scholarly journals Myocardial Infarction Type 2 and Myocardial Injury

2017 ◽  
Vol 63 (1) ◽  
pp. 101-107 ◽  
Author(s):  
Yader Sandoval ◽  
Kristian Thygesen
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Thrombotic Event ◽  
High Sensitivity ◽  
Diagnostic Strategies ◽  
Atherothrombotic Event ◽  
Patients At Risk ◽  
Poor Outcomes

Abstract BACKGROUND The development and implementation of sensitive and high-sensitivity cardiac troponin assays has not only expedited the early ruling in and ruling out of acute myocardial infarction, but has also contributed to the identification of patients at risk for myocardial injury with necrosis, as confirmed by the presence of cardiac troponin concentrations above the 99th percentile. Myocardial injury with necrosis may occur either in the presence of overt ischemia from myocardial infarction, or in the absence of overt ischemia from myocardial injury accompanying other conditions. Myocardial infarction type 2 (T2MI) has been a focus of attention; conceptually T2MI occurs in a clinical setting with overt myocardial ischemia where a condition other than an acute atherothrombotic event is the major contributor to a significant imbalance between myocardial oxygen supply and/or demand. Much debate has surrounded T2MI and its interrelationship with myocardial injury. CONTENT We provide a detailed overview of the current concepts and challenges regarding the definition, diagnosis, management, and outcomes of T2MI, as well as the interrelationship to myocardial injury, and emphasize several critical clinical concepts for both clinicians and researchers moving forward. SUMMARY T2MI and myocardial injury are frequently encountered in clinical practice and are associated with poor outcomes in both the short term and long term. Diagnostic strategies to facilitate the clinical distinction between ischemic myocardial injury with or without an acute atheroma-thrombotic event vs non–ischemic-mediated myocardial injury conditions are urgently needed, as well as evidence-based therapies tailored toward improving outcomes for patients with T2MI.

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

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

Understanding cardiac troponin part 1: avoiding troponinitis

2017 ◽  
Vol 35 (2) ◽  
pp. 120-125 ◽  
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.

scholarly journals No additional value of conventional and high-sensitivity cardiac troponin over clinical scoring systems in the differential diagnosis of type 1 vs. type 2 myocardial infarction

2018 ◽  
Vol 56 (5) ◽  
pp. 702-709 ◽  
Author(s):  
Luciano Consuegra-Sánchez ◽  
Juan José Martínez-Díaz ◽  
Luis García de Guadiana-Romualdo ◽  
Samantha Wasniewski ◽  
Patricia Esteban-Torrella ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Characteristic Curve ◽  
High Sensitivity ◽  
St Segment ◽  
Clinical Scoring

AbstractBackground:The distinction of type 1 and type 2 myocardial infarction (MI) is of major clinical importance. Our aim was to evaluate the diagnostic ability of absolute and relative conventional cardiac troponin I (cTnI) and high-sensitivity cardiac troponin T (hs-cTnT) in the distinction between type 1 and type 2 MI in patients presenting at the emergency department with non-ST-segment elevation acute chest pain within the first 12 h.Methods:We measured cTnI (Dimension Vista) and hs-cTnT (Cobas e601) concentrations at presentation and after 4 h in 200 patients presenting with suspected acute MI. The final diagnosis, based on standard criteria, was adjudicated by two independent cardiologists.Results:One hundred and twenty-five patients (62.5%)were classified as type 1 MI and 75 (37.5%) were type 2 MI. In a multivariable setting, age (relative risk [RR]=1.43, p=0.040), male gender (RR=2.22, p=0.040), T-wave inversion (RR=8.51, p<0.001), ST-segment depression (RR=8.71, p<0.001) and absolute delta hs-cTnT (RR=2.10, p=0.022) were independently associated with type 1 MI. In a receiver operating characteristic curve analysis, the discriminatory power of absolute delta cTnI and hs-cTnT was significantly higher compared to relative c-TnI and hs-cTnT changes. The additive information provided by cTnI and hs-cTnT over and above the information provided by the “clinical” model was only marginal.Conclusions:The diagnostic information provided by serial measurements of conventional or hs-cTnT is not better than that yielded by a simple clinical scoring model. Absolute changes are more informative than relative troponin changes.

Myeloid-related protein 8/14 and high-sensitivity cardiac troponin I to differentiate type 2 myocardial infarction

2020 ◽  
Vol 304 ◽  
pp. 144-147 ◽  
Author(s):  
Johanna Bormann ◽  
Dimitrios A. Psyrakis ◽  
Beatrice von Jeinsen ◽  
Dimitri Grün ◽  
Laura K. Elsner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
High Sensitivity ◽  
Cardiac Troponin I ◽  
Related Protein

scholarly journals Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to High-Sensitivity Cardiac Troponin I

2017 ◽  
Vol 130 (12) ◽  
pp. 1431-1439.e4 ◽  
Author(s):  
Yader Sandoval ◽  
Stephen W. Smith ◽  
Anne Sexter ◽  
Sarah E. Thordsen ◽  
Charles A. Bruen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
High Sensitivity ◽  
Cardiac Troponin I ◽  
Clinical Transition

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

Circulation ◽  
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

High-sensitivity cardiac troponin assays and unstable angina

2016 ◽  
Vol 7 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Yader Sandoval ◽  
Fred S Apple ◽  
Stephen W Smith
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Unstable Angina ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Necrosis ◽  
High Sensitivity ◽  
Clinical Context ◽  
Over Time

The term unstable angina has been conventionally applied to patients with myocardial ischemia without myocardial necrosis. However, while the clinical context has remained constant over time, the biomarkers of myocardial injury and acute myocardial infarction have evolved. High-sensitivity cardiac troponin assays have several key analytical differences from prior cardiac troponin assay generations, which may alter the diagnosis and frequency of unstable angina, as well as affect our understanding of previously developed risk stratification strategies. This document reviews the current challenges in regards to unstable angina when using high-sensitivity cardiac troponin I and T assays.

249High-sensitivity cardiac troponin and the universal definition of myocardial infarction: a randomised controlled trial

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A R Chapman ◽  
P D Adamson ◽  
A Anand ◽  
A S V Shah ◽  
K K Lee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Primary Outcome ◽  
Controlled Trial ◽  
High Sensitivity ◽  
Cardiovascular Death ◽  
Acute Myocardial Injury ◽  
Universal Definition

Abstract Background The Universal Definition of Myocardial Infarction recommends the 99th centile diagnostic threshold using a high-sensitivity cardiac troponin (hs-cTn) assay and the classification of patients by the etiology of myocardial injury. Whether implementation of this definition improves risk stratification, treatment or outcomes is unknown. Methods In a stepped-wedge cluster randomized controlled trial, we implemented a high-sensitivity troponin assay and the recommendations of the Universal Definition in 48,282 consecutive patients with suspected acute coronary syndrome across ten hospitals. In a pre-specified secondary analysis, we compared the primary outcome of myocardial infarction or cardiovascular death, and secondary outcome of non-cardiovascular death at one year across diagnostic categories as per the Fourth Universal Definition. We applied competing risks methodology in all analyses, using a cumulative incidence function and determining the cause-specific hazard ratio (csHR) for competing outcomes. Results Cardiac troponin concentrations were elevated in 21.5% (10,360/48,282) of all trial participants. Implementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4,471), type 2 myocardial infarction by 22% (205/916), acute myocardial injury by 36% (443/1,233) and chronic myocardial injury by 43% (389/898). The risk and rate of the primary outcome was highest in those with type 1 myocardial infarction, whereas the risk and rate of non-cardiovascular death was highest in those with acute myocardial injury (Table, Figure). Despite increases in anti-platelet therapy and coronary revascularization after implementation, the primary outcome was unchanged in patients with type 1 myocardial infarction (csHR 1.00, 95% CI 0.82 to 1.21), or in any other category. Adjusted csHR for competing outcomes Myocardial infarction or cardiovascular death Non-cardiovascular death Adjusted csHR (95% CI) Adjusted csHR (95% CI) Type 1 myocardial infarction 5.64 (5.12 to 6.22) 0.83 (0.72 to 0.96) Type 2 myocardial infarction 3.50 (2.94 to 4.15) 1.72 (1.44 to 2.06) Acute myocardial injury 4.38 (3.80 to 5.05) 2.65 (2.33 to 3.00) Chronic myocardial injury 3.88 (3.31 to 4.55) 2.06 (1.77 to 2.40) Cox regression models adjusted for age, sex, diabetes, ischaemic heart disease, season, days since trial onset and site of recruitment (as a random effect). Cumulative incidence and number at risk Conclusions Implementation of the recommendations of the Universal Definition identified patients with different risks of future cardiovascular and non-cardiovascular events, but did not improve outcomes. Greater understanding of the underlying mechanisms and effective strategies for the investigation and treatment of patients with myocardial injury and infarction are required if we are to improve outcomes. Acknowledgement/Funding British Heart Foundation

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