Abstract
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.