Estimated Stressed Blood Volume and Outcomes in Cardiac Amyloidosis

A single-center retrospective analysis of patients with cardiac amyloidosis undergoing right heart catheterization evaluated whether a model-derived intravascular volume metric—estimated stressed blood volume (eSBV)—tracked with invasive filling pressures and related to short-term outcomes.

eSBV is derived from routinely acquired catheterization and clinical inputs rather than a directly measured volume. In the outcome analyses, higher eSBV was linked to higher 1-year all-cause mortality in the subgroup with left ventricular ejection fraction (LVEF) >40%.

The cohort included 388 patients with cardiac amyloidosis, comprising transthyretin (ATTR) and light-chain (AL) subtypes. Analyses were stratified by LVEF. eSBV was estimated using a simulation-based cardiovascular model (HARVI) supplied with patient-specific inputs recorded at rest during right heart catheterization and contemporaneous clinical assessment. Inputs included heart rate, cardiac output, mean right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), pulmonary artery systolic and diastolic pressures, systolic and diastolic aortic pressures, and LVEF. The model algorithm searched parameter space to match measured hemodynamics with model outputs while optimizing parameters that included ventricular elastances and eSBV, which the authors reported scaled as mL per 70 kg body weight. In this design, eSBV functioned as a computed output derived from standard invasive measurements rather than an additional procedure-specific measurement.

In hemodynamic profiling, the authors described the cohort as generally exhibiting a “warm-and-wet” phenotype characterized by elevated biventricular filling pressures with preserved cardiac output. Within the LVEF >40% stratum, higher eSBV was reported to align with markers of right-sided congestion, with regression and discrimination analyses highlighting RAP and pulmonary artery pressure measures as predictors of higher eSBV; PCWP was noted as the key left-sided marker with predictive signal. Correlation analyses in the same stratum were described as weak but directionally positive between eSBV and RAP and PCWP. The article also reported an inverse correlation between eSBV and left ventricular end-systolic elastance (LV Ees), an output of the modeling framework used to quantify contractility. The study positioned higher eSBV as clustering with more congestive invasive profiles, as summarized by the authors.

For outcomes, the primary endpoint was 1-year all-cause mortality, evaluated separately in patients with LVEF >40% versus those with LVEF ≤40%. In the LVEF >40% group, Kaplan–Meier analysis separated high versus low eSBV strata, and Cox modeling showed a hazard ratio (HR) of 1.84 (95% CI 1.12–3.01; p=0.015) for higher versus lower eSBV. In a multivariable model adjusted for age, sex, smoking, body mass index, LVEF, and NT-proBNP, higher eSBV remained associated with all-cause mortality (HR 2.19, 95% CI 1.19–4.03; p=0.012). The article reported that eSBV was not predictive of poor outcome in the LVEF ≤40% subgroup, and it noted that an attempted ROC-based approach did not yield a robust eSBV cutpoint for adverse outcomes. In this cohort, the reported prognostic signal for eSBV was concentrated in the LVEF >40% stratum after adjustment.

The authors noted overlap between eSBV and RAP in the LVEF >40% subgroup. Across individual hemodynamic models incorporating PCWP, cardiac output, RAP/PCWP ratio, and PVR, elevated eSBV predicted all-cause mortality, but this risk signal was attenuated after additional adjustment for RAP. To further explore interdependence, they reported analyses combining high/low RAP with high/low eSBV (based on medians) and described persistent separation on unadjusted Kaplan–Meier curves, including a pattern in which elevated eSBV was associated with worse outcomes even when RAP was low.

Key Takeaways:

• In this retrospective cardiac amyloidosis cohort, eSBV was estimated from standard right heart catheterization inputs using a simulation-based HARVI model and reported normalized to body weight.
• Higher eSBV was reported to track with invasive markers of higher filling pressures and right-sided congestion in the LVEF >40% stratum, alongside an inverse association with modeled LV end-systolic elastance.
• Among patients with LVEF >40%, higher eSBV was independently associated with higher 1-year all-cause mortality after multivariable adjustment, while high eSBV was not predictive of poor outcome in the LVEF ≤40% subgroup.