Discrimination of myocardial infarction and myocardial injury using a multibiomarker approach

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Neumann ◽  
N.A Soerensen ◽  
T.S Hartikainen ◽  
P.M Haller ◽  
J Lehmacher ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Area Under The Curve ◽  
Funding Source ◽  
Multivariable Model ◽  
Multivariable Logistic Regression Model ◽  
Wide Range ◽  
Universal Definition ◽  
Definition Of

Abstract Background In the Universal Definition of Myocardial Infarction (MI) myocardial injury was introduced as a specific diagnosis in patients with elevated troponin concentrations, but without evidence of acute myocardial ischemia. However, their differentiation within the acute setting might be challenging. Therefore, we sought to investigate a multibiomarker panel in these patients and determine the discriminative capacity to differentiation MI from myocardial injury. Methods We use a cohorts of acute patients presenting to the emergency department. All final diagnoses were adjudicated by two physicians in a blinded fashion and based on the fourth universal definition of MI. In case of disagreement a third physician referred. For the present analyses only patients diagnosed with MI or myocardial injury were used. A panel of 28 biomarkers was measured in blood samples collected directly at admission. Spearman correlations were calculated. A multivariable logistic regression model using MI as the dependent variable was used and the predictors were chosen via backward step-back selection. Odds ratios (OR) were calculated for each predictor. Results We included 359 patients; 138 were diagnosed as having MI and 221 has having myocardial injury. The median age of the study population was 73 years and 59.1% were males. Hypertension was diagnosed in 80.4%, dyslipidemia in 45.4% and diabetes in 19.0%.The biomarker panel showed a wide range of correlations (Figure 1). In the multivariable model five logarithmized biomarkers (N-terminal prohormone of brain natriuretic peptide [OR 0.62], pulmonary and activation-regulated chemokine [OR 0.51], tumor-necrosis-factor-receptor 2 [OR 2.22], copeptin [OR 1.59] and high-sensitivity troponin I [OR 1.80]) were significant discriminators between MI and myocardial injury. Internal validation of the model via bootstrap shows a for overoptimism corrected area under the curve of 0.84. Conclusion In the multivariable model five biomarkers were discriminators between MI and myocardial injury. Spearman correlations Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Research fellowship by the Deutsche Forschungsgemeinschaft

Multibiomarker model to discriminate Type 1 and Type 2 myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Neumann ◽  
N.A Soerensen ◽  
T.S Hartikainen ◽  
P.M Haller ◽  
J Lehmacher ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Emergency Department ◽  
Troponin I ◽  
External Validation ◽  
Area Under The Curve ◽  
High Sensitivity ◽  
Funding Source ◽  
Multivariable Logistic Regression Model

Abstract Background The discrimination of patients with type 1 myocardial infarction (T1MI) from patients with type 2 MI (T2MI) is often challenging in the emergency department. Earlier we presented a discrimination model, which based on clinical variables, as well as on troponin concentrations. In the present analyses we sought to investigate the discriminative power of 28 biomarkers in patients with T1MI and T2MI. Methods Patients presenting to the emergency department with symptoms suggestive of MI were recruited. The final diagnosis of all patients was adjudicated by two physicians in a blinded fashion and based on the fourth universal definition of MI. For the present analyses only patients with T1MI and T2MI were used. In total 28 biomarkers were measured in blood samples collected directly at admission. A multivariable logistic regression model for T1MI vs T2MI as the dependent variable was used and the predictors were chosen via backward step-down selection. Results In total 138 patients (107 T1MI and 31 T2MI) were available for the analyses. The median age of the study population was 65 years and 66.7% were males. Hypertension was present in 77.4% and dyslipidemia in 41.3%. In the multivariable model four biomarkers (apolipoprotein A-II, n-terminal prohormone of brain natriuretic peptide, copeptin and high-sensitivity troponin I) were significant discriminators between T1MI and T2MI (Table 1). Internal validation of the model via bootstrap shows a for overoptimism corrected area under the curve of 0.82. Conclusion Using a multibiomarker approach discrimination between T1MI and T2MI could be improved. External validation of our findings is warranted. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Research fellowship by the Deutsche Forschungsgemeinschaft

scholarly journals Incidence and outcomes of perioperative myocardial infarction/injury diagnosed by high-sensitivity cardiac troponin I

2021 ◽  
Author(s):  
Danielle M. Gualandro ◽  
◽  
Christian Puelacher ◽  
Giovanna Lurati Buse ◽  
Noemi Glarner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
High Sensitivity ◽  
Prognostic Impact ◽  
Perioperative Myocardial Infarction ◽  
Important Complication ◽  
All Cause Mortality ◽  
Universal Definition ◽  
Definition Of

Abstract Background  Perioperative myocardial infarction/injury (PMI) diagnosed by high-sensitivity troponin (hs-cTn) T is frequent and a prognostically important complication of non-cardiac surgery. We aimed to evaluate the incidence and outcome of PMI diagnosed using hs-cTnI, and compare it to PMI diagnosed using hs-cTnT. Methods We prospectively included 2455 patients at high cardiovascular risk undergoing 3111 non-cardiac surgeries, for whom hs-cTnI and hs-cTnT concentrations were measured before surgery and on postoperative days 1 and 2. PMI was defined as a composite of perioperative myocardial infarction (PMIInfarct) and perioperative myocardial injury (PMIInjury), according to the Fourth Universal Definition of Myocardial Infarction. All-cause mortality was the primary endpoint. Results Using hs-cTnI, the incidence of overall PMI was 9% (95% confidence interval [CI] 8–10%), including PMIInfarct 2.6% (95% CI 2.0–3.2) and PMIInjury 6.1% (95% CI 5.3–6.9%), which was lower versus using hs-cTnT: overall PMI 15% (95% CI 14–16%), PMIInfarct 3.7% (95% CI 3.0–4.4) and PMIInjury 11.3% (95% CI 10.2–12.4%). All-cause mortality occurred in 52 (2%) patients within 30 days and 217 (9%) within 1 year. Using hs-cTnI, both PMIInfarct and PMIInjury were independent predictors of 30-day all-cause mortality (adjusted hazard ratio [aHR] 2.5 [95% CI 1.1–6.0], and aHR 2.8 [95% CI 1.4–5.5], respectively) and, 1-year all-cause mortality (aHR 2.0 [95% CI 1.2–3.3], and aHR 1.8 [95% CI 1.2–2.7], respectively). Overall, the prognostic impact of PMI diagnosed by hs-cTnI was comparable to the prognostic impact of PMI using hs-cTnT. Conclusions Using hs-cTnI, PMI is less common versus using hs-cTnT. Using hs-cTnI, both PMIInfarct and PMIInjury remain independent predictors of 30-day and 1-year mortality. Graphic abstract

Circulating Erythrocyte Microparticles and the Biochemical Extent of Myocardial Injury in ST Elevation Myocardial Infarction

Cardiology ◽  
2016 ◽  
Vol 136 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Georgios Giannopoulos ◽  
Dimitrios A. Vrachatis ◽  
Georgios Oudatzis ◽  
Georgios Paterakis ◽  
Christos Angelidis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Multivariable Analysis ◽  
Area Under The Curve ◽  
Myocardial Damage ◽  
Primary Angioplasty ◽  
St Elevation Myocardial Infarction ◽  
Vascular Effects ◽  
St Elevation

Objectives: Red blood cell microparticles (RBCm) have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI). The purpose of this study is to investigate their relationship with biochemical infarct size. Methods: RBCm were quantified with flow cytometry in blood drawn from 60 STEMI patients after a primary angioplasty. The creatine kinase-myocardial brain fraction (CK-MB) was measured at predefined time points and the area under the curve (AUC) was calculated. Results: RBCm count was correlated with CK-MB AUC (Spearman's ρ = 0.83, p < 0.001). The CK-MB AUC values per RBCm quartile (lower to upper) were: 3,351 (2,452-3,608), 5,005 (4,450-5,424), 5,903 (4,862-10,594), and 8,406 (6,848-12,782) ng × h/ml, respectively. From lower to upper quartiles, the maximal troponin I values were: 42.2 (23.3-49.3), 49.6 (28.8-54.1), 59.2 (41.4-77.3), and 69.1 (48.0-77.5) ng/ml (p = 0.005). In multivariable analysis, RBCm remained a significant predictor of CK-MB AUC (standardized β = 0.63, adjusted p = 0.001). Conclusions: Erythrocyte microparticles appear to be related to the total myocardial damage biomarker output. The exact pathophysiologic routes, if any, for this interaction remain to be identified. However, these results suggest that erythrocytes may be a - thus far virtually ignored - player in the pathogenesis of ischemic injury.

Abstract 19710: Causes for Increased Cardiac Troponin I Using Gender-Specific 99th Percentiles From a High Sensitivity Assay in a US Population

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yader Sandoval ◽  
Stephen W Smith ◽  
Karen M Schulz ◽  
MaryAnn M Murakami ◽  
Fred S Apple
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Plaque Rupture ◽  
High Sensitivity ◽  
The United States ◽  
Universal Definition ◽  
Definition Of ◽  
Gender Specific

Introduction: High-sensitivity cardiac troponin (hs-cTn) assays have not yet been FDA cleared for clinical use in the United States (US). Pending expected approval of hs-cTn assays, which will use gender-specific cutoffs (GSC), it is relevant to recognize the causes of cTn increases using hs-cTnI assays in a US population. Our purpose was to describe the frequency of distinct etiologies of hs-cTnI assay increases using GSC. Methods: Retrospective study of 310 patients with serial hs-cTnI (Abbott ARCHITECT, 99th percentiles: F:16 ng/L; M:34 ng/L) measurements. Patients with an increased hs-cTnI were adjudicated into categories according to the 3rd Universal Definition of MI. Categories included, A: primary myocardial ischemia (i.e. plaque rupture); B: injury secondary to supply/demand imbalance; C: injury not related to myocardial ischemia (i.e. cardiac contusion, ablation, shock, surgery); D: multifactorial or indeterminate myocardial injury (i.e. heart failure, critically ill, pulmonary HTN, sepsis, stroke, renal failure, pulmonary embolism); E: Unknown. Results: 127 (41%) had an increased hs-cTnI above the GSC 99th percentile, whereas 183 (59%) had a normal hs-cTnI. The most common causes of hs-cTnI increases were: a) multifactorial or indeterminate injury - 43% among all patients and 52% in males, and b) supply/demand imbalance - 39% in women (Table). Injury related to primary myocardial ischemia was present in 10% (n=13). Females had more injury related to supply/demand ischemia than males (39% vs. 18%, p=0.01), whereas males had more multifactorial or indeterminate injury (52% vs. 33%, p=0.05). Conclusions: Most increased hs-cTnI values were explained by non-plaque rupture conditions. Males tended to have hs-cTnI increases due to multifactorial/indeterminate causes, whereas in women supply/demand imbalance was the most common etiology. Investigations are needed to better understand if etiologies of myocardial injury have gender differences.

Abstract 350: Assessment of Clinicians’ Attitudes and Knowledge About Cardiac Troponin Testing

2020 ◽  
Vol 13 (Suppl_1) ◽  
Author(s):  
Sandeep Jain ◽  
Andrew Hammes ◽  
Eric Rudofker ◽  
Karen Ream ◽  
Andrew E Levy
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
The United States ◽  
Advanced Practice ◽  
Attitudes And Knowledge ◽  
Universal Definition ◽  
Definition Of ◽  
Attending Physicians

In the United States, the positive predictive value (PPV) of cardiac troponin for type 1 myocardial infarction is substantially lower than in Europe (15% vs. 50%). Further, even with publication of the 4 th Universal Definition of Myocardial Infarction, recent studies have shown that inaccurate classification of myocardial injury is common among clinicians in the United States. These findings are at least partly attributable to clinicians’ knowledge and attitudes about cardiac troponin testing; a survey of these parameters has never been conducted. Clinicians at the University of Colorado completed a brief 8-question multiple-choice survey related to troponin use, definitions of myocardial infarction and clinical assessment of elevated troponin levels. The survey was distributed via secure email and administered electronically using the Qualtrics™ platform. Responses were anonymous, completion was estimated to take 3 minutes and a lottery award system was used as an incentive for participation. Respondents included trainees, advanced practice providers and attending physicians from internal medicine, emergency medicine and medical subspecialties. We plan to obtain a total of 300 responses with descriptive findings of preliminary results included below. The survey was completed by 114 clinicians: 37 interns (32%), 45 residents (39%), 9 advanced practice providers (8%), 11 fellows (10%), and 12 attending physicians (11%). Regarding indications for troponin testing, 93% (106/114) indicated that they “usually” or “always” check troponin levels in patients with chest pain. More interestingly, 46% (52/112) reported checking troponin on “undifferentiated patients” at least half the time. For troponin interpretation, 97% (110/114) of participants identified that troponin levels alone cannot rule in or rule out coronary artery disease. In contrast, only 36% (41/114) and 55% (63/114), respectively, identified the NPV and PPV of a contemporary troponin assay for type 1 MI. Further, only 50% (57/114) of respondents identified that the likelihood of type 1 MI increases as troponin levels increase. Three brief clinical vignettes revealed that, while 78% (89/114) and 74% (45/61) of participants, respectively, identified type 1 MI and type 2 MI presentations, only 40% (21/53) of respondents correctly identified a vignette for non-ischemic myocardial injury. Concordant with this finding, 54% (61/114) of clinicians correctly identified the 4 th Universal Definition of Myocardial Infarction. These preliminary findings highlight important facets of clinician attitudes and knowledge about troponin testing that help explain the poor PPV for troponin and diagnostic misclassification observed among U.S. clinicians. These results could help guide curricular and clinical decision support interventions designed to improve the use and interpretation of cardiac troponin testing.

scholarly journals Discordance between ICD-Coded Myocardial Infarction and Diagnosis according to the Universal Definition of Myocardial Infarction

2017 ◽  
Vol 63 (1) ◽  
pp. 415-419 ◽  
Author(s):  
Jorge Díaz-Garzón ◽  
Yader Sandoval ◽  
Stephen W Smith ◽  
Sara Love ◽  
Karen Schulz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Troponin I ◽  
High Sensitivity ◽  
International Classification Of Diseases ◽  
Healthcare Management ◽  
Clinical Indication ◽  
Kappa Index ◽  
Universal Definition ◽  
Definition Of

Abstract BACKGROUND International Classification of Diseases (ICD) coding is the standard diagnostic tool for healthcare management. At present, type 2 myocardial infarction (T2MI) classification by the Universal Definition of Myocardial Infarction (MI) remains ignored in the ICD system. We determined the concordance for the diagnosis of MI using ICD-9 coding vs the Universal Definition. METHODS Cardiac troponin I (cTnI) was measured by both contemporary (cTnI) and high-sensitivity (hs-cTnI) assays in 1927 consecutive emergency department (ED) patients [Use of TROPonin In Acute coronary syndromes (UTROPIA) cohort] who had cTnI ordered on clinical indication. All patients were adjudicated using both contemporary and hs-cTnI assays. The Kappa index and McNemar test were used to assess concordance between ICD-9 code 410 and type 1 MI (T1MI) and type 2 MI (T2MI). RESULTS Among the 249 adjudicated MIs using the contemporary cTnI, only 69 (28%) were ICD-coded MIs. Of 180 patients not ICD coded as MI, 34 (19%) were T1MI and 146 (81%) were T2MI. For the ICD-coded MIs, 79% were T1MI and 21% were T2MI. A fair Kappa index, 0.386, and a McNemar difference of 0.0892 (P &lt; 0.001) were found. Among the 207 adjudicated MIs using the hs-cTnI assay, 67 (32%) were ICD coded as MI. Of the 140 patients not ICD coded as MI, 27 (19%) were T1MI and 113 (81%) were T2MI. For the ICD-coded MIs, 85% were T1MI and 15% T2MI. A moderate Kappa index, 0.439, and a McNemar difference of 0.0674 (P &lt; 0.001) were found. CONCLUSIONS ICD-9–coded MIs captured only a small proportion of adjudicated MIs, primarily from not coding T2MI. Our findings emphasize the need for an ICD code for T2MI.

scholarly journals Acute myocardial damage in new coronavirus infection (COVID-19)

2021 ◽  
Vol 20 (5) ◽  
pp. 98-104
Author(s):  
N. V. Izmozherova ◽  
A. A. Popov ◽  
A. I. Tsvetkov ◽  
M. A. Shambatov ◽  
I. P. Antropova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Medical Care ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Damage ◽  
True Incidence ◽  
Wide Range ◽  
Acute Myocardial Injury ◽  
Coronavirus Infection

Introduction. Acute respiratory distress syndrome (ARDS) and cardiovascular events, acute myocardial injury being the most frequent of the latter, are among the leading causes of death in COVID-19 patients. The lack of consensus on acute myocardial injury pathogenesis mechanisms, the patients management, treatment an rehabilitation logistics, the anticoagulant treatment in identified SARS-CoV-2 or suspected COVID-19 patients setting indicates the need to assess, analyze and summarize the available data on the issue.Materials and methods. Scientific publications search was carried out in PubMed, Google Scholar databases for the period from December 2019 to September 2021.Results and Discussion. Cardiospecific troponin I increase beyond reference limits is reported to occur in at least every tenth patient with identified SARS-CoV-2, the elevated troponin detection rate increasing among persons with moderate to severe course of the infection. The mechanisms of acute myocardial injury in patients with COVID-19 are poorly understood. By September 2021, there are several pathogenesis theories. A high frequency viral myocarditis direct cardiomyocytes damage is explained by the high SARS-CoV-2 affinity to ACE2 expressed in the myocardium. The cytokine storm related myocardial damage is reported a multiple organ failure consequence. Coagulopathy may also trigger myocardial microvessels damage. Up to every third death of SARS-CoV-2 infected persons is related to the acute myocardial injury. At the same time, due to the high incidence of the acute myocardial injury, it is rather difficult to assess the true incidence of acute myocardial infarction in patients with COVID-19. In the pandemic setting, the waiting time for medical care increases, the population, trying to reduce social contacts, is less likely to seek medical help. In this regard, in order to provide effective medical care to patients with acute myocardial infarction, it is necessary to develop algorithms for providing care adapted to the current epidemiological situation.Conclusion. The treatment of patients with probable development of acute myocardial damage against the background of new coronavirus infection should be performed in accordance with the current clinical guidelines. Anticoagulant therapy should be administered in a prophylactic dose under control of hemostasis parameters and a wide range of biochemical parameters.

scholarly journals Concordance, Variance, and Outliers in 4 Contemporary Cardiac Troponin Assays: Implications for Harmonization

2012 ◽  
Vol 58 (1) ◽  
pp. 274-283 ◽  
Author(s):  
Jacobus P J Ungerer ◽  
Louise Marquart ◽  
Peter K O'Rourke ◽  
Urs Wilgen ◽  
Carel J Pretorius
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Analytical Imprecision ◽  
Universal Definition ◽  
Definition Of ◽  
Abbott Architect ◽  
Roche Cobas

Abstract BACKGROUND Data to standardize and harmonize the differences between cardiac troponin assays are needed to support their universal status in diagnosis of myocardial infarction. We characterized the variation between methods, the comparability of the 99th-percentile cutoff thresholds, and the occurrence of outliers in 4 cardiac troponin assays. METHODS Cardiac troponin was measured in duplicate in 2358 patient samples on 4 platforms: Abbott Architect i2000SR, Beckman Coulter Access2, Roche Cobas e601, and Siemens ADVIA Centaur XP. RESULTS The observed total variances between the 3 cardiac troponin I (cTnI) methods and between the cTnI and cardiac troponin T (cTnT) methods were larger than expected from the analytical imprecision (3.0%–3.7%). The between-method variations of 26% between cTnI assays and 127% between cTnI and cTnT assays were the dominant contributors to total variances. The misclassification of results according to the 99th percentile was 3%–4% between cTnI assays and 15%–17% between cTnI and cTnT. The Roche cTnT assay identified 49% more samples as positive than the Abbott cTnI. Outliers between methods were detected in 1 patient (0.06%) with Abbott, 8 (0.45%) with Beckman Coulter, 10 (0.56%) with Roche, and 3 (0.17%) with Siemens. CONCLUSIONS The universal definition of myocardial infarction should not depend on the choice of analyte or analyzer, and the between- and within-method differences described here need to be considered in the application of cardiac troponin in this respect. The variation between methods that cannot be explained by analytical imprecision and the discordant classification of results according to the respective 99th percentiles should be addressed.

scholarly journals Troponin elevation pattern and subsequent cardiac and non-cardiac outcomes: Implementing the Fourth Universal Definition of Myocardial Infarction and high-sensitivity troponin at a population level

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248289
Author(s):  
Anthony (Ming-yu) Chuang ◽  
Mau T. Nguyen ◽  
Ehsan Khan ◽  
Dylan Jones ◽  
Matthew Horsfall ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Arrhythmia ◽  
Myocardial Injury ◽  
High Sensitivity ◽  
Cardiac Outcomes ◽  
High Sensitivity Troponin ◽  
Acute Myocardial Injury ◽  
Acute Mi ◽  
Universal Definition ◽  
Definition Of

Background The Fourth Universal Definition of Myocardial Infarction (MI) differentiates MI from myocardial injury. We characterised the temporal course of cardiac and non-cardiac outcomes associated with MI, acute and chronic myocardial injury. Methods We included all patients presenting to public emergency departments in South Australia between June 2011–Sept 2019. Episodes of care (EOCs) were classified into 5 groups based on high-sensitivity troponin-T (hs-cTnT) and diagnostic codes: 1) Acute MI [rise/fall in hs-cTnT and primary diagnosis of acute coronary syndrome], 2) Acute myocardial injury with coronary artery disease (CAD) [rise/fall in hs-cTnT and diagnosis of CAD], 3) Acute myocardial injury without CAD [rise/fall in hs-cTnT without diagnosis of CAD], 4) Chronic myocardial injury [elevated hs-cTnT without rise/fall], and 5) No myocardial injury. Multivariable flexible parametric models were used to characterize the temporal hazard of death, MI, heart failure (HF), and ventricular arrhythmia. Results 372,310 EOCs (218,878 individuals) were included: acute MI (19,052 [5.12%]), acute myocardial injury with CAD (6,928 [1.86%]), acute myocardial injury without CAD (32,231 [8.66%]), chronic myocardial injury (55,056 [14.79%]), and no myocardial injury (259,043 [69.58%]). We observed an early hazard of MI and HF after acute MI and acute myocardial injury with CAD. In contrast, subsequent MI risk was lower and more constant in patients with acute injury without CAD or chronic injury. All patterns of myocardial injury were associated with significantly higher risk of all-cause mortality and ventricular arrhythmia. Conclusions Different patterns of myocardial injury were associated with divergent profiles of subsequent cardiac and non-cardiac risk. The therapeutic approach and modifiability of such excess risks require further research.

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