Angiotensin I and angiotensin II concentrations and their ratio in catecholamine-resistant vasodilatory shock. Bellomo, R., Wunderink, R. G., Szerlip, H., English, S. W., Busse, L. W., Deane, A. M., Khanna, A. K., McCurdy, M. T., Ostermann, M., Young, P. J., Handisides, D. R., Chawla, L. S., Tidmarsh, G. F., & Albertson, T. E. Critical Care, 24(1):43, December, 2020.
Angiotensin I and angiotensin II concentrations and their ratio in catecholamine-resistant vasodilatory shock [link]Paper  doi  abstract   bibtex   
Abstract Background In patients with vasodilatory shock, plasma concentrations of angiotensin I (ANG I) and II (ANG II) and their ratio may reflect differences in the response to severe vasodilation, provide novel insights into its biology, and predict clinical outcomes. The objective of these protocol prespecified and subsequent post hoc analyses was to assess the epidemiology and outcome associations of plasma ANG I and ANG II levels and their ratio in patients with catecholamine-resistant vasodilatory shock (CRVS) enrolled in the Angiotensin II for the Treatment of High-Output Shock (ATHOS-3) study. Methods We measured ANG I and ANG II levels at baseline, calculated their ratio, and compared these results to values from healthy volunteers (controls). We dichotomized patients according to the median ANG I/II ratio (1.63) and compared demographics, clinical characteristics, and clinical outcomes. We constructed a Cox proportional hazards model to test the independent association of ANG I, ANG II, and their ratio with clinical outcomes. Results Median baseline ANG I level (253 pg/mL [interquartile range (IQR) 72.30–676.00 pg/mL] vs 42 pg/mL [IQR 30.46–87.34 pg/mL] in controls; P  \textless  0.0001) and median ANG I/II ratio (1.63 [IQR 0.98–5.25] vs 0.4 [IQR 0.28–0.64] in controls; P  \textless  0.0001) were elevated, whereas median ANG II levels were similar (84 pg/mL [IQR 23.85–299.50 pg/mL] vs 97 pg/mL [IQR 35.27–181.01 pg/mL] in controls; P  = 0.9895). At baseline, patients with a ratio above the median (≥1.63) had higher ANG I levels ( P  \textless  0.0001), lower ANG II levels ( P  \textless  0.0001), higher albumin concentrations ( P  = 0.007), and greater incidence of recent (within 1 week) exposure to angiotensin-converting enzyme inhibitors ( P  \textless  0.00001), and they received a higher norepinephrine-equivalent dose ( P  = 0.003). In the placebo group, a baseline ANG I/II ratio \textless1.63 was associated with improved survival (hazard ratio 0.56; 95% confidence interval 0.36–0.88; P  = 0.01) on unadjusted analyses. Conclusions Patients with CRVS have elevated ANG I levels and ANG I/II ratios compared with healthy controls. In such patients, a high ANG I/II ratio is associated with greater norepinephrine requirements and is an independent predictor of mortality, thus providing a biological rationale for interventions aimed at its correction. Trial registration ClinicalTrials.gov identifier NCT02338843 . Registered 14 January 2015.
@article{bellomo_angiotensin_2020,
	title = {Angiotensin {I} and angiotensin {II} concentrations and their ratio in catecholamine-resistant vasodilatory shock},
	volume = {24},
	issn = {1364-8535},
	url = {https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-2733-x},
	doi = {10.1186/s13054-020-2733-x},
	abstract = {Abstract
            
              Background
              In patients with vasodilatory shock, plasma concentrations of angiotensin I (ANG I) and II (ANG II) and their ratio may reflect differences in the response to severe vasodilation, provide novel insights into its biology, and predict clinical outcomes. The objective of these protocol prespecified and subsequent post hoc analyses was to assess the epidemiology and outcome associations of plasma ANG I and ANG II levels and their ratio in patients with catecholamine-resistant vasodilatory shock (CRVS) enrolled in the Angiotensin II for the Treatment of High-Output Shock (ATHOS-3) study.
            
            
              Methods
              We measured ANG I and ANG II levels at baseline, calculated their ratio, and compared these results to values from healthy volunteers (controls). We dichotomized patients according to the median ANG I/II ratio (1.63) and compared demographics, clinical characteristics, and clinical outcomes. We constructed a Cox proportional hazards model to test the independent association of ANG I, ANG II, and their ratio with clinical outcomes.
            
            
              Results
              
                Median baseline ANG I level (253 pg/mL [interquartile range (IQR) 72.30–676.00 pg/mL] vs 42 pg/mL [IQR 30.46–87.34 pg/mL] in controls;
                P
                 {\textless}  0.0001) and median ANG I/II ratio (1.63 [IQR 0.98–5.25] vs 0.4 [IQR 0.28–0.64] in controls;
                P
                 {\textless}  0.0001) were elevated, whereas median ANG II levels were similar (84 pg/mL [IQR 23.85–299.50 pg/mL] vs 97 pg/mL [IQR 35.27–181.01 pg/mL] in controls;
                P
                 = 0.9895). At baseline, patients with a ratio above the median (≥1.63) had higher ANG I levels (
                P
                 {\textless}  0.0001), lower ANG II levels (
                P
                 {\textless}  0.0001), higher albumin concentrations (
                P
                 = 0.007), and greater incidence of recent (within 1 week) exposure to angiotensin-converting enzyme inhibitors (
                P
                 {\textless}  0.00001), and they received a higher norepinephrine-equivalent dose (
                P
                 = 0.003). In the placebo group, a baseline ANG I/II ratio {\textless}1.63 was associated with improved survival (hazard ratio 0.56; 95\% confidence interval 0.36–0.88;
                P
                 = 0.01) on unadjusted analyses.
              
            
            
              Conclusions
              Patients with CRVS have elevated ANG I levels and ANG I/II ratios compared with healthy controls. In such patients, a high ANG I/II ratio is associated with greater norepinephrine requirements and is an independent predictor of mortality, thus providing a biological rationale for interventions aimed at its correction.
            
            
              Trial registration
              
                ClinicalTrials.gov identifier
                NCT02338843
                . Registered 14 January 2015.},
	language = {en},
	number = {1},
	urldate = {2021-05-07},
	journal = {Critical Care},
	author = {Bellomo, Rinaldo and Wunderink, Richard G. and Szerlip, Harold and English, Shane W. and Busse, Laurence W. and Deane, Adam M. and Khanna, Ashish K. and McCurdy, Michael T. and Ostermann, Marlies and Young, Paul J. and Handisides, Damian R. and Chawla, Lakhmir S. and Tidmarsh, George F. and Albertson, Timothy E.},
	month = dec,
	year = {2020},
	pages = {43},
}
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