2009, Volume 16, Supplement 3: Multi-management of ischaemic heart disease: do we have the COURAGE of our convictions?

September 2009 Br J Cardiol 2009;16(Suppl 3):S3

Multi-management of ischaemic heart disease: do we have the COURAGE of our convictions?

Rachel Arthur

Abstract

A report from a satellite symposium at the British Cardiovascular Society Annual Scientific Conference. Highlights from the A Menarini Pharma UK SRL and CV Therapeutics Europe-sponsored symposium at the British Cardiovascular Society Annual Scientific Conference 2009....

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September 2009 Br J Cardiol 2009;16(Suppl 3):S3-S4

Treating chronic stable angina: who’s winning, who’s losing and why

Harry Hemingway

Abstract

The extent of the problem: Most people with stable angina, irrespective of treatment, will get symptoms again over a prolonged follow-up period. The ACRE (Appropriateness of Coronary Revascularisation) study, for example, showed that in a consecutive unselected patient series of 1,020 patients, more than 50% treated with percutaneous coronary intervention (PCI) or medical treatment had symptoms at six years.(1)...

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September 2009 Br J Cardiol 2009;16(Suppl 3):S5-S6

Perspectives to ponder: pills, pipework or both?

William E Boden

Abstract

Evidence from randomised trials supports percutaneous coronary intervention (PCI) in patients with acute coronary syndromes (ACS): PCI has been shown to improve clinical outcomes and to reduce events. Its role in the broader group of patients with chronic angina and stable coronary artery disease has been less certain, however. ...

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September 2009 Br J Cardiol 2009;16(Suppl 3):S7-S8

Chronic stable angina and the late sodium current

John Camm

Abstract

The pathological paradigm: The use of a slow sodium inhibitor may improve angina pectoris. This is based on the following pathological paradigm. The transient, or peak, sodium current occurs at the beginning of the action potential: the rapid influx of sodium causes the upstroke of the action potential. This current does not immediately die away: it has a tail, known as the late, delayed or slow sodium current. In an abnormal situation, the late sodium current can be enhanced. Normally this current transports about half the sodium from outside the cell to the inside but under certain situations, when it becomes enhanced, it transports far more sodium into the cell and sodium accumulates within the cell. An enhanced current prolongs the action potential and, with it, the QT interval. There is a mechanical consequence to this enhancement: instead of the simple phasic twitch when myocardium is activated, the pattern of mechanical contraction is phasic followed by a tonic component. This tonic component extends into diastole, meaning that muscle is still tense during the early part of diastole....

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