Elevation of cardiac troponins and creatinine kinase is frequently observed in setting of systemic inflammatory response syndrome (SIRS), sepsis, or septic shock. Underlying pathophysiologic mechanism for such troponin leak, its clinical significance, and what different could be done in such settings remain elusive. In this paper we have briefly overviewed the proposed pathogenic mechanisms for SIRS, sepsis, or septic shock-related troponin elevation (SRTE) and have provided brief overview on its clinical significance. Upon review of the relevant literature we found that majority of patients with the SRTE with no prior history of coronary artery disease (CAD) upon testing are found not to have any CADs. We have also briefly discussed the possible pharmacologic agents and potential targets which are important from pathophysiologic and pharmacologic point of view that may alter the outcomes of SRTE-related myocardial depression in near future. 1. Introduction Elevation of cardiac troponins and creatinine kinase (CK) is observed in 31%–80% of patients in setting of systemic inflammatory response syndrome (SIRS), sepsis, or septic shock (SIRS, sepsis, or septic shock related troponin elevations (SRTE)) [1–3]. Skeletal muscle ischemia due to sepsis-related hypotension explains the elevated CK [3]. Cardiac troponins are elevated only when there is an insult to cardiac myocytes; what causes this insult in the setting of sepsis is not known. Different theories have been hypothesized to explain the SRTE. From academic as well as from a clinical standpoint defining the etiopathogenesis of the SRTE and its significance will have important clinical implications. There are no consensus guidelines on how to approach patients with SRTE. Majority of SRTE patients without any prior history of coronary artery disease (CAD) on testing are found not to have any significant CADs [3–5] (Table 1). Troponin elevation in setting of sepsis has been proposed as a biomarker for underlying myocardial dysfunction [6]. Sepsis-related mortality has been reported to equal the mortality due to myocardial infarction [7, 8] and myocardial dysfunction has been shown to be a common complication in the setting of sepsis [7, 8]. Table 1 The purpose of this paper is to briefly review three basic questions: what causes SRTE, what is its clinical significance and what different can be done in such cases? 2. What Is Cardiac Troponin? Troponin is a complex of three regulatory proteins (troponin I, TnI, troponin C, TnC, troponin T, TnT) [6] and TnT binds to tropomyosin that lies in between the
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