Albumin cobalt binding and ischemia modified albumin generation: An endogenous response to ischemia?

Myocardial ischemia has become the leading cause of mortality in western countries and this unfavorable trend is unlikely to reverse in the near future. The events progression leading to acute coronary syndrome involves a physiological continuum that traditionally spans from plaque instability to rupture, intracoronary thrombus, reduced blood flow, myocardial ischemia, reversible damage and necrosis [1]. From this biological perspective, myocardial necrosis is time-dependent and occurs when the action of the endogenous mechanisms of response to ischemia is finally overwhelmed. During acute ischemic conditions, the metal binding capacity of albumin for transition metals, like copper, nickel and cobalt is reduced, generating a metabolic variant of the protein, commonly known as ischemia modified albumin (IMA). IMA measurement has recently been proposed as the first US FDA-cleared sensitive marker for the diagnosis of myocardial ischemia in patients presenting with typical acute chest pain [2]