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“Ischemia modified albumin”: a new biochemical marker of myocardial ischaemia
  1. A Sacchetti
  1. Correspondence to:
 Dr A Sacchetti
 Our Lady of Lourdes Medical Center, 1600 Haddon Avenue, Camden, New Jersey, USA;

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Biochemical marker that has the potential to change management of chest pains

Periodically in the course of a medical career a new technological advance occurs that dramatically changes the direction of our patient care. The brief history of emergency medicine has unveiled a few such marvels. Those of us who have been in practice for many years have on occasion boasted to our younger colleagues of the challenges of managing SVTs without adenosine, or diagnosing unconscious patients with no computed tomography scans. The report by Sinha et al on an “Ischemia modified albumin” (IME) assay in this issue of the journal has the potential to create a similar management change for the emergency department care of chest pain patients.1

Differentiating transient myocardial ischaemia or angina from non-cardiac causes of chest pain is a major diagnostic challenge. Emergency physicians have a very limited number of answers they can provide a chest pain patient. We can identify an acute ST elevation myocardial infarction (MI) through examination of a standard 12 lead electrocardiogram, in most instances. We can also recognise a non-STE MI, and acute coronary syndromes though detection of raised myocardial enzymes. But once we have excluded either of these two conditions, we cannot readily tell a chest pain patient if they are at risk for any acute myocardial event. Our inability to identify occult cardiac disease is compounded by the potential for sudden cardiac death in patients with unrecognised significant coronary artery lesions.

Diagnostic options for chest pain patients in the ED include clinical assessment, provocative testing, or advanced imaging studies. None of these truly meet the practice needs of most emergency practitioners or our patients.

Unstructured use of a patient’s history and physical examination may be reliable in patients with classic presentations but it is certainly fraught with false positives and more significantly false negatives. The introduction of the Goldman criteria provided a formalised history and physical examination scoring system and demonstrated improved diagnostic accuracy in chest pain patients but still had sensitivities below 60%.2 Unfortunately, the accuracy of this approach is limited by both the ability of the interviewer to obtain an accurate history and that of the patient to correctly answer questions. Most experienced clinicians are well aware of the difficulties in interpreting an ambiguous or varying description of chest pain.

Provocative tests such as exercise and chemical stress tests have well established credibility in identifying patients with coronary artery lesions. Sensitivity for these tests range from 46% to 85% for simple exercise tests and up to 94% for nuclear medicine assisted tests.34 Unfortunately, emergency medicine utilisation of these tests is frequently limited by the logistics of arranging such tests or access to the consultants needed to interpret them. Even the most well designed rapid rule out units still require personnel and equipment to perform the exercise portion of the test and specialists to interpret either the nuclear medicine scans or echocardiograms. All of this takes control of the patient out of the hands of the emergency physician and forces us into a dependent role in patient decision making. More recently, magnetic resonance cardiology has been described, although access to this technology will be even more limited.

Coronary artery angiography is certainly an option, and occasionally the most reasonable diagnostic study for patients with extremely suspect histories and normal electrocardiograms. However, again, the emergency physician’s management revolves around additional services and consultants.

The introduction of the IMA assay for the first time provides emergency physicians with an objective diagnostic study to determine the presence of myocardial ischaemia completely within the control of the emergency department.

The IMA assay presents a quantitative accurate laboratory determination of the occurrence of an ischaemic myocardial event, angina. Unlike previous serum studies that identify myocardial damage after the fact, this test allows emergency physicians to determine which patients have potential coronary artery lesions before occlusion occurs. The study in this month’s journal demonstrates a 95% sensitivity for the IMA assay when combined with the ECG and troponin T. This matches that of any other diagnostic modality short of coronary artery catheterisation. Considering the potential consequences for missing the presence of clinically significant coronary lesions the introduction of an objective decisions tool for these patients is a welcome aid to even the most confident clinician.

More important than the existence of this diagnostic test itself is the decision making capabilities it provides emergency physicians. The test can be performed and returned to the ordering physician in about 30 minutes providing a disposition point well within the limits of the typical ED visit. This compares very favourably with the 9–12 hour periods for chest pain unit stress testing or the multiple day admissions for inpatient evaluations.

Placing such management control completely within the initial ED visit will have dramatic effects on hospital bed and resource utilisation. Considering the universal prevalence of ED crowding, the safe discharge to home of chest pain patients will free in patient beds for those admitted patients now boarding in ED hallways.

For as promising as the IMA assay appears some degree of caution is still indicated. Before we relinquish all those acute coronary syndrome beds and renovate the cardiac stress laboratory there are a number of questions on IMA testing that need to be established. Specifics on the timing of blood sampling in relation to the onset of chest pain must be established as well as other conditions that may cause false positive or negative results. Sindha’s study is certainly methodologically sound and supports other reports on the diagnostic value of assaying IMA concentrations in chest pain patients. If indeed this test bears up under additional scrutiny the next generation of emergency physicians may listen amazed at our care of chest pain patients without a serum marker for angina.

Biochemical marker that has the potential to change management of chest pains


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