Atrial fibrillation in the setting of acute myocardial infarction: the GUSTO-I experience. Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries.
OBJECTIVE
We examined the clinical predictors and angiographic and clinical outcomes associated with atrial fibrillation in the setting of acute myocardial infarction (MI).


BACKGROUND
This condition has been studied primarily in prethrombolytic era small trials.


METHODS
We compared baseline clinical characteristics, short-term clinical and angiographic outcomes and 1-year mortality of patients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial with atrial fibrillation on admission electrocardiography (n = 1,026 [2.5%]) or after enrollment (n = 3,254 [7.9%]) and those without atrial fibrillation (n = 36,611 [89.6%]). Univariable and multivariable analyses were used to assess relations between baseline factors and the development of atrial fibrillation.


RESULTS
Patients with any atrial fibrillation more often had three-vessel coronary artery disease and initial Thrombolysis in Myocardial Infarction (TIMI) grade < 3 flow than those without the arrhythmia. In-hospital stroke was increased in patients with atrial fibrillation (3.1% vs. 1.3%, p = 0.0001), mainly ischemic stroke (1.8% vs. 0.5%, p = 0.0001). Significant multivariable predictors of later atrial fibrillation included advanced age, higher peak creatine kinase levels, worse Killip class and increased heart rate. The unadjusted mortality rate was significantly higher at 30 days (14.3% vs. 6.2%, p = 0.0001) and at 1 year (21.5% vs. 8.6%, p < 0.0001) in patients with atrial fibrillation. The adjusted 30-day mortality rate remained significantly higher with any (odds ratio [OR] 1.3, 95% confidence interval [CI] 1.2 to 1.4) or later (OR 1.4, 95% CI 1.3 to 1.5) atrial fibrillation but not with baseline atrial fibrillation (OR 1.1, 95% CI 0.88 to 1.3).


CONCLUSIONS
Atrial fibrillation in the setting of acute MI independently predicts stroke and 30-day mortality. More aggressive treatment strategies in this subgroup may be warranted and deserve further study.
Crenshaw
B S
BS
Duke Clinical Research Institute, Durham, North Carolina. crenshaw.cards@mhs.unc.edu
Ward
S R
SR
Granger
C B
CB
Stebbins
A L
AL
Topol
E J
EJ
Califf
R M
RM
D001281:Atrial Fibrillation / Q000209:etiology* / Q000401:mortality; D002561:Cerebrovascular Disorders / Q000209:etiology; D017023:Coronary Angiography; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000401:mortality; D010960:Plasminogen Activators / Q000627:therapeutic use*; D013300:Streptokinase / Q000627:therapeutic use*; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*
D013300:Streptokinase; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator