The medication tilarginine, a drug that was believed could be beneficial for patients who develop cardiogenic shock (low blood pressure due to impaired cardiac function) after a heart attack, did not reduce the risk of death up to six months after a heart attack, according to a JAMA study published online March 26. The study is being released early to coincide with its presentation at the American College of Cardiology's annual conference.
Cardiogenic shock is the leading cause of death among hospitalized patients with acute myocardial infarction (MI; heart attack), with rates of death in excess of 50 percent. Early revascularization improves survival; however, early death rates remain high, particularly among patients with continued shock after revascularization, according to background information in the article. "Systemic inflammation, including expression of inducible nitric oxide synthase (NOS [enzyme that promotes nitric oxide]) and generation of excess nitric oxide, is believed to contribute to the pathogenesis and inappropriate vasodilatation [widening of blood vessels] of persistent cardiogenic shock. Preliminary, single-center studies suggested a beneficial effect of NOS inhibition on hemodynamics, renal [kidney] function, and survival in patients with cardiogenic shock."
Judith S. Hochman, M.D., of the New York University School of Medicine, New York, and the TRIUMPH (Tilarginine Acetate Injection in a Randomized lnternational Study in Unstable MI Patients With Cardiogenic Shock) trial investigators tested the effect of NOS inhibition with the drug tilarginine on risk of death on heart attack patients with cardiogenic shock. The study included 398 patients at 130 centers in eight countries. Participants were enrolled between January 2005 and August 2006 when the study was terminated early. Patients received either 1-mg/kg tilarginine intravenously followed by 1.0 mg/kg per hour of intravenous infusion for 5 hours, or matching placeb
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