CMR extracellular volume identifies low-output hemodynamic phenotype in cardiac amyloidosis and refines risk beyond ejection fraction

Background Cardiac amyloidosis often presents with preserved EF despite advanced functional limitation. Non-invasive identification of low-output hemodynamic phenotype may improve risk stratification and advanced therapy planning. Purpose To assess the association of CMR extracellular volume (ECV) with invasive hemodynamics in cardiac amyloidosis. Methods We analyzed adults with suspected or confirmed cardiac amyloidosis who underwent CMR (native T1 and ECV) and RHC within 60 days (2021–2025). Low-output phenotype was defined as cardiac index <2.2 L/min/m². Associations were evaluated using correlation and multivariable models. Results Eighty-six patients were included (mean age 66±10 years; 63% male); median EF was 52% (IQR 45–58) (Table 1). Low-output phenotype was present in 34 (40%). ECV was higher in low-output versus preserved output patients (39±6% vs 33±5%, p<0.001) and correlated inversely with cardiac index (r=−0.46, p<0.001) (Figure 1). EF did not reliably discriminate low output (AUC 0.61), whereas ECV showed better discrimination (AUC 0.78). After adjustment for age and EF, ECV remained independently associated with low-output phenotype (adjusted OR 1.3 per 3% increase, 95% CI 1.1–1.6) (Figure 2). Conclusion In cardiac amyloidosis, CMR ECV identifies a clinically relevant low-output hemodynamic phenotype and refines risk beyond EF, supporting its role in integrated care pathways.