Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release

Background Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. Methods The study included 50 ICU patients with SS (n = 25) and NSS (n = 25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop−). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. Results ACStrop+ (1525 [25th–75th percentile: 790–3820] pg/L) and NSS (687 [254–1552]) patients showed increased NT-proBNP levels above those of UAtrop− patients (107 [43–450], p < 0.001) and controls (52 [42–99], p < 0.001), but SS patients exhibited still higher levels (11,335 [4716–25,769], p < 0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specifity (area under ROC curve: 0.946 [95% confidence interval, 0.872–1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p < 0.001) and SS patients (p = 0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p < 0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. Conclusions SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.