Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers Are Associated With Improved Outcome but Do Not Prevent New-Onset Atrial Fibrillation After Acute Myocardial Infarction.
BACKGROUND
Treatment with renin-angiotensin system (RAS) inhibitors might restrain the structural/electrical remodeling associated with atrial fibrillation (AF). Limited evidence exists regarding the potential benefits of RAS inhibition post-acute myocardial infarction (AMI) in patients with AF. This study sought to assess the association between RAS inhibition and all-cause mortality and new-onset AF in patients with/without congestive heart failure (CHF) post-AMI.


RESULTS
Patients hospitalized for AMI between 2006 and 2012 were identified in Swedish registries. Patients were stratified in 4 subgroups; patients with CHF and AF (n=11 489); patients with CHF without AF (n=31 676); patients with AF without CHF (n=10 066); and patients without both CHF and AF (n=59 417). Patients exposed to RAS inhibition were compared to nontreated. Three-year risk of all-cause mortality and new-onset AF was assessed using adjusted Cox regression analyses. At discharge, 83 291 (73.9%) patients received RAS inhibition. RAS inhibition was associated with lower 3-year risk of all-cause mortality in CHF patients with AF, adjusted hazard ratio (HR) with 95% CI 0.75 (0.70-0.81), CHF patients without AF, HR 0.65 (0.60-0.69), AF patients without CHF, HR 0.82 (0.75-0.90), and in patients without CHF and AF, HR 0.76 (0.72-0.81), respectively. RAS inhibition was not associated with lower 3-year risk of new-onset AF in patients without AF but with/without CHF; HR 0.96 (0.84-1.10) and 1.12 (1.02-1.22), respectively.


CONCLUSIONS
RAS inhibition post-AMI was associated with lower risk of all-cause mortality. In patients with/without CHF, RAS inhibition was not associated with lower incidence of new-onset AF.
Uppsala Clinical Research Center, Uppsala, Sweden gorav.batra@ucr.uu.se.|Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Gorav
G
Batra
Uppsala Clinical Research Center, Uppsala, Sweden.
Lars
L
Lindhagen
Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden.|Skåne University Hospital, Lund, Sweden.
Pontus
P
Andell
Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden.|Skåne University Hospital, Lund, Sweden.
David
D
Erlinge
Uppsala Clinical Research Center, Uppsala, Sweden.|Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Stefan
S
James
Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
Jonas
J
Spaak
Uppsala Clinical Research Center, Uppsala, Sweden.|Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Jonas
J
Oldgren
D000368:Aged; D000369:Aged, 80 and over; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000453:epidemiology*; D016022:Case-Control Studies; D002423:Cause of Death; D015897:Comorbidity; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000453:epidemiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009026:Mortality; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000453:epidemiology; D016016:Proportional Hazards Models; D065840:Protective Factors; D012042:Registries; D012189:Retrospective Studies; D013548:Sweden / Q000453:epidemiology; D016896:Treatment Outcome
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors
atrial fibrillation; myocardial infarction