 An estimated 120,000 to 160,000 patients annually are diagnosed with cardiogenic shock CS in North America and Europe. CS complicates approximately 5-14 of all cases of acute myocardial infarction AMI and is the most common cause of death in patients hospitalized with AMI. Cardiogenic shock developing during the course of AMI is the end result of a pathophysiological cycle secondary to a sudden and significant decrease in cardiac contractility due to infarction, ischemia, and stunning of large myocardial segments. It is not anticipated that further advances in reperfusion or revascularization therapy will have a significant additional impact on survival in patients with CS. Modalities that protect the myocardium during ischemia and reperfusion are likely to be the next major advance in improving outcome in the setting of acute myocardial infarction MI, especially in patients with large infarcts complicated by shock. Preliminary studies investigating nitric oxide synthase NOS inhibition suggest that improvements in cardiovascular function and survival are possible by limiting formation of toxic NO. The primary objective of the TRIUMPH study is to establish the efficacy of Tilarginine Acetate Injection compared to placebo in reducing all cause mortality at 30 days post randomization in patients with cardiogenic shock complicating acute myocardial infarction MI. Safety objectives of this study include an evaluation of adverse events and serious adverse events, and key laboratory parameters. 