LEADING ARTICLE
Ischaemia-modified albumin: clinical utility and pitfalls in measurement
1 Department of Chemical Pathology, St George’s Hospital and Medical School, Blackshaw Road, London SW17 0QT, UK
2 Department of Cardiology, St George’s Hospital and Medical School, Blackshaw Road, London SW17 0QT, UK
Correspondence to:
Dr Paul O Collinson, Department of Chemical Pathology, 2nd Floor Jenner Wing, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK; paul.collinson@stgeorges.nhs.uk
Accepted 11 March 2008
| The first 150 words of the full text of this article appear below. |
Ischaemia occurs when there is a supply demand mismatch in cardiac blood flow. In unstable angina, this occurs due to partial or total occlusion of a coronary artery due to plaque rupture. In stable angina, there is progressive vascular occlusion resulting ultimately in a stenosis of more than 70%, impairing blood flow. Occasionally it may arise on a background of impaired blood flow and extreme oxygen demand. In this case, the area of myocardium affected will typically be one at the watershed of one or more arterial supplies. If the ischaemia is reversible, no myocardial damage occurs. If the ischaemia is prolonged there will be cellular necrosis and myocardial infarction. The interventional challenge for medicine is to be able to identify acutely impaired myocardial perfusion before necrosis has occurred. Currently, the only strategy for this is to detect ST segment changes on the ECG. Reperfusion therapy can then be initiated
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