Prognostic Impact of Myocardial Injury Related to Various Cardiac and Noncardiac Conditions

Sarkisian, Laura; Saaby, Lotte; Poulsen, Tina Svenstrup; Gerke, Oke; Hosbond, Susanne; Jangaard, Nikolaj; Diederichsen, Axel Cosmus Pyndt; Thygesen, Kristian; Mickley, Hans

doi:10.1016/j.amjmed.2015.12.009

Cited by 64 publications

(56 citation statements)

References 50 publications

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“…[1] One recent study of all troponin tests ordered by treating physicians in a hospital system found 42% of these tests to be positive; 29% were secondary to a non-thrombotic (type 2) troponin elevation as compared to 13% from an acute MI diagnosis. [3] Mortality was 59% at 3.2 years in the patients with non-thrombotic (type 2) troponin elevations. [3] Troponin is further limited by the fact that it is a measure of myocardial necrosis, the outcome of the triggering event, rather than the cause and therapeutic target itself (i.e., plaque disruption and ensuing thrombosis).…”

Section: Discussionmentioning

confidence: 99%

“…[3] Mortality was 59% at 3.2 years in the patients with non-thrombotic (type 2) troponin elevations. [3] Troponin is further limited by the fact that it is a measure of myocardial necrosis, the outcome of the triggering event, rather than the cause and therapeutic target itself (i.e., plaque disruption and ensuing thrombosis). Therefore, troponin elevations often fail to confirm the diagnosis of acute MI before the induction of irreversible myocardial necrosis, even with highly sensitive cardiac troponin assays.…”

Section: Discussionmentioning

confidence: 99%

“…[2] One recent study of all troponin tests ordered by treating physicians in a hospital system found 42% of troponin tests to be positive; 29% were secondary to non-thrombotic (type 2) etiologies compared with 13% from an acute thrombotic MI diagnosis. [3] Mortality was 59% at 3.2 years in the patients with non-thrombotic (type 2) troponin elevations. [3] Furthermore, while circulating levels of troponin are specific indicators of myocardial necrosis, the levels of these proteins often do not increase for several hours after the start of an acute MI.…”

Section: Introductionmentioning

confidence: 99%

“…[3] Mortality was 59% at 3.2 years in the patients with non-thrombotic (type 2) troponin elevations. [3] Furthermore, while circulating levels of troponin are specific indicators of myocardial necrosis, the levels of these proteins often do not increase for several hours after the start of an acute MI. [4] Therefore, current diagnostic criteria for acute MI are unable to delineate the cause of acute MI and often fail to confirm the diagnosis before the induction of irreversible myocardial necrosis, even with modern “super sensitive” cardiac troponin assays.…”

Section: Introductionmentioning

confidence: 99%

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Identification of a plasma metabolomic signature of thrombotic myocardial infarction that is distinct from non-thrombotic myocardial infarction and stable coronary artery disease

et al. 2017

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AimsCurrent non-invasive diagnostics for acute myocardial infarction (MI) identify myocardial necrosis rather than the primary cause and therapeutic target—plaque disruption and resultant thrombosis. The aim of this study was to identify changes specific to plaque disruption and pathological thrombosis that are distinct from acute myocardial necrosis.Methods and resultsWe quantified 1,032 plasma metabolites by mass spectrometry in 11 thrombotic MI, 12 non-thrombotic MI, and 15 stable coronary artery disease (CAD) subjects at two acute phase (time of catheterization [T0], six hours [T6]) and one quiescent (>3 months follow-up) time points. A statistical classifier was constructed utilizing baseline (T0) abundances of a parsimonious set of 17 qualifying metabolites. Qualifying metabolites were those that demonstrated a significant change between the quiescent phase and the acute phase and that were distinct from any change seen in non-thrombotic MI or stable CAD subjects. Classifier performance as estimated by 10-fold cross-validation was suggestive of high sensitivity and specificity for differentiating thrombotic from non-thrombotic MI and stable CAD subjects at presentation.Nineteen metabolites demonstrated an intra-subject change from time of acute thrombotic MI presentation to the quiescent state that was distinct from any change measured in both the non-thrombotic MI and stable CAD subjects undergoing cardiac catheterization over the same time course (false discovery rate <5%).ConclusionsWe have identified a candidate metabolic signature that differentiates acute thrombotic MI from quiescent state after MI, from acute non-thrombotic MI, and from stable CAD. Further validation of these metabolites is warranted given their potential as diagnostic biomarkers and novel therapeutic targets for the prevention or treatment of acute MI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Identification of a plasma metabolomic signature of thrombotic myocardial infarction that is distinct from non-thrombotic myocardial infarction and stable coronary artery disease

et al. 2017

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“…The rise and fall profiles of both the hs-cTnT and CK-MB concentrations seen in our study resemble those of an evolving acute myocardial infarction and the development of acute nonischemic myocardial injury. 37,38 A number of causes for nonischemic myocardial injury include cardiac contusion, cardiac pulmonary resuscitation, repetitive defibrillation shocks, coronary angiography, heart failure, critical illness, and postcardiac arrest syndrome. 12,39 This diversity of potential causes, reflecting the multifactorial conditions after out-of-hospital cardiac arrest, may explain the large variability of the biomarker measurements in our study which has also been demonstrated by others.…”

Section: Assessment Of Myocardial Injury By Cardiac Biomarkersmentioning

confidence: 99%

The Extent of Myocardial Injury During Prolonged Targeted Temperature Management After Out-of-Hospital Cardiac Arrest

Grejs

Gjedsted

Thygesen

et al. 2017

The American Journal of Medicine

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This study of comatose out-of-hospital cardiac arrest survivors showed no difference between the extents of myocardial injury estimated by hs-cTnT of prolonged targeted temperature management of 48 hours vs 24 hours, although the CK-MB was significantly higher during 48 hours vs 24 hours. Hence, it seems unlikely that the duration of targeted temperature management has a beneficial effect on the extent of myocardial injury after out-of-hospital cardiac arrest, and may even have a worsening effect.

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Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

et al. 2019

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Prognostic Impact of Myocardial Injury Related to Various Cardiac and Noncardiac Conditions

Cited by 64 publications

References 50 publications

Identification of a plasma metabolomic signature of thrombotic myocardial infarction that is distinct from non-thrombotic myocardial infarction and stable coronary artery disease

Identification of a plasma metabolomic signature of thrombotic myocardial infarction that is distinct from non-thrombotic myocardial infarction and stable coronary artery disease

The Extent of Myocardial Injury During Prolonged Targeted Temperature Management After Out-of-Hospital Cardiac Arrest

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

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