Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure

Abstract

Background: Although cardiac troponin (cTn) is a cornerstone marker in the assessment and management of patients with acute coronary syndrome (ACS) and heart failure (HF), cTn is not diagnostically specific for any single myocardial disease process. This narrative review discusses increases in cTn that result from acute and chronic diseases, iatrogenic causes, and myocardial injury other than ACS and HF.Content: Increased cTn concentrations have been reported in cardiac, vascular, and respiratory disease and in association with infectious processes. In cases involving acute aortic dissection, cerebrovascular accident, treatment in an intensive care unit, and upper gastrointestinal bleeding, increased cTn predicts a longer time to diagnosis and treatment, increased length of hospital stay, and increased mortality. cTn increases are diagnostically and prognostically useful in patients with cardiac inflammatory diseases and in patients with respiratory disease; in respiratory disease cTn can help identify patients who would benefit from aggressive management. In chronic renal failure patients the diagnostic sensitivity of cTn for ACS is decreased, but cTn is prognostic for the development of cardiovascular disease. cTn also provides useful information when increases are attributable to various iatrogenic causes and blunt chest trauma.Summary: Information on the diagnostic and prognostic uses of cTn in conditions other than ACS and heart failure is accumulating. Although increased cTn in settings other than ACS or heart failure is frequently considered a clinical confounder, the astute physician must be able to interpret cTn as a dynamic marker of myocardial damage, using clinical acumen to determine the source and significance of any reported cTn increase.

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

“…Some pathophysiological factors should be borne in mind when comparing and explaining the differences in cTn release in ischemic and non-ischemic injury in patients with cardiac disease [74][75][76] and that in healthy patients following physical exercise. The kinetic profile of cTnI and cTnT circulating levels after strenuous exercise in apparently healthy subjects [25,40,[52][53][54][55][56][77][78][79][80][81][82][83][84][85][86][87][88][89][90] is different from that usually observed in patients with AMI.…”

Myocarditis in a 72-year-old woman with late onset systemic lupus erythematous

“…Interestingly, CK-MB was elevated while myoglobin and troponin had unremarkable levels. Troponin is a biomarker for the detection of myocarditis, but false positive/ negative results occur related to the troponin sensitivity (53%), negative predictive value (56%), specificity (94%) and positive predictive value of 93% 19 . The hypothesis of immunoassay interference seems strengthened in the present case, based on the usual concordance between results of CK-MB (non-immunoassay) and troponin in patients with myocarditis 20 .…”

Comparison of High-Sensitive Cardiac Troponin-T Changes between Non-ST-Segment Elevation Myocardial Infarction and Non-Coronary Artery Patients

“…In addition, there are several noncoronary-related conditions, known to cause an increase in cTn, which should be considered in the differential diagnosis of patients presenting with troponin elevation (5)(6)(7)(8). Also, there are several factors which can influence the upper reference limits of hs-cTnT (97.5th and 99th…”