Ischaemia-modified albumin: clinical utility and pitfalls in measurement

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 and is life-saving, and results in myocardial salvage. The majority of patients who present with chest pain do not have acute myocardial infarction (AMI). The sensitivity of the admission ECG is typically around 50%. There is therefore a need for a strategy that could detect ischaemia before necrosis occurs and result in prompt revascularisation. The challenge is to use additional quantitative risk stratification tools that could be biomarkers for ischaemia. Currently, three markers have been proposed: choline, free fatty acids and ischaemia-modified albumin (IMA).1 Of these, only IMA is currently available as a licensed test for routine clinical application. The N-terminal portion of human serum albumin is known to be a binding site for transition metal ions, binding cobalt, copper and nickel in their (II) forms.2 It is also known that the N-terminal portion of human serum albumin is susceptible to biochemical degradation and is less stable than …