Anticoagulation for Atrial Fibrillation in Acute Myocardial Infarction

Abstract & Commentary

By Michael H. Crawford, MD, Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer.

Synopsis: In daily clinical practice, OAC was only given to a minority (30%) of AMI patients with AF, despite the fact that OAC was associated with a 29% relative and 7% absolute reduction in 1-year mortality after adjustment for confounding variables. The results emphasize the importance of OAC treatment for AF after AMI.

Source: Stenestrand U, et al. Anticoagulation Therapy in Atrial Fibrillation in Combination with Acute Myocardial Infarction Influences Long-Term Outcome: A Prospective Cohort Study from the Register of Information and Knowledge. Circulation. 2005;112:3225-3231.

Although the ACC/AHA guidelines recommend oral anticoagulants for atrial fibrillation (AF) complicating myocardial infarction (MI), it is not always given. Thus, Stenestrand and colleagues from the Register of Information and Knowledge about the Swedish Heart Intensive Care Admissions studied oral anticoagulation (OAC) usage in post-MI patients with AF, and evaluated its effect on mortality at one year. Patients admitted to Swedish hospitals with acute MI discharged alive between 1995 and 2002 were assessed. There were 6182 patients with acute MI and AF on the discharge ECG (7.6% of the total MI population). The incidence of AF increased with age. Most (78%) had AF on admission. In 29%, OAC was prescribed at discharge, 60% were given aspirin or thienopyridine and 11% received no antiplatelet or anticoagulant therapy. Mortality at one year was highest for those on nothing (45%) as compared to those on platelet inhibitors only (31%) and those on OAC (22%). Of those on OACs at discharge, 46% were taking it on admission. There was no difference between the treatment groups with regard to reperfusion therapy and heart failure. OAC use reduced one-year mortality (RR .73) primarily due to reduced ischemic cardiac death (55.6 vs 62%). Fatal stroke was reduced from 7.5 to 5.7% in the OAC group. No subgroup benefited more than others. Stenestrand et al concluded that OAC use in post-MI AF patients was associated with a significant reduction in one-year mortality.


Although this is an observational study, there are no prospective trials of therapy for AF complicating acute MI. The AF trials excluded acute MI patients. Yet this is an important issue since about 10% of acute MI patients have AF. In this cohort, about one-third were treated with OACs and all the rest received antiplatelet drugs. Those treated with OACs clearly did better in terms of one-year mortality.

Prior studies of aspirin plus fixed low-dose OAC (CARS, CHAMP) in post acute MI patients showed no benefit. However, INR > 2.0 adjusted OAC plus aspirin in 2 trials in post MI patients did show a reduction in the combined end point of death, reinfarction, and stroke (ASPECT-2, WARIS-2). However, bleeding rates doubled. In this study, bleeding rates were not higher on OAC.

Although deaths due to vascular causes were reduced in this study by OACs, other causes of death were increased on OACs from 21.9% to 27.6%. Most patients died of the acute MI or other ischemic complications. Stroke deaths were in the 6-7% range and were reduced by OAC. Nonfatal strokes were also reduced from 10% to 8%. Thus, the usual recommendation for oral anticoagulants for AF in any setting would seem to apply to acute MI patients. In this group, like any other, aspirin and other antiplatelet drugs are not as effective. This study supports the general conclusions of the AF OAC studies. What is surprising is that only one-third of post MI patients with AF got OAC. Some may have had contradictions to their use, but more likely physicians were afraid to load up the drugs that can cause bleeding in this patient group. This fear seems unfounded in this observational study. The benefits of OAC exceeded the risks.