ReviewCureus2026
Cardiac Troponin Elevation Beyond Type 1 Myocardial Infarction: A Systematic Review of Prognostic Significance and Cardiovascular Risk Stratification.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac troponin elevation is central to the diagnosis of myocardial injury, but its clinical interpretation remains challenging when type 1 myocardial infarction is absent. This systematic review evaluated the clinical and prognostic significance of elevated cardiac troponin in adults without type 1 myocardial infarction, with particular emphasis on type 2 myocardial infarction, critical illness-related myocardial injury, suspected acute coronary syndrome populations with minor myocardial injury, and acute or chronic heart failure-related myocardial injury. A systematic search of PubMed/MEDLINE, Scopus, and Web of Science identified six eligible clinical studies. The included evidence comprised prospective and retrospective cohort studies, secondary biomarker analyses of randomized trials, and trial-derived heart failure cohorts. Across heterogeneous clinical settings, troponin elevation was consistently associated with adverse outcomes, including all-cause mortality, cardiovascular mortality, heart failure hospitalization, cardiovascular death or heart failure rehospitalization, and greater clinical severity. In type 2 myocardial infarction and critical illness, troponin elevation identified high-risk patients despite the absence of classic plaque-rupture acute coronary syndrome. In heart failure populations, troponin appeared to function as a dynamic marker of myocardial stress, residual risk, and treatment-responsive injury. High-sensitivity assays further suggest that troponin may convey prognostic information across a continuum rather than only above binary diagnostic thresholds. These findings support a phenotype-based approach in which troponin elevation outside type 1 myocardial infarction is interpreted according to mechanism, clinical context, biomarker trajectory, and follow-up needs. Although current evidence does not define a uniform treatment pathway, it indicates that troponin-positive patients without type 1 myocardial infarction should not be considered low risk solely because acute coronary syndrome has been excluded. Future prospective studies should determine which troponin-positive phenotypes benefit most from structured cardiovascular reassessment, targeted investigation, and post-discharge surveillance.
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