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Angiotensin Receptor-Neprilysin Inhibition in Acute Myocardial Infarction
Marc A Pfeffer1, Brian Claggett1, Eldrin F Lewis1
1From the Cardiovascular Division (M.A.P., B.C., S.D.S., K.J., E.B.) and the Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division (E.B.), Brigham and Women's Hospital and Harvard Medical School, Boston; the Division of Cardiovascular Medicine, Stanford University School of Medicine, Palo Alto (E.F.L.), and the Heart Failure and Preventive Cardiology Programs, Department of Veterans Affairs Greater Los Angeles, University of California, Los Angeles, Los Angeles (F.V.M.) - both in California; Duke University Medical Center, Durham, NC (C.B.G.); Rigshospitalet, Blegdamsvej, University of Copenhagen (L.K.), and the Department of Cardiology, Herlev-Gentofte University Hospital (M. Schou) - both in Copenhagen; National Association of Hospital Cardiologists Research Center, Florence (A.P.M.), and the Cardiovascular Department, Hospital Papa Giovanni XXIII, Bergamo (M. Senni) - both in Italy; Washington University School of Medicine, St. Louis (D.L.M.); British Heart Foundation Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom (J.J.V.M., M.C.P.); Montreal Heart Institute, University of Montreal, Montreal (J.-L.R.); Université de Paris, Assistance Publique-Hôpitaux de Paris, French Alliance for Cardiovascular Trials and INSERM Unité 1148, Paris (P.G.S.); Academic Research Organization, Hospital Israelita Albert Einstein, São Paulo (O.B.); the Department of Cardiovascular Diseases, University Hospital Center Zagreb, University of Zagreb School of Medicine, Zagreb, Croatia (M.C.); the Department of Cardiovascular Medicine, Flinders Medical Centre, Adelaide, SA, Australia (C.G.D.P.); Baylor Soltero CV Research Center, Baylor Scott and White Heart and Vascular Hospital, Dallas (C.E.); Cardiology Service, Sanatorio Modelo Quilmes, Quilmes, Argentina (A.F.); the Department of Cardiology, German Center for Cardiovascular Research Partner Site Berlin, Berlin Institute of Health, Charité-Universitätsmedizin Berlin, Berlin (U.L.); Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York (R.M.); the Heart and Vascular Center, Semmelweis University, Budapest, Hungary (B.M.); Acibadem City Clinic Cardiovascular Center, Sofia, Bulgaria (I.P.); National Heart Center Singapore, Singapore (D.S.); the Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands (P.M.); and Novartis, East Hanover, NJ (M.L., Y.Z., J.G.).
Sacubitril-valsartan did not significantly reduce cardiovascular death or heart failure events compared to ramipril in acute myocardial infarction patients. Further research is needed to clarify its role post-myocardial infarction.
Area of Science:
- Cardiology
- Clinical Trials
- Pharmacology
Background:
- Sacubitril-valsartan is effective for symptomatic heart failure, outperforming ACE inhibitors.
- Limited data exists on its use in acute myocardial infarction (MI).
Purpose of the Study:
- To compare sacubitril-valsartan with ramipril in patients following acute MI.
- To assess the impact on cardiovascular death and heart failure events.
Main Methods:
- A randomized trial of 5661 patients with acute MI.
- Patients received either sacubitril-valsartan or ramipril plus standard care.
- Primary outcome: cardiovascular death or incident heart failure.
Main Results:
- No significant difference in primary outcome between sacubitril-valsartan and ramipril groups (11.9% vs 13.2%).
- Similar rates for cardiovascular death, heart failure hospitalizations, and all-cause mortality.
- Adverse event discontinuation rates were comparable.
Conclusions:
- Sacubitril-valsartan did not show a significant benefit over ramipril in reducing cardiovascular death or heart failure post-MI.
- The study did not establish superiority of sacubitril-valsartan in this specific patient population.
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