The fact that even in healthy people raised levels of cTnT, and cTnI, as well as BNP are found after prolonged strenuous exercise, and that after a triathlon LVEF, fractional shortening, and stroke volume have been shown to be significantly different from prerace values despite unchanged preload and even decreased afterload, and to recover to baseline levels within 48 h, strengthens the assumption that transient myocardial depression with short-lasting troponin leakage in the absence of myocyte necrosis and BNP release following an inflammatory process (eg, sepsis and extreme endurance exercise) does really exist. Interestingly, experimental evidence for a direct up-regulation of the BNP gene by lipopoly-saccharides has come from a study in rats. Regarding the weak correlation between BNP level and hemodynamic parameters, a similar up-regulation of proBNP synthesis and the release of BNP and NT-pro-BNP mediated by cytokines must be strongly considered to explain the sometimes extraordinarily high BNP levels in patients with sepsis. In addition, anemia could also play a role, as a relationship between low hemoglobin levels and elevated BNP and NT-proBNP levels has been demonstrated in patients without sepsis. Figure 2 summarizes the possible mechanisms contributing to elevated serum BNP and troponin levels in patients with severe sepsis and septic shock. The speculative and incomplete nature of the proposed diagram needs to be emphasized. other
However, it remains to be established whether BNP levels provide additional information to that obtained by the measurement of cardiac troponin levels, and whether an approach relying on information coming from both of these biomarker could optimize the assessment of sepsis-associated myocardial dysfunction.
There is evidence from several small studies that elevated cardiac troponin levels in patients with sepsis indicate myocardial dysfunction and a poor prognosis. As far as the diagnosis of sepsis is obvious, and other conditions such as ACS, pulmonary embolism, or end-stage renal failure are excluded, elevated cardiac troponin levels may help to identify high-risk patients, who should undergo echocardiography, invasive hemodynamic monitoring, and optimized therapy.
Figure 2. Schematic visualization of possible mechanisms leading to elevated cardiac troponin (cTn) and BNP levels in patients with severe sepsis and septic shock. Dashed lines indicate a more speculative nature of the suggested mechanism. ALI = acute lung injury; IL = interleukin; LV = left ventricular; RV = right ventricular; RVEDP = right ventricular end-diastolic pressure; RVSWI = right ventricular stroke work index; TNF = tumor necrosis factor.