Trial reportCritical care (London, England)2025
An index of the initial blood pressure response to angiotensin II treatment and its association with clinical outcomes in vasodilatory shock.
Trial report in Critical care (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Toward endotype-guided renin-angiotensin-aldosterone system modulation in septic shock.Critical care (London, England) · 2026Article
- Renin-dependent association between oxidative stress and organ dysfunction in acute hypoxemic respiratory failure.Journal of anesthesia, analgesia and critical care · 2026Article
- Circulating DPP3 limits efficacy of angiotensin II infusion in septic shock.Critical care (London, England) · 2026Article
- Vasopressor use in septic shock: separating evidence, practice, and future directions.Intensive care medicine · 2026Article
- Absolute, weight-based, fixed-dose, or phenotype-guided? Rethinking the meaning of vasopressor dose in critical care.Annals of intensive care · 2026Article
- The therapeutic horizon of acute kidney injury in critical care: exploring pathology, promises, pitfalls, and progress.Current opinion in critical care · 2025Review
- Effects of angiotensin 2 infusion on the RAAS and alternative RAAS pathway.Critical care (London, England) · 2025Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNo standardized index exists to assess cardiovascular responsiveness to angiotensin-II. We hypothesized that a standardized index of initial blood pressure response to angiotensin-II treatment would be associated with clinical outcomes.
methodsUsing data from the Angiotensin Therapy for High Output Shock (ATHOS-3) trial, we developed an Angiotensin-II Initial MAP Response Index of Treatment Effect (AIMRITE) defined as (MAP at hr1 - MAP at baseline)/study drug dose. We assessed AIMRITE continuously and, based on observed distributions, we additionally categorized patients as "responsive" or "resistant", with responsiveness defined by an AIMRITE ≥ 0.90 mmHg/ng/kg/min. The primary clinical outcome was 28-day mortality. Secondary outcomes included days alive and vasopressor- or ventilator- or renal replacement therapy-free at day-7. Biological outcomes included baseline renin, angiotensin-II, and renin/angiotensin-II ratio, and their change at hr3.
resultsOf 158 placebo patients, as expected, 157 (99%) had AIMRITE < 0.90 mmHg/ng/kg/min (median AIMRITE 0.02; IQR - 0.03-0.10). In contrast, 163 patients assigned to angiotensin-II had a median AIMRITE of 1.43 mmHg/ng/kg/min (IQR 0.35-2.83). Of these, 97 (60%) were responsive (median AIMRITE 2.55; IQR 1.66-4.12) and 66 (40%) were resistant (median AIMRITE 0.24; IQR 0.10-0.52). Each 1.0-unit increase in AIMRITE was associated with a 16% lower hazard of death (HR: 0.84 per-mmHg/ng/kg/min [95% CI 0.74-0.95], p = 0.0062). Responsive patients had half the mortality hazard than resistant patients (HR: 0.50 [95% CI 0.32-0.78], p = 0.0026) and placebo patients (HR 0.58 [95% CI 0.40-0.86], p = 0.0064). Resistant patients had a similar mortality hazard to placebo (HR 1.17 [95% CI 0.80-1.72], p = 0.41). Compared to resistant patients, responsive patients had lower baseline renin and renin/angiotensin-II ratio, but a greater decrease in both at hr3. When stratified by baseline renin level, mortality was highest in placebo patients with high renin (69%) and angiotensin-II resistant patients with low renin (61%).
conclusionsAmong patients with catecholamine-refractory vasodilatory shock treated with angiotensin-II, the AIMRITE was associated with mortality at day-28. Responsive angiotensin-II patients had higher survival versus both angiotensin-II resistant patients and those treated with placebo plus standard vasopressors. This index may serve as a prognostic indicator and early identifier of patients most likely to benefit from angiotensin-II.
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