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J Am Coll Cardiol, 2005; 45:1775-1780, doi:10.1016/j.jacc.2005.02.061 © 2005 by the American College of Cardiology Foundation |
* Department of Medicine, George Washington University, Washington, DC
Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota
Columbia University Medical Center and The Cardiovascular Research Foundation, New York, New York
Keck School of Medicine, Division of Cardiovascular Medicine, University of Southern California and the Heart Institute of Good Samaritan Hospital, Los Angeles, California
|| Department of Medicine, Emory University School of Medicine, Atlanta, Georgia
Manuscript received October 15, 2004; revised manuscript received December 28, 2004, accepted February 14, 2005.
* Reprint requests and correspondence: Dr. R. Wayne Alexander, Department of Medicine, Emory University Hospital, H-153, 1364 Clifton Road NE, Atlanta, Georgia 30322. (Email: ralexan{at}emory.edu).
OBJECTIVES: The purpose of this research was to determine the effect of intravenous adenosine on clinical outcomes and infarct size in ST-segment elevation myocardial infarction (STEMI) patients undergoing reperfusion therapy.
BACKGROUND: Previous small studies suggest that adenosine may reduce the size of an evolving infarction.
METHODS: Patients (n = 2,118) with evolving anterior STEMI receiving thrombolysis or primary angioplasty were randomized to a 3-h infusion of either adenosine 50 or 70 µg/kg/min or of placebo. The primary end point was new congestive heart failure (CHF) beginning >24 h after randomization, or the first re-hospitalization for CHF, or death from any cause within six months. Infarct size was measured in a subset of 243 patients by technetium-99m sestamibi tomography.
RESULTS: There was no difference in the primary end point between placebo (17.9%) and either the pooled adenosine dose groups (16.3%) or, separately, the 50-µg/kg/min dose and 70-µg/kg/min groups (16.5% vs. 16.1%, respectively, p = 0.43). The pooled adenosine group trended toward a smaller median infarct size compared with the placebo group, 17% versus 27% (p = 0.074). A dose-response relationship with final median infarct size was seen: 11% at the high dose (p = 0.023 vs. placebo) and 23% at the low dose (p = NS vs. placebo). Infarct size and occurrence of a primary end point were significantly related (p < 0.001).
CONCLUSIONS: Clinical outcomes in patients with STEMI undergoing reperfusion therapy were not significantly improved with adenosine, although infarct size was reduced with the 70-µg/kg/min adenosine infusion, a finding that correlated with fewer adverse clinical events. A larger study limited to the 70-µg/kg/min dose is, therefore, warranted.
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