Author + information
- Received September 13, 2015
- Revision received January 8, 2016
- Accepted January 28, 2016
- Published online April 12, 2016.
- S0735109716005106-119bc90a8ea47ec75682d045d835c884Marie Evans, MD, PhDa,∗ (, )
- S0735109716005106-71e7cb21627efcca6463df273a0d7f9aJuan-Jesus Carrero, PhDa,b,
- S0735109716005106-167978b3a64fcb716da562a54c12075aKarolina Szummer, MD, PhDc,
- S0735109716005106-bb1a9239975ac28a6ceee13a9b2aa6cfAxel Åkerblom, MD, PhDd,e,
- S0735109716005106-b5a5b435da72f36292c01f44cdf8195dRobert Edfors, MDc,
- S0735109716005106-a94e8998df82b3daf97e92151b2e9807Jonas Spaak, MD, PhDf,
- S0735109716005106-eb41c9e213e5fb40ee0fc00d14c5bb7aStefan H. Jacobson, MD, PhDf,
- S0735109716005106-305604ffd95180b66835cb10f76b5840Pontus Andell, MDg,
- S0735109716005106-d6d31792942dcbcaa8de67b69be58dfeLars Lindhagen, PhDe and
- S0735109716005106-ff150441fa9e691d1248b6d623f93eccTomas Jernberg, MD, PhDc
- aRenal Medicine, CLINTEC, Karolinska Institutet, Stockholm, Sweden
- bInstitute for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden
- cDepartment of Medicine, Huddinge, Section of Cardiology, Karolinska Institutet, and Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden
- dDepartment of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden
- eUppsala Clinical Research Center, Uppsala, Sweden
- fDepartment of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden
- gDepartment of Cardiology, Clinical Sciences, Lund University, Lund, Sweden
- ↵∗Reprint requests and correspondence:
Dr. Marie Evans, Renal Department M99, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Sweden.
Background There is no consensus whether angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB) should be used for secondary prevention in all or in only high-risk patients after an acute myocardial infarction (AMI).
Objectives This study sought to investigate whether ACEI/ARB treatment after AMI is associated with better outcomes across different risk profiles, including the entire spectrum of estimated glomerular filtration rates.
Methods This study evaluated discharge and continuous follow-up data on ACEI/ARB use among AMI survivors (2006 to 2009) included in a large Swedish registry. The association between ACEI/ARB treatment and outcomes (mortality, myocardial infarction, stroke, and acute kidney injury [AKI]) was studied using Cox proportional hazards models (intention-to-treat and as treated).
Results In total, 45,697 patients (71%) were treated with ACEI/ARB. The 3-year mortality was 19.8% (17.4% of ACEI/ARB users and 25.4% of nonusers). In adjusted analysis, significantly better survival was observed for patients treated with ACEI/ARB (3-year hazard ratio: 0.80; 95% confidence interval: 0.77 to 0.83). The survival benefit was consistent through all kidney function strata, including dialysis patients. Overall, those treated with ACEI/ARB also had lower 3-year risk for myocardial infarction (hazard ratio: 0.91; 95% confidence interval: 0.87 to 0.95), whereas treatment had no significant effect on stroke risk. The crude risk for AKI was in general low (2.5% and 2.0% for treated and nontreated, respectively) and similar across estimated glomerular filtration rate categories but was significantly higher with ACEI/ARB treatment. However, the composite outcome of AKI and mortality favored ACEI/ARB treatment.
Conclusions Treatment with ACEI/ARB after AMI was associated with improved long-term survival, regardless of underlying renal function, and was accompanied by low rates of adverse renal events.
This work was supported by a grant from the Swedish Foundation for Strategic Research, the Swedish Heart and Lung Foundation, and the Stockholm County Council (ALF project [Drs. Carrero and Jernberg], post-doctoral project [Drs. Evans and Szummer]). The sponsor was not involved in the design and conduct of the study; collection, management, analysis, or interpretation of the data; or review or approval of the manuscript. Drs. Evans and Jacobson have received payment for lectures from Amgen. Dr. Szummer has received payment for lectures from AstraZeneca and Aspen. Dr. Åkerblom has received institutional research grants from AstraZeneca. Dr. Spaak has received grant funding from AbbVie; payment for lectures from Abbot and Merck (Merck Sharp and Dohme); payment for the development of educational presentations from Merck Sharp and Dohme; and travel accommodations from Medtronic. Dr. Jacobson has received payment for lectures from Fresenius Medical Care. Dr. Jernberg has received fees for lectures from AstraZeneca and Aspen unrelated to this work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 13, 2015.
- Revision received January 8, 2016.
- Accepted January 28, 2016.
- American College of Cardiology Foundation