Cardiac troponins and natriuretic peptides provide different information about myocardial dysfunction. Troponin release indicates minimal myocyte damage or loss of cell membrane integrity, and thus gives structural information, whereas BNP reflects wall stress, and thus provides functional information. Raised levels of both cardiac troponins and natriuretic peptides have been found in patients with a variety of conditions associated with overload or the damage of either or both cardiac ventricles other than ACS and CHF, including pulmonary embolism, pulmonary hypertension, sepsis, and drug toxicity. However, there have been only a few studies available that have assessed cardiac troponins and natriuretic peptides simultaneously in patients with sepsis. In the study by Charpentier et al, plasma levels of cTnI increased at days 2 and 3 in patients with myocardial dysfunction and returned to normal after day 3, which was very similar to the pattern seen for BNP. Whereas BNP levels were significantly higher in nonsurvivors compared to survivors at days 2 and 3, this was not the case for cTnI levels.
In the study by Cuthbertson et al, BNP and cTnI levels on ICU admission were higher in patients with sepsis than in other ICU patients. However, neither BNP nor cTnI levels on ICU admission or at 24 h after ICU admission were predictive for outcome in the whole study group or in the sepsis subgroup. In the analysis by Roch and coworkers, both NT-pro-BNP and cTnI levels were higher in nonsurvivors compared to survivors. However, only NT-pro-BNP level was a significant predictor of ICU death. A recent study in 57 patients with severe sepsis found a fairly good correlation between NT-proBNP and cTnI levels (r = 0.68), which might indicate a relationship between the degree of structural myocyte damage and functional myocardial impairment.
Interestingly, one study revealed that in about 50% of patients with advanced CHF cTnI levels were detectable in the absence of ACS, and that patients with elevated cTnI levels had higher PCWP, cardiac index, and BNP levels, and higher mortality than cTnI-negative patients. It has been hypothesized that, in response to wall stress, intracellular signaling cascades are activated, resulting in myocyte apoptosis and thus troponin release. However, regarding the elevation of interleukin-6 both in patients with sepsis and CHF (to a lesser degree in CHF patients, however),.. troponin leakage following the up-regulation of inflammatory cytokines has to be considered as an alternative explanation.