April 2002

From Lancet

Nicorandil could improve outcome for angina patients

Please note that if you are outside North America the embargo date for all Lancet press material is 0001hours UK time Friday 29 March 2002

Results of a UK study in this week°¶s issue of THE LANCET suggest that the antianginal drug nicorandil could reduce the risk of cardiovascular disease associated with angina.

Angina occurs in 10% of men aged older than 60 years in the UK (10-15 years later in women), and is a common underlying cause of coronary heart disease (CHD). Aspirin, angiotensin-converting-enzyme (ACE) inhibitors, and statins reduce the risk of cardiovascular events in subgroups of patients with stable angina; however, the effect of specific antianginal treatment in these patients is unknown. The antianginal drug nicorandil is thought to have cardioprotective properties in addition to its anti-ischaemic effects. Henry Dargie from the Western Infirmary, Glasgow, UK, and the Impact Of Nicorandil in Angina (IONA) investigators did a randomised trial to find out whether nicorandil could reduce the frequency of coronary events in men and women who had stable angina and additional risk factors for CHD.

5126 patients from 226 centres in the UK were randomly assigned 20 mg nicorandil twice daily or identical placebo in addition to standard antianginal therapy (É“-blockers, calcium-channel blockers, or long-acting nitrates). Average follow-up time was 1.6 years.

15.5% of patients in the placebo group and 13.1% in the nicorandil group had a primary endpoint (death due to coronary heart disease, non-fatal heart attack, or unplanned hospital admission because of chest pain). The rate of acute coronary syndromes was 7.6% in the placebo group and 6.1% in the nicorandil group; the corresponding rates for all cardiovascular events were 17% and 14.7%, respectively.

An accompanying Commentary (p 1262) by Edward Lesnefsky from Louis Stokes Veterans Affairs Medical Center, Cleveland, USA, concludes: °•The results of IONA provide strong evidence that the cellular effectors of ischaemic preconditioning will continue to emerge as key therapeutic targets in the development of strategies to manage ischaemic heart disease.°¶

Contact: Professor HJ Dargie, Department of Cardiology, Western Infirmary, Glasgow G11 6NT, UK; T) +44 (0)141 211 2637; F) +44 (0)141 211 1791; E) H.Dargie@bio.gla.ac.uk

Dr Edward J Lesnefsky, Department of Medicine, Division of Cardiology, Case Western Reserve University and Medical Service/Geriatric Research, Education and Clinical Center, Louis Stokes Veterans Affairs Medical Center, Cleveland, Oh 44106, USA; E) EXL9@po.cwru.edu











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