High-Sensitivity Troponin T in Stable Heart Failure
High-Sensitivity Troponin T in Stable Heart Failure
Cardiac troponin levels are known to be elevated in the HF population. The proportion of HF patients with baseline elevations varies in studies depending on population subtypes, troponin assay used, and cut-off point defined for raised levels. In this study, 84.4% of patients had detectable levels in plasma and 43.8% had levels above the 99 percentile for the normal range, which is a higher proportion than that described in many previous studies of patients with both acute and chronic HF, even when using a high-sensitivity assay. One previous study, using a high-sensitivity troponin assay, described a similar proportion of patients with detectable circulating troponin levels (92%), although this was using a pre-commercial assay. Interestingly, there was no significant difference between baseline levels of hsTnT in patients with ischaemic (13.9 ng/L, 95% CI 11.8–20.2) and non-ischaemic (13.7 ng/L, 95% CI 4.6–26.3) aetiologies (p=0.8). The mechanisms hypothesised to account for troponin elevations in HF, other than ischaemia, include neurohormonal activation, cytotoxic effect of inflammatory cytokines, cell stretch and the effect of oxidative stress, which may lead to chronic low-level troponin elevations. It could be hypothesised, therefore, that in clinically stable disease, the final mechanisms leading to chronic troponin elevation are similar in ischaemic and non-ischaemic aetiologies. Certainly, a history of major epicardial vessel ischaemia did not result in greater troponin elevations in this group.
In this study, hsTnT levels appeared to be stable over a relatively short period of time. This is important to consider when the diagnosis of infarction is based, not only on elevated levels, but also on demonstrating a delta change in troponin levels. Elevations due to HF should remain relatively stable over short periods of time, with a median change of less than 10% demonstrated in this study.
Discussion
Cardiac troponin levels are known to be elevated in the HF population. The proportion of HF patients with baseline elevations varies in studies depending on population subtypes, troponin assay used, and cut-off point defined for raised levels. In this study, 84.4% of patients had detectable levels in plasma and 43.8% had levels above the 99 percentile for the normal range, which is a higher proportion than that described in many previous studies of patients with both acute and chronic HF, even when using a high-sensitivity assay. One previous study, using a high-sensitivity troponin assay, described a similar proportion of patients with detectable circulating troponin levels (92%), although this was using a pre-commercial assay. Interestingly, there was no significant difference between baseline levels of hsTnT in patients with ischaemic (13.9 ng/L, 95% CI 11.8–20.2) and non-ischaemic (13.7 ng/L, 95% CI 4.6–26.3) aetiologies (p=0.8). The mechanisms hypothesised to account for troponin elevations in HF, other than ischaemia, include neurohormonal activation, cytotoxic effect of inflammatory cytokines, cell stretch and the effect of oxidative stress, which may lead to chronic low-level troponin elevations. It could be hypothesised, therefore, that in clinically stable disease, the final mechanisms leading to chronic troponin elevation are similar in ischaemic and non-ischaemic aetiologies. Certainly, a history of major epicardial vessel ischaemia did not result in greater troponin elevations in this group.
In this study, hsTnT levels appeared to be stable over a relatively short period of time. This is important to consider when the diagnosis of infarction is based, not only on elevated levels, but also on demonstrating a delta change in troponin levels. Elevations due to HF should remain relatively stable over short periods of time, with a median change of less than 10% demonstrated in this study.