ESC heart failure · 2026
Non-invasive quantification of haemodynamic imbalance in acute heart failure.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Morishita Hiroshi
Аннотация
BACKGROUND AND AIMS: Acute heart failure (AHF) is commonly regarded as a worsening stage of chronic heart failure (CHF), yet the haemodynamic transition to decompensation remains incompletely defined. This study evaluated whether a non-invasive physiology-guided approach based on venous return (VR)-cardiac output (CO) balance can provide a framework to characterize transitional circulatory states preceding overt AHF.
METHODS: A total of 193 patients with chronic heart failure, hypertensive heart disease, or AHF were analysed. Mean circulatory filling pressure and right atrial pressure were estimated non-invasively using inferior vena cava diameter indexed to body surface area and extracellular-to-total body water ratio, respectively. VR-CO imbalance was quantified using a composite mismatch index.
RESULTS: The distribution of VR-CO mismatch demonstrated a bimodal pattern on Gaussian mixture modelling, with two components (means ± SD: 2.25 ± .96 and 5.25 ± 2.61). All overt AHF cases were localized within the higher-mismatch component. Intermediate states exhibited increasing mismatch while maintaining relatively preserved forward flow, consistent with buffered circulatory states. A subset of patients exhibited marked haemodynamic mismatch without clinical congestion, representing a highly buffered pre-decompensated state.
CONCLUSIONS: AHF may represent a failure of circulatory compensation in which venous return loading exceeds the capacity of forward flow. A non-invasive VR-CO framework reveals a continuum from compensated to buffered to overtly decompensated states and identifies a previously unrecognized highly buffered state preceding clinical deterioration. This physiology-guided approach may enable earlier detection of circulatory instability and provide a quantitative framework for risk stratification and therapeutic monitoring.
METHODS: A total of 193 patients with chronic heart failure, hypertensive heart disease, or AHF were analysed. Mean circulatory filling pressure and right atrial pressure were estimated non-invasively using inferior vena cava diameter indexed to body surface area and extracellular-to-total body water ratio, respectively. VR-CO imbalance was quantified using a composite mismatch index.
RESULTS: The distribution of VR-CO mismatch demonstrated a bimodal pattern on Gaussian mixture modelling, with two components (means ± SD: 2.25 ± .96 and 5.25 ± 2.61). All overt AHF cases were localized within the higher-mismatch component. Intermediate states exhibited increasing mismatch while maintaining relatively preserved forward flow, consistent with buffered circulatory states. A subset of patients exhibited marked haemodynamic mismatch without clinical congestion, representing a highly buffered pre-decompensated state.
CONCLUSIONS: AHF may represent a failure of circulatory compensation in which venous return loading exceeds the capacity of forward flow. A non-invasive VR-CO framework reveals a continuum from compensated to buffered to overtly decompensated states and identifies a previously unrecognized highly buffered state preceding clinical deterioration. This physiology-guided approach may enable earlier detection of circulatory instability and provide a quantitative framework for risk stratification and therapeutic monitoring.