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Tilarginine in Patients With Acute Myocardial Infarction and Cardiogenic Shock
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To the Editor: The report of the TRIUMPH investigators1 showed a lack of benefit of NOS inhibition by L-NMMA in patients with MI complicated by cardiogenic shock. L-NMMA is closely related to ADMA. Both compounds are endogenously produced during the process of protein turnover and inhibit NOS with about equal potency.2 Plasma concentrations of ADMA were found to predict adverse outcome in patients with multiorgan failure,3 a common cause of death in cardiogenic shock.
Achan et al2 showed that infusion of ADMA in healthy volunteers increased systemic vascular resistance and blood pressure and decreased cardiac output. The most rapid change seen in response to intravenous ADMA administration was a significant fall in heart rate, well before blood pressure had increased, suggesting that the drop in cardiac output was not secondary to increased vascular resistance, but rather resulted from a direct effect of ADMA on the heart. Kielstein et al4 showed . . . [Full Text of this Article]
Tom Teerlink, PhD
t.teerlink@vumc.nl
Department of Clinical Chemistry
VU University Medical Center
Amsterdam, the Netherlands
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Tilarginine in Patients With Acute Myocardial Infarction and Cardiogenic Shock
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JAMA. 2007;298(9):971.
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Tilarginine in Patients With Acute Myocardial Infarction and Cardiogenic Shock—Reply
Robert A. Harrington, John H. Alexander, Judith S. Hochman, Harmony R. Reynolds, Vladimir Dzavik, and Frans J. Van de Werf
JAMA. 2007;298(9):972-973.
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Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and Cardiogenic Shock: The TRIUMPH Randomized Controlled Trial
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JAMA. 2007;297(15):1657-1666.
ABSTRACT
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