Our review of the literature emphasizes that differences between hs-cTnT and hs-cTnI exist in several aspects. This is illustrated both by the often surprisingly low correlation between both hs-cTn () and by variations in their distribution pattern with narrower ranges of hs-cTnI compared to hs-cTnT [, ]. Analytical issues or preanalytical interferences appear only to a minor degree to explain these discrepancies. It is thus, conceivable that they rather signify variations in the mechanisms of cardiac affections resulting in hs-cTn elevation, and of differences in cTn release and clearance patterns.
cTnT is tighter bound to tropomyosin [] and thus, released into the circulation at a slower rate compared to cTnI in case of cardiomyocyte injury [, ], [], [], []. cTnT moreover, is to a stronger degree affected by renal dysfunction but even diabetes [], [], [], [, , , ], i.e. entities reflecting general morbidity. Along this line, hs-cTnT appears to be a stronger predictor of mortality, in particular of non-CV mortality as demonstrated by the results from the GS:SFH study []. cTnI in contrast, appears to be more sensitive to myocardial ischemia [], [], [], [], [, ], [], []. It is however, hard to believe that higher hs-cTnI elevations reflect acute subclinical cardiac insults. The consequence would be a substantial loss of viable cardiomoycytes over time in patients with moderately raised concentrations, not observed in clinical studies. As to whether other mechanisms, e.g. cellular aging or increased cellular stress, might contribute to differences in release patterns and prognostic implications of both cTn remains to be elucidated.
The causes of the discrepancies between concentrations of hs-cTnT and hs-cTnI are multifactorial, and we just have started to understand the underlying cellular mechanisms []. Further preclinical studies are clearly needed. Even longitudinal investigations on the associations of temporal concentration changes for either hs-cTn with ischemic or non-ischemic outcomes, respectively would be of interest. This also applies to studies on the impact of directed medical interventions on changes of either hs-cTnT or hs-cTnI concentrations. Finally, as only the Roche and Abbott hs-assays have been used in the comparison studies, it needs to be established whether differences between both hs-cTn are generalizable to other assays.
To summarize, the preference regarding the use of either hs-cTnT or hs-cTnI for assessment of stable populations depends ultimately on the objective for testing. The current accumulated evidence suggests that hs-cTnT rather is an indicator of general CV illness whereas hs-cTnI is a stronger predictor of CAD and ischemic risk. However, the predictive differences between both hs-cTn are not tremendous and probably of minor importance when it comes to real-life clinical applications. Combination testing for both hs-cTn might be an option to improve risk prediction in stable populations but will inevitably increase the complexity of result interpretation and is for this reason not recommended. This is at difference to acutely diseased patients in whom the hs-cTnI/T ratio appears to carry some information on underlying disease mechanisms [, ]. The choice regarding the use of hs-cTnT or hs-cTnI needs also to be embedded in each respective clinical environment. The used hardware at the central laboratory needs to be considered in this context together with established pathways for patient management. Nonetheless, having the possibility to choose between either hs-cTnT or I might be an option for framing individualized CV assessment in the future.
