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European Heart Journal 2003 24(14):1282-1284; doi:10.1016/S0195-668X(03)00318-X
Copyright © 2003 by the European Society of Cardiology.
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Editorial

Nicorandil: a drug for many purposes: too good to be true?

Eric Eeckhouta,*

a Service de Cardiology, Centre Hospital Universitaire Vaudois, 1011 Lausanne, Switzerland

* Corresponding author: Tel.: +41/21-3140-012; fax: +41/213-140-067
E-mail address: eric.eeckhout@chuv.hospvd.ch

Received 4 June 2003; revised 4 June 2003; accepted 5 June 2003

The first 10% of the full text of this article appears below.

See doi:10.1016/S1095-668X(03)00202-1 and doi:10.1016/S1095-668X(03)00236-7 for the article to which this editorial refers

Nicorandil, a drug approved for the treatment of ischaemic heart disease, is believed to have a dual properties. The intrinsic mechanism of the drug (selective activation of K+ATPchannels at the sarcolemmal and mitrochondrial level) allows coronary and peripheral vasodilatation with subsequent reduction of preload and afterload. Secondly, because of the role K+ATPchannels in ischaemic preconditioning, nicorandil has been attributed cardioprotective effects.1

The drug has been available in Europe for years, classified as a new class of therapy for coronary artery disease, but failed till now to truly penetrate on the ‘European market’. The large scaled, randomized IONA trial evaluated the efficacy of nicorandil on top of ‘conventional’ antianginal drugs for the . . . [Full Text of this Article]


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