DOI: 10.1093/ejhf/xuag193.209 ISSN: 1388-9842

Silent hypoperfusion in acute heart failure: prevalence, physiologic discordance, and clinical outcomes despite preserved blood pressure

X Zalazar, P Darko, B Otchere, C Chinnatambi, P Berchie, A Krishnamoorthy, B Demoss, R Singh, R Loungani, K Bauza, E Molina, C Marti

Abstract

Introduction

Blood pressure is commonly used to assess perfusion in acute heart failure but incompletely reflects tissue-level circulation. Normotension may coexist with impaired end-organ perfusion due to low-flow states, venous congestion, or microcirculatory dysfunction. Biochemical and physiological markers such as lactate elevation, oliguria, and narrowed pulse pressure can signal occult hypoperfusion, yet the prevalence and prognostic significance of this discordance in routine ward-level care remain poorly defined.

Purpose

To determine the prevalence of silent hypoperfusion among normotensive heart failure admissions and to evaluate its association with acute kidney injury and in-hospital mortality.

Methods

We conducted a retrospective cohort study of adult heart failure hospitalisations using the medical information mart for intensive care IV (MIMIC-IV) database. Early blood pressure metrics were derived from the first 6 hours of admission, while perfusion signals were assessed over 24–48 hours. Silent hypoperfusion was defined as normotension with at least one hypoperfusion marker (elevated lactate, low urine output, or narrow pulse pressure). Patients were categorised into blood pressure–perfusion concordance groups. Primary outcomes were acute kidney injury (AKI) within 48 hours and in-hospital mortality. Associations were evaluated using Firth penalised logistic regression to address outcome separation.

Results

The analytic cohort included 80,612 hospitalised adults with acute heart failure (mean age 70 years; median 71, interquartile range 61–81). Women comprised 46.9% of admissions. Silent hypoperfusion was identified in 17,056 patients, representing 21.2% of normotensive admissions. Event rates increased stepwise across blood pressure–perfusion categories. Patients with normotension and no hypoperfusion signals had the lowest rates of AKI (16.1%) and mortality (2.5%). Normotensive patients with silent hypoperfusion had substantially higher risks of AKI (28.2%) and in-hospital mortality (9.9%). The highest event rates occurred in hypotensive patients with hypoperfusion signals (AKI 42.1%, mortality 26.9%). In adjusted analyses, silent hypoperfusion was independently associated with AKI (odds ratio [OR] 1.59, 95% confidence interval [CI] 1.47–1.71) and in-hospital mortality (OR 1.39, 95% CI 1.24–1.56), independent of early mean arterial pressure and pulse pressure.

Conclusion

Silent hypoperfusion is common among hospitalised patients with acute heart failure, affecting more than one in five normotensive admissions. Despite preserved blood pressure, these patients experience markedly higher risks of acute kidney injury and in-hospital death. Reliance on blood pressure alone fails to identify a large, high-risk subgroup with occult circulatory insufficiency. Early integration of biochemical and physiological perfusion markers may improve risk stratification and enable earlier intervention in acute heart failure.For image description, please refer to the figure legend and surrounding text.

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