Renin-Angiotensin System Inhibition Effect on Post-MI Mortality and New-Onset Atrial Fibrillation

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No association was observed between RAS inhibition and lower risk of new-onset AF in patients with no AF history and with congestive heart failure.
No association was observed between RAS inhibition and lower risk of new-onset AF in patients with no AF history and with congestive heart failure.

A retrospective observational cohort study reported in the Journal of the American Heart Association found that inhibition of the renin-angiotensin system (RAS) reduced the risk of mortality post-acute myocardial infarction (AMI) in patients with and without congestive heart failure (CHF).1

In previous research involving patients with CHF and/or left ventricular dysfunction, inhibition of the RAS with angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) decreased the risk of recurring AMI, hospitalization, and death.2-4 In addition, these agents have been shown to have antiarrhythmic properties.5

Guidelines from the United States and Europe recommend RAS inhibition for this patient group and further suggest that it may prevent new-onset atrial fibrillation (AF).6,7 

To elucidate the benefits of ACEI and ARB, the researchers investigated whether their use was associated with lower cardiovascular and all-cause mortality, stroke, and reinfarction in patients who were post-AMI with and without CHF and/or AF.

They further aimed to determine whether the risk of new-onset AF was lower with RAS inhibition in patients with no AF history or in-hospital AF diagnosis post-AMI. 

The final sample included 112,648 adult patients (median age, 72; 35.5% women) across 72 coronary care units in Sweden who had been admitted for a first AMI; 73.9% were treated with ACEI or ARB or both.

RAS inhibition was linked with a reduced 3-year risk of all-cause mortality in each of the study's 4 subgroups:

  • Patients with CHF and AF (n=11,489; hazard ratio [HR]: 0.75; 95% CI, 0.70-0.81)
  • Patients with CHF without AF (n=31,676; HR: 0.65; 95% CI, 0.60-0.69)
  • Patients with AF without CHF (n=10,066; HR: 0.82; 95% CI, 0.75-0.90)
  • Patients without either CHF or AF (n=59,417; HR: 0.76; 95% CI, 0.72-0.81)

No association was observed between RAS inhibition and a lower 3-year risk of new-onset AF in patients with no history of AF and with CHF (HR: 0.96; 95% CI, 0.84-1.10) or without CHF (HR: 1.12; 95% CI, 1.02-1.22).

These results align with those of prior research, including the Survival and Ventricular Enlargement (SAVE) trial and the Valsartan in Acute Myocardial Infarction (VALIENT) trial, among others.8,4

“The lower risk of mortality observed in our study, and in previous trials, might be a result of reduction in myocardial infarct expansion, ventricular remodeling, and ventricular dilatation observed with RAS inhibition,” the investigators wrote.

Disclosures: Dr Andell reports receiving speaker fees from AstraZeneca; Dr Spaak reports receiving honoraria from Abbott/AbbVie, MSD, AstraZeneca, and Bristol-Myers Squibb; and Dr Oldgren reports receiving consultant and lecture fees from Bayer, Boehringer Ingelheim, and Bristol-Myers Squibb/Pfizer. 

References

  1. Batra G, Lindhagen L, Andell P, et al. 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 [published online March 20, 2017]. J Am Heart Assoc. doi:10.1161/JAHA.116.005165
  2. Køber L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 1995;333(25):1670-1676. doi:10.1056/NEJM199512213332503
  3. Torp-Pedersen C, Køber L. Effect of ACE inhibitor trandolapril on life expectancy of patients with reduced left-ventricular function after acute myocardial infarction. Lancet. 1999;354(9172):9-12. 
  4. Pfeffer MA, McMurray JJV, Velazquez EJ, et al; for the Valsartan in Acute Myocardial Infarction Trial Investigators. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003;349(20):1893-1906. doi:10.1056/NEJMoa032292 
  5. Khatib R, Joseph P, Briel M, Yusuf S, Healey J. Blockade of the renin-angiotensin-aldosterone system (RAAS) for primary prevention of non-valvular atrial fibrillation: a systematic review and meta analysis of randomized controlled trials. Int J Cardiol. 2013;165(1):17-24. doi:10.1016/j.ijcard.2012.02.009 
  6. O'Gara PT, Kushner FG, Ascheim DD, et al; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4):e362-425. doi:10.1161/CIR.0b013e3182742cf6 
  7. Steg PG, James SK, Atar D, et al; for the Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33(20):2569-2619. doi:10.1093/eurheartj/ehs215 
  8. Flather MD, Yusuf S, Køber L, et al. Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group. Lancet. 2000;355(9215):1575-1581.
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