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Correspondence to:
Correspondence to:
Alistair.Lindsay@btinternet.com
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GENERAL CARDIOLOGY

Cardiogenic shock carries a mortality rate in excess of 50%. Induction of nitric oxide synthase (NOS), leading to the generation of excess nitric oxide, is believed to contribute to the inappropriate vasodilatation seen in cardiogenic shock. Tilarginine acts as an NOS inhibitor and early studies have suggested a potential clinical benefit. The TRIUMPH (Tilarginine Acetate Injection in a Randomized International Study in Unstable MI Patients With Cardiogenic Shock) planned to enrol 658 patients at 130 centres, however the study was terminated early after 398 patients had been enrolled. All patients were in refractory cardiogenic shock after myocardial infarction (MI) despite revascularisation. The primary outcome was all-cause mortality among patients who received the study drug. Secondary outcomes included shock resolution and duration, NYHA class at 30 days, and 6-month mortality. Enrolment was stopped in August 2006 and the 6-month follow-up completed in February 2007. No difference in 30-day all-cause mortality was
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