Key result
Impaired organ perfusion pressure linked to ~144% higher mortality and increased AKI in the vasodilator cohort.
Why the study?
This study aimed to assess the feasibility of organ perfusion pressure (OPP) and its predictiveness for clinical outcomes throughout diverse heart failure cohorts.
Does impaired organ perfusion pressure predict adverse clinical outcomes in patients with advanced heart failure and venous congestion?
Cohort (n=376)
Does impaired organ perfusion pressure predict adverse clinical outcomes in patients with advanced heart failure and venous congestion?
Impaired organ perfusion pressure (≤60 mmHg) is a valuable hemodynamic metric that predicts kidney dysfunction and mortality in patients with advanced heart failure and volume overload.
Answers are grounded in this paper and cite their sources.
May warrant closer monitoring in advanced HF on vasodilators; hypothesis-generating for perfusion pressure as target pending prospective trials.
Background Organ perfusion pressure (OPP) is an integrative metric of mean arterial pressure and central venous pressure, thereby reflecting both afterload and preload. Recent research demonstrated valuable predictive capacity of the novel hemodynamic metric OPP in acute decompensated heart failure (ADHF) and cardiogenic shock patients for acute kidney injury (AKI) and in-hospital mortality. This study aims to assess the feasibility of OPP and its predictiveness for clinical outcomes throughout diverse heart failure cohorts. Our objective is to assess OPP as a novel hemodynamic metric for organ perfusion throughout a diversity of heart failure cohorts. Methods Organ perfusion pressure was calculated by subtracting mean arterial pressure (MAP) with central venous pressure (CVP) in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial (N=200) and in an ADHF cohort treated with nitroprusside (N=176). The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality, cardiac rehospitalization and heart transplant. Results In the ESCAPE cohort, impaired OPP (≤60 mmHg) was associated with an increased likelihood for developing AKI (OR 2.01, 95%CI 1.05-3.84), and serum blood urea nitrogen >50 mg/dL (OR 3.22, 95%CI 1.62-6.49). In the Vasodilator trial, impaired OPP (≤60 mmHg) was not associated with an increased likelihood for developing AKI (OR 1.55, 95%CI 0.74-3.24). Yet, there was a significant higher odds of developing elevated and blood urea nitrogen >50 mg/dL (OR 2.72, 95%CI 1.43-5.25). Cox regression analysis demonstrated that impaired OPP was not associated with a higher risk to reach the composite endpoint of all-cause mortality, cardiac rehospitalization and heart transplant after adjusting for highly prevalent cardiovascular risk factors (HR 1.38, 95%CI 0.96-1.98). However, in the Vasodilator cohort, impaired OPP (≤60 mmHg) was associated with a higher risk to reach the endpoint of all-cause mortality (HR 2.24, 95%CI 1.29–3.88), even after adjustment for highly prevalent cardiovascular risk factors (HR 2.44, 95%CI 1.26–4.70). Conclusion Impaired OPP in the context of venous congestion portends kidney dysfunction and adverse outcomes in patients with ADHF and volume overload.
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Vanhentenrijk et al. (2026) conducted a cohort in Advanced heart failure and venous congestion (n=376). Impaired organ perfusion pressure (≤60 mmHg) vs. Normal organ perfusion pressure (>60 mmHg) was evaluated on composite endpoint of all-cause mortality, cardiac rehospitalization and heart transplant (HR 1.38, 95% CI 0.96-1.98). Impaired organ perfusion pressure (≤60 mmHg) predicted acute kidney injury (OR 2.01; 95% CI 1.05-3.84) and all-cause mortality in the vasodilator cohort (adjusted HR 2.44; 95% CI 1.26-4.70).
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