Cardiac ischemia in patients with septic shock randomized to vasopressin or norepinephrine
1 Department of Medicine and Interdepartmental Division of Critical Care Medicine, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada
2 University Health Network-General Division, University of Toronto, Toronto, Ontario, Canada
3 Intensive Care, Charing Cross Hospital, Imperial College, London, UK
4 Departments of Medicine, Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Ontario, Canada
5 Department of Medicine and Division of Cardiology, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada
6 Department of Respiratory Medicine, Changi General Hospital, Singapore
7 School of Population and Public Health, Centre for Health Evaluation and Outcome Sciences, and University of British Columbia, Vancouver, British Columbia, Canada
8 Critical Care Research Laboratories, Heart and Lung Institute, St. Paul's Hospital, and University of British Columbia, Vancouver, British Columbia, Canada
9 Alfred Hospital, Monash University, Melbourne, Australia
10 Kelowna General Hospital, Kelowna, and University of British Columbia, Kelowna, British Columbia, Canada
11 Ottawa Hospital-General Campus, and University of Ottawa, Ottawa, Ontario, Canada
12 Mater Health Services, University of Queensland and Monash University, South Brisbane Queensland, Australia
Critical Care 2013, 17:R117 doi:10.1186/cc12789
See related commentary by Gradwohl-Matis and Dunser, http://ccforum.com/content/17/5/1002Published: 20 June 2013
Cardiac troponins are sensitive and specific biomarkers of myocardial necrosis. We evaluated troponin, CK, and ECG abnormalities in patients with septic shock and compared the effect of vasopressin (VP) versus norepinephrine (NE) on troponin, CK, and ECGs.
This was a prospective substudy of a randomized trial. Adults with septic shock randomly received, blinded, a low-dose infusion of VP (0.01 to 0.03 U/min) or NE (5 to 15 μg/min) in addition to open-label vasopressors, titrated to maintain a mean blood pressure of 65 to 75 mm Hg. Troponin I/T, CK, and CK-MB were measured, and 12-lead ECGs were recorded before study drug, and 6 hours, 2 days, and 4 days after study-drug initiation. Two physician readers, blinded to patient data and drug, independently interpreted ECGs.
We enrolled 121 patients (median age, 63.9 years (interquartile range (IQR), 51.1 to 75.3), mean APACHE II 28.6 (SD 7.7)): 65 in the VP group and 56 in the NE group. At the four time points, 26%, 36%, 32%, and 21% of patients had troponin elevations, respectively. Baseline characteristics and outcomes were similar between patients with positive versus negative troponin levels. Troponin and CK levels and rates of ischemic ECG changes were similar in the VP and the NE groups. In multivariable analysis, only APACHE II was associated with 28-day mortality (OR, 1.07; 95% CI, 1.01 to 1.14; P = 0.033).
Troponin elevation is common in adults with septic shock. We observed no significant differences in troponin, CK, and ECGs in patients treated with vasopressin and norepinephrine. Troponin elevation was not an independent predictor of mortality.