ESC Congress 2026 Abstract · Oct 26, 2026
Heart failure therapy optimization in myocardial infarction patients with systolic dysfunction during Phase 2 and 3 Cardiac Rehabilitation
By Cardona-Tercero S, Marques-Cano N, Merenciano-Gonzalez H et al.
Background: Systolic dysfunction after myocardial infarction (MI) is not uncommon, particularly in patients with ST-segment elevation MI (STEMI). Optimization of heart failure (HF) pharmacotherapy is essential for both symptomatic relief and prognostic improvement. Purpose: We aimed to analyse the evolution of HF therapy in our local post-MI Cardiac Rehabilitation Program (CRP), focusing on treatment adjustments during Phase 2 and extended follow-up in Phase 3 (one year after MI). Methods: Patients with MI and systolic dysfunction (defined as left ventricular ejection fraction [LVEF] <50%) between November 2021 and November 2024 who completed our Phase 2 CRP and at least a one-year follow-up visit in extended Phase 3 were included in a prospective registry. We evaluated the changes in HF therapy, including beta-blockers, angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARB), neprilysin and angiotensin receptor inhibitors (ARNI), mineralocorticoid receptor antagonists (MRA), sodium-glucose cotransporter-2 inhibitors (SGLT2i), and other diuretics. Relative equivalent doses (ED, standardized to reference doses) and achievement of target doses were assessed for each drug class. Results: Our cohort comprised 87 patients (mean age 63.83±12 years, 80.5% males, 46% previous smokers), mainly presenting with anterior (n=52, 59.8%) and inferior (n=24, 27.6%) STEMI. The mean LVEF was 40.34±4.43%, with 52.9% showing mildly reduced (40–49%), 36.8% moderately reduced (30–39%), and 10.3% severely reduced (<30%) LVEF. HF therapy optimization was performed in 72 (82.8%) patients during Phase 2 and in 12 (13.8%) patients at one year. Beta-blocker therapy was nearly universal (n=84, 96.6% at one year) with no significant changes during follow-up. A trend toward reduced use of ACEI (32.2% to 25.3%) and ARB (28.7% to 23%) was observed, accompanied by a significant increase in ARNI use (25.3% to 41.4%) and ED (from 1 [0.5-1] to 1 [0.5-2] sacubitril-valsartan 24/26mg ED, p<0.001). Both the use and ED of MRA increased (39.1% and 1 [0.5-1] to 73.6% and 1 [1-1] eplerenone 25mg ED, p<0.001). Use of SGLT2i rose markedly (49.4% to 89.7%, p<0.001), as did the use of other diuretics (26.4% to 36.8%, p=0.006). After one year, most patients had not achieved target doses for any drug class except SGLT2i (89.7%). NTproBNP levels decreased significantly from 2154 [1063.5-3796.5] pg/mL before Phase 2 to 375.5 [195.75-624.5] pg/mL after Phase 2 and 342.5 [170.25-661] pg/mL 1 year after MI (p<0.001). Conclusion: Substantial optimization of HF pharmacotherapy can be achieved during Phase 2 and Phase 3 CRP, particularly for MRA and SGLT2i. However, most patients do not reach guideline-recommended target doses, potentially due to symptomatic hypotension or LVEF recovery. The clinical implications of this treatment strategy warrant further investigation.Figure.HF therapy changes during CRPTable.HF therapy changes during CRP