Estimated Stressed Blood Volume in Patients With Cardiac Amyloidosis
Abstract
Hemodynamic profiles in cardiac amyloidosis (CA) patients differ from traditional heart failure phenotypes. Stressed blood volume is a main determinant of intravascular pressures and affect cardiac filling pressures. We hypothesized that estimated stressed blood volume (eSBV) may help us better understand hemodynamic derangements in patients with CA and its relation to adverse outcomes. We reviewed 462 consecutive patients who underwent right heart catheterization at a tertiary care institution for eSBV based on basic hemodynamic measurements. Median eSBV was used to stratify for high versus low eSBV. The primary outcome was all-cause mortality of high versus low eSBV in CA patients with left ventricular ejection fraction (LVEF) >40% or LVEF ≤ 40%. In our final cohort of 388 patients, of which 225 (58%) had transthyretin CA and 163 (42%) had light-chain CA, the median eSBV was 2,191 ml/70 kg. Among those with LVEF > 40%, 42 (16.6%) patients with high eSBV, while 27 (10.7%) patients with low eSBV developed adverse events (log-rank p = 0.018). Higher eSBV was independently associated with a higher risk of all-cause mortality (HR 1.84, 95% cardiac index 1.12 to 3.01, p = 0.015) even after adjustments for traditional cardiovascular risk factors, LVEF, and NT-proBNP (HR 2.19, 95% cardiac index 1.19 to 4.03, p = 0.012). Conversely, high eSBV did not predicted poor outcome in the LVEF ≤ 40% cohort. In conclusion, eSBV is an independent predictor of all-cause mortality in patients with CA and LVEF > 40% even after adjustment for traditional cardiovascular risk factors. Modelling eSBV through integrating established invasive hemodynamic parameters may become a valuable asset in the contemporary heart failure unit to guide treatment decision-making and prognosis.
Fields of Study & Subjects
Amyloidosis: Diagnosis
Treatment
Outcomes
Cardiovascular Function and Risk Factors
Takotsubo Cardiomyopathy and Associated Phenomena
Publication details
- Journal / source
- The American Journal of Cardiology
- Publisher
- Elsevier BV
- Volume
- 266
- Pages
- 59–66
- Publication date
- 13 February 2026
- Language
- EN