Patrick M Wieruszewski1, Erica D Wittwer2, Kianoush B Kashani3, Daniel R Brown2, Simona O Butler4, Angela M Clark4, Craig J Cooper5, Danielle L Davison6, Ognjen Gajic7, Kyle J Gunnerson8, Rachel Tendler9, Kristin C Mara10, Erin F Barreto11. 1. Department of Pharmacy, Mayo Clinic, Rochester, MN; Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN. 2. Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN. 3. Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN; Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN; Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN. 4. Department of Pharmacy, Michigan Medicine, Ann Arbor, MI. 5. Department of Pharmacy, Northwestern Memorial Hospital, Chicago, IL. 6. Departments of Anesthesiology and Critical Care Medicine, George Washington University, Washington, DC. 7. Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN; Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN. 8. Departments of Emergency Medicine, Anesthesiology, and Internal Medicine, Michigan Medicine, Ann Arbor, MI. 9. Department of Pharmacy, Emory University, Atlanta, GA. 10. Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN. 11. Department of Pharmacy, Mayo Clinic, Rochester, MN; Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN; Robert D. and Patricia E. Kern Center for the Science of Health Care Delivery, Mayo Clinic, Rochester, MN. Electronic address: barreto.erin@mayo.edu.
Abstract
BACKGROUND: Vasodilatory shock refractory to catecholamine vasopressors and arginine vasopressin is highly morbid and responsible for significant mortality. Synthetic angiotensin II is a potent vasoconstrictor that may be suitable for use in these patients. RESEARCH QUESTION: What is the safety and effectiveness of angiotensin II and what variables are associated with a favorable hemodynamic response? STUDY DESIGN AND METHODS: We performed a multicenter, retrospective study at five tertiary medical centers in the United States. The primary end point of hemodynamic responsiveness to angiotensin II was defined as attainment of mean arterial pressure (MAP) of ≥ 65 mm Hg with a stable or reduced total vasopressor dosage 3 h after drug initiation. RESULTS: Of 270 included patients, 181 (67%) demonstrated hemodynamic responsiveness to angiotensin II. Responders showed a greater increase in MAP (+10.3 mm Hg vs +1.6 mm Hg, P < .001) and reduction in vasopressor dosage (-0.20 μg/kg/min vs +0.04 μg/kg/min; P < .001) compared with nonresponders at 3 h. Variables associated with favorable hemodynamic response included lower lactate concentration (OR 1.11; 95% CI, 1.05-1.17, P < .001) and receipt of vasopressin (OR, 6.05; 95% CI, 1.98-18.6; P = .002). In severity-adjusted multivariate analysis, hemodynamic responsiveness to angiotensin II was associated with reduced likelihood of 30-day mortality (hazard ratio, 0.50; 95% CI, 0.35-0.71; P < .001). Arrhythmias occurred in 28 patients (10%) and VTE was identified in 4 patients. INTERPRETATION: In postmarketing use for vasopressor-refractory shock, 67% of angiotensin II recipients demonstrated a favorable hemodynamic response. Patients with lower lactate concentrations and those receiving vasopressin were more likely to respond to angiotensin II. Patients who responded to angiotensin II experienced reduced mortality.
BACKGROUND: Vasodilatory shock refractory to catecholamine vasopressors and arginine vasopressin is highly morbid and responsible for significant mortality. Synthetic angiotensin II is a potent vasoconstrictor that may be suitable for use in these patients. RESEARCH QUESTION: What is the safety and effectiveness of angiotensin II and what variables are associated with a favorable hemodynamic response? STUDY DESIGN AND METHODS: We performed a multicenter, retrospective study at five tertiary medical centers in the United States. The primary end point of hemodynamic responsiveness to angiotensin II was defined as attainment of mean arterial pressure (MAP) of ≥ 65 mm Hg with a stable or reduced total vasopressor dosage 3 h after drug initiation. RESULTS: Of 270 included patients, 181 (67%) demonstrated hemodynamic responsiveness to angiotensin II. Responders showed a greater increase in MAP (+10.3 mm Hg vs +1.6 mm Hg, P < .001) and reduction in vasopressor dosage (-0.20 μg/kg/min vs +0.04 μg/kg/min; P < .001) compared with nonresponders at 3 h. Variables associated with favorable hemodynamic response included lower lactate concentration (OR 1.11; 95% CI, 1.05-1.17, P < .001) and receipt of vasopressin (OR, 6.05; 95% CI, 1.98-18.6; P = .002). In severity-adjusted multivariate analysis, hemodynamic responsiveness to angiotensin II was associated with reduced likelihood of 30-day mortality (hazard ratio, 0.50; 95% CI, 0.35-0.71; P < .001). Arrhythmias occurred in 28 patients (10%) and VTE was identified in 4 patients. INTERPRETATION: In postmarketing use for vasopressor-refractory shock, 67% of angiotensin II recipients demonstrated a favorable hemodynamic response. Patients with lower lactate concentrations and those receiving vasopressin were more likely to respond to angiotensin II. Patients who responded to angiotensin II experienced reduced mortality.
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