with sex-specific 99th percentiles based on the third
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D, Peterson ED, Sabatine MS, Smalling RW, Zieman SJ; American College of
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Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 64 (24):
e139-228.
Figure 1. 180-day all-cause mortality and post discharge major adverse cardiac events
Figure 2. 180-day Kaplan-Meier survival curve for patients without myonecrosis (no
myocardial infarction with cTnI <99th percentile), type 1 myocardial infarction, type 2
Figure 3. 2-year Kaplan-Meier survival curve for type 1 myocardial infarction, type 2
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Table 1. Baseline characteristics for patients with type 1 myocardial infarction, type 2
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and/or other stimulant use
n (%)
History of tobacco use n 23 (30) 52 (37) 85 (30) 0.33 0.28 0.16
(%)
Presenting symptom
Chest discomfort n (%) 38 (49) 22 (16) 41 (15) <0.0001 <0.0001 0.77
Dyspnea n (%) 40 (52) 72 (51) 98 (35) 0.001 0.94 0.001
Arm and/or shoulder 30 (39) 15 (11) 18 (6) <0.0001 <0.0001 0.12
discomfort n (%)
Jaw and/or neck discomfort 12 (16) 6 (4) 9 (3) <0.0001 0.004 0.58
n (%)
Epigastric discomfort n (%) 8 (10) 8 (6) 14 (5) 0.21 0.21 0.76
Nausea and/or vomiting n 25 (33) 25 (18) 46 (16) 0.006 0.01 0.71
(%)
Fatigue n (%) 5 (7) 5 (4) 14 (5) 0.62 0.33 0.51
Diaphoresis n (%) 16 (21) 16 (11) 17 (6) 0.0005 0.06 0.05
Vitals signs
Body mass index (BMI) 31 (8) 29 (8) 30 (9) 0.20 0.05 0.32
mean (SD)
Heart rate (beats per minute) 85 (19) 100 (30) 90 (24) <0.0001 <0.0001 0.0002
mean (SD)
Temperate (C) mean (SD) 36.5 (0.7) 36.6 (0.9) 36.7 (1.5) 0.64 0.57 0.59
Systolic blood pressure 153 (27) 154 (39) 144 (33) 0.005 0.89 0.005
(mmHg) mean (SD)
Diastolic blood pressure 86 (19) 92 (27) 82 (23) 0.0003 0.06 <0.0001
(mmHg) mean (SD)
Pulse oximetry mean (SD) 95 (10) 94 (9) 95 (9) 0.032 0.51 0.13
Laboratory measurements, biochemistry
Baseline sensitive 1.8 (6.6) 0.07 (0.1) 0.1 (0.2) <0.0001 0.003 0.21
contemporary cTnI
concentration (g/L) mean
(SD) (n=497)
Baseline sensitive 1.4 (5.9) 0.07 (0.1) 0.1 (0.2) <0.0001 0.007 0.11
contemporary cTnI
concentration (g/L),
excluding STEMIs mean
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(SD) (n=490)
Maximum sensitive 9.9 (18) 0.6 (2.0) 0.2 (0.4) <0.0001 <0.0001 0.001
contemporary cTnI
concentration (g/L) mean
(SD) (n=497)
Maximum sensitive 7.5 (15.1) 0.6 (2.1) 0.2 (0.4) <0.0001 <0.0001 0.001
contemporary cTnI
concentration (g/L),
excluding STEMIs mean
(SD) (n=490)
Creatinine (mg/dL) mean 1.4 (1.5) 2.2 (3.6) 3.2 (7.3) 0.04 0.08 0.12
(SD) (n=477)
Estimated glomerular 83 (44) 73 (49) 62 (43) 0.001 0.15 0.02
-1
filtration rate, mL min (1.73
2 -1
m) mean (SD) (n=488)
Blood urea nitrogen (mg/dL) 19.6 (16) 28.3 (26) 30.4 (27) 0.01 0.01 0.45
(n=***)
Hemoglobin (g/dL) mean 13.3 (2) 12.8 (3) 12.3 (3) 0.01 0.16 0.07
(SD) (n=492)
Hematocrit (%) mean (SD) 39.7 (6) 38.7 (8) 36.7 (8) 0.002 0.30 0.01
(n=490)
NT-terminal pro-brain 3715 2974 7409 0.01 0.83 0.01
natriuretic peptide (ng/L) (4450) (3628) (12626)
mean (SD) (n=165)
Lactate (mmol/L) mean 3.2 (3.0) 4.3 (3.8) 2.9 (2.6) 0.02 0.26 0.01
(SD) (N=171)
12-lead electrocardiogram (ECG) at presentation
Adjudicated as a diagnostic 6 (8) 1 (1) 0 (0) <0.0001* 0.01* 0.33*
ECG with ischemic ST-
segment elevation changes
(STEMI) n (%)
Any ST-segment elevation 24 (31) 31 (22) 58 (21) 0.15 0.14 0.74
n (%)
ST depression and/or T wave 40 (52) 74 (53) 101(36) 0.001 0.90 0.001
changes n (%)
Pathological Q wave n (%) 15 (20) 16 (11) 50 (18) 0.17 0.10 0.09
Nonspecific ST-T wave 18 (23) 56 (40) 89 (32) 0.04 0.01 0.10
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changes n (%)
Atrial fibrillation/flutter n (%) 3 (4) 22 (16) 28 (10) 0.02 0.01 0.09
*Indicates that Fishers Exact Test was used
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Table 2. Concordance between contemporary cTnI and hs-cTnI assays for patients
(K=0.53, 95% CI 0.45-0.60, 93% concordance) and myocardial injury (K=0.58, 95% CI
different test result. Boxes that are not shaded (except for those representing total
results) represent discordant diagnoses due to adjudication only, not due to a different
test result.
infarction infarction
myonecrosis
Type 1 10 56 2 9 77
myocardial
infarction
Type 2 31 8 68 33 140
myocardial
infarction
injury
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