|Trial||Agent||Mechanism of Action||n||Primary End Point(s)||Results|
|TIMI-2 (80)||IV metoprol||Lowers oxygen demand||1,390||EF at discharge||Negative (50.5% vs. 50.0%)|
|TAMI-4 (81)||Prostacyclin||Inhibits neutrophils; scavenges free radicals||50||IRA patency, EF||Negative (both lower)|
|TAMI-9 (82)||Fluosol||Inhibits neutrophils; improves oxygen delivery||430||Infarct size||Negative (22% vs. 17%)|
|ISIS-4 (83)||Magnesium||Stabilizes myocardial membranes||58,050||Death at 35 days||Negative (7.6% vs. 7.2%)|
|CORE (84)||RheothRx||Improves oxygen delivery||2,780||Death/shock/repeat MI||Negative (13.6% vs. 12.7%)|
|AMISTAD (85)||Adenosine||Inhibits neutrophils; scavenges free radicals||236||Infarct size||Positive (13% vs. 19.5%)∗|
|HALT-MI (86)||Hu23F2G||Inhibits neutrophil adhesion to endothelial cells||420||Infarct size||Neutral (17.1% vs. 19.3%)†|
|ADMIRE (87)||AMP579||Inhibits neutrophils; scavenges free radicals||311||Infarct size||Negative (11.8% vs. 9.9%)‡|
↵∗ The primary end point included a multivariable regression analysis, which revealed a 33% relative reduction in infarct size with adenosine treatment (p = 0.03).
↵† High dose Hu23F2G versus placebo.
↵‡ High dose AMP579 versus placebo.
↵legend ADMIRE = AMP579 Delivery for Myocardial Infarction REduction; AMISTAD = Acute Myocardial Infarction STudy of ADenosine; CORE = Collaborative Organization for RheothRx Evaluation; EF = ejection fraction; HALT-MI = Hu23F2G antiAdhesion to Limit cytoToxic injury following acute Myocardial Infarction; IRA = infarct-related artery; ISIS = International Study of Infarct Survival; MI = myocardial infarction; TAMI = Thrombolysis and Angioplasty in Myocardial Infarction; TIMI = Thrombolysis In Myocardial Infarction.
legend Adapted from Granger (79), with permission.