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Proteolytic Digestion of Serum Cardiac Troponin I as Marker of Ischemic Severity
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- Author(s) / Creator(s)
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Background: The serum troponin assay is the biochemical gold standard for detecting myocardial infarction
(MI). A major diagnostic issue is that some believe troponin levels can rise with reversible injury, in the absence of
radiologically detectable infarct.
Hypothesis: Because cell death activates intracellular proteases, troponin released by irreversible infarct will be
more proteolyzed than that released by milder processes. Our goal was to quantify proteolytic digestion of cardiac
troponin I in patients with varying degrees of myocardial injury.
Methods: Serum or plasma samples from 29 patients with cardiac troponin I elevations were analyzed for
proteolytic degradation, using 3 different sandwich ELISAs designed to specifically detect the N-terminal, core, or
C-terminal regions of cardiac troponin I.
Results: As predicted, the degree of proteolytic digestion increased with increasing severity of injury, as estimated
by the total troponin level, and this trend was more pronounced for C-terminal (vs N-terminal) degradation.
The highest degree of proteolytic digestion was observed in patients with ST-elevation MI; the least, in type 2 MI
(supply–demand ischemia rather than acute thrombus formation).
Conclusions: The proteolytic degradation pattern of cardiac troponin I may be a better indicator of clinically
significant MI than total serum troponin level. Distinguishing between intact and degraded forms of troponin may
be useful for (a) identifying those patients with clinically significant infarct in need of revascularization, (b) monitoring
intracellular proteolysis as a possible target for therapeutic intervention, and (c) providing an impetus for
standardizing the epitopes used in the troponin I assay -
- Date created
- 2018-02-13
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- Subjects / Keywords
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- Type of Item
- Article (Published)
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- License
- Attribution 4.0 International