The odyssey to dethrone LV ejection fraction continues: the prognostic value of LV global function index in heart failure

Abstract

\n \n \n Left Ventricular (LV) Global Function index (LVGFi) is a parameter that combines data from global systolic performance and volumetric anatomical information, measurable by non-contrast Cardiac Magnetic Resonance (CMR). We aimed to evaluate whether LVGFi predicts major cardiovascular outcomes and outperforms LV ejection fraction (LVEF) in Heart Failure (HF).\n \n \n \n We conducted a retrospective single-centre study of consecutive patients with HF who were referred to and had a LVEF <50% at CMR. Other than inadequate images for endocardial or epicardial border delineation, there were no exclusion criteria. LVEF was determined by 3D measurement. LVGFi was calculated as the LV stroke volume to the LV global volume ratio (Figure 1). The primary endpoint was a composite of time to all-cause death or HF hospitalization.\n \n \n \n The cohort was comprised of 433 HF patients (mean age 64±12 years, 74.1% male, ischaemic HF 53.1%, NYHA I-II 83.9%) with a mean LVEF of 33.5±10.0% and LVGFi of 22.8±7.4%. Over a median follow-up of 27 (17–37) months, 85 (19.6%) met the primary endpoint and 42 (9.7%) died. Patients with an event of the primary endpoint had markers of more severe HF, as noted by a reduced functional capacity (NYHA I-II: 63.5 vs. 89.0%; p<0.001) and increased natriuretic peptides [NT-proBNP: 2664 (1022–27242) vs. 791 (337–7258); p<0.001). Likewise, CMR showed higher LV volumes (e.g., LV end-diastolic volume index: 137±50 vs. 120±43mL/m2; p=0.001) and reduced LV performance indices, namely LVEF (29.2±10.6 vs 34.5±9.6%; p<0.001) and LVGFi (19.8±7.4 vs 23.6±7.3%; p<0.001). Both LVEF and LVGFi independently predicted the primary endpoint in multivariate analysis (separately imputed into a model adjusted for NYHA, NT-proBNP and creatinine). The LVEF model was more powerful than that of LVGFi. Similarly, LVGFi did not provide incremental prognostic information over LVEF in c-statistics analysis (0.653 vs. 0.622; p=0.645) (Figure 2).\n \n \n \n While LVGFi independently predicted major outcomes in patients with HF and LVEF <50%, it did not surpass LVEF. Our findings contrast to those demonstrating LVGFi as a powerful variable that outperforms LVEF in hypertrophic cardiomyopathy, cardiac amyloidosis, and healthy subjects at risk of developing structural heart disease. We hypothesize that LVGFi might be primarily useful in the prognostic stratification of patients with preserved LVEF.\n \n \n \n Type of funding sources: None. Figure 1 Figure 2\n