Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation

Aims: Exposure to bacterial endotoxin, perhaps due to bowel congestion or i schaemia and altered gut permeability, may result in immune activation that is characteristic for patients with severe heart failure. It is known that blood procalcitonin rises in response to bacterial endotoxin exposure. Met hods: We measured procalcitonin in a group of 29 patients with acute cardio genic shock and no sign of infection (all without bacteraemia) and 26 with septic shock. Blood was analysed for procalcitonin, interleukin-6, tumour n ecrosis factor-alpha (TNF-alpha), c-reactive protein (CRP) and neopterin. P atients were managed conventionally in an intensive care unit with no furth er experimental procedures. Results: Three cardiogenic (10%) and seven sept ic shock patients (27%) survived. Most patients with acute heart failure su rviving 12 h or more (18 of 20) developed a pyrexia (738.0 degrees C) of un known origin in the absence of positive cultures, with a rise in procalcito nin (1.4 +/- 0.8 to 48.0 +/- 16.2 ng/ml, P < 0.001), CRP (76.5 +/- 16.4 to 154.7 +/- 22.9 mg/l, P < 0.001) and neopterin (20.7 +/- 3.5 to 41.2 +/- 6.7 nmol/l, P < 0.001). Patients with septic shock had higher initial levels o f cytokines, and higher peak levels. Those with heart failure surviving (n = 3) and those dying in the first 12 h (n = 9) had no rise in cytokine leve ls. The patients with high procalcitonin had a higher temperature (38.9 +/- 0.3 vs. 37.3 +/- 0.23 degrees C, P < 0.05), TNF-alpha (43.95 +/- 9.64 vs. 16.43 +/- 4.33 pg/ml; P < 0.005) and CRP (146.1 +/- 18.4 vs. 68.2 +/- 39.6 mg/ml, P < 0.005). Peak procalcitonin levels correlated with peak temperatu re (r = 0.74, P < 0.001). Conclusions: Cardiogenic shock causes a pyrexia o f unknown origin in patients surviving for 12 h and that is associated with a rise in procalcitonin levels. This lends support to the hypothesis that patients with cardiogenic shock may be being exposed to bacterial endotoxin at a time when bowel wall congestion and or ischaemia is likely to be pres ent. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.