DOI: 10.1093/eurheartj/ehag785.1296 ISSN: 0195-668X

Heart failure therapy optimization in myocardial infarction patients with systolic dysfunction during Phase 2 and 3 Cardiac Rehabilitation

S Cardona-Tercero, N Marques-Cano, H Merenciano-Gonzalez, C Bertolin-Boronat, M L Martinez Mas, P Palau, J I Climent Alberola, L Lopez Bueno, B Diaz Diaz, N Perez-Sole, A Paya Rubio, J Nunez, J Sanchis, V Bodi, V Marcos Garces

Abstract

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

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