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. 2019 Sep 22:25:7115-7125.
doi: 10.12659/MSM.915830.

Elevated Cardiac Troponin in Clinical Scenarios Beyond Obstructive Coronary Artery Disease

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Elevated Cardiac Troponin in Clinical Scenarios Beyond Obstructive Coronary Artery Disease

Michael Sternberg et al. Med Sci Monit. .

Abstract

In this systematic review article, we aim to summarize the most up-to-date evidence regarding elevations of cardiac troponin, especially in clinical scenarios other than obstructive coronary artery disease. The accurate interpretation of raised cardiac troponin is challenging because it relies on unconfirmed postulations and dogmatic knowledge (e.g., the exclusive provenience of cardiac troponin from cardiac myocytes), based on which every troponin elevation is assumed to definitely indicate myocardial damage. Indeed, the investigation of the pathophysiologic mechanism leading to the release in the bloodstream of cardiac biomarkers should be the first step of the diagnostic process to fully understand the clinical significance of the elevated serum levels and identify the best management. A prominent effort should be put in place to identify the contribution of potential confounding factors, both cardiac and non-cardiac in etiology, with the ability to affect synthesis and clearance of cardiac biomarkers. Regardless of the underlying cause, it is well established that cardiovascular biomarkers are increasingly useful to further risk stratification and prognosticate patients. Accordingly, we sought to clarify the meaning and impact of elevated cardiac troponin in those frequently encountered real-world scenarios presenting clinicians with a diagnostic dilemma, with the final goal of facilitating the diagnosis and help optimize individually tailored treatment strategies.

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Conflict of interest statement

Conflicts of interest

None.

Figures

Figure 1
Figure 1
Various clinical scenarios causing an elevation in cardiac troponins.
Figure 2
Figure 2
Physiology of contraction-relaxation cycle in cardiac myocytes and role of troponin [10].
Figure 3
Figure 3
Postulated biochemical mechanisms responsible for hypercatabolic protein breakdown.

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