The role of T1 mapping and Extracellular Volume (ECV) in predicting cardiac reverse remodelling and response to Heart Failure with reduced Ejection Fraction (HFrEF) therapy

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background Adverse cardiac remodelling results from an insult such as myocardial infarction, or as seen in Heart Failure (HF), maladaptive neurohormonal activation. Reverse remodelling describes improvement in cardiac geometry; the left ventricle (LV) recovers more normal structure with improved function and prognosis. Cardiovascular Magnetic Resonance imaging (CMR) allows gold standard assessment of LV volumes and function, diffuse and focal fibrosis and estimation of extracellular volume (ECV) by T1 mapping. Purpose Elevated T1 and ECV values are associated with worse outcome in many cardiac conditions. We conducted the first prospective study to investigate whether T1 mapping and ECV can predict cardiac reverse remodelling in response to treatment, in a cohort of patients hospitalised with a new HF diagnosis. Methods This was a single centre observational study. Inclusion criteria were admission with new HF, LVEF ≤50% or elevated NTproBNP and being treated with intravenous furosemide. Only patients with Heart Failure with reduced Ejection Fraction (HFrEF) and EF <40% on baseline echocardiography were included in this analysis. 36 consecutive eligible participants were included and had both echocardiogram and CMR studies to establish anatomy, function, and myocardial tissue characteristics at baseline. Participants were treated according to international HF guidelines and underwent reviews and repeat echocardiography at 6, 12–18 and 24–30 months. "Responders" to guideline directed HFrEF therapy were defined as those who had an increase in LVEF of ≥10% to a value of ≥40% between their baseline and latest follow-up echocardiogram. Baseline CMR volumes, function, presence of Late Gadolinium Enhancement (LGE), septal and whole heart T1 and ECV values were compared between responder and non-responder groups. Results Median follow-up was 26 months. 27 (75%) participants were responders to therapy. There were no differences in baseline characteristics between groups. There was high uptake of HFrEF medical therapy in both groups. (Table 1) There was no significant difference found between septal or whole heart T1 or ECV values between responder and non-responder groups. There was a trend towards lower whole heart ECV values (29% vs. 35%; p = 0.06) in the responder group but this did not reach statistical significance. (Figure 1) Overall, there was no difference in rates of LGE presence between groups but there was a significantly higher proportion of participants with non-ischaemic LGE pattern in the responder group compared to non-responder group (48% vs 11%; p = 0.05). Conclusions In this cohort of patients hospitalised with a new HFrEF diagnosis, the majority demonstrated reverse remodelling in response to therapy by 26 months. Whole heart ECV (%) as a surrogate marker for fibrosis calculated by whole heart T1 mapping may play a role in understanding which patients are likely to respond to HF therapy but further larger studies are required.