Use of myoglobin for cardiac injury

Studies are continuing to quickly and accurately diagnose chest pain in the ER. I was recently having a discussion where the topic of serum myoglobin came up as a routine part of the cardiac enzyme panel at some institutions.

The hospitals that I work at typically only include the CK, CK-MB and troponin I as markers for cardiac injury – I was less familiar with the myoglobin. The serum myoglobin is relevant for early diagnosis of cardiac injury, since elevation occurs more rapidly than the other two markers (a 1-4 hour onset of elevation for myoglobin vs 3-12 hour onset for CK and troponin I).

There is a study that suggests that a combination of troponin I and myoglobin can effectively exclude myocardial infarction with a negative predictive value of 99.6% within 90 minutes:

Sensitivity and negative predictive value for point-of-care combination of myoglobin and troponin I by 90 minutes was 96.9% and 99.6%, respectively.

CONCLUSIONS: Acute myocardial infarction can be excluded rapidly in the emergency department by use of point-of-care measurements of myoglobin and troponin I during the first 90 minutes after presentation.

So, why isn’t the serum myoglobin used routinely in more cardiac enzyme panels? UptoDate points to two reasons:

There are two limitations to the use of serum myoglobin for the diagnosis of acute MI. First, the rapid release and metabolism of myoglobin can result in an undulating or “staccato” pattern characterized by increases and decreases in the plasma myoglobin concentration that can lead to clinical confusion.

The second problem is that, like LD, it lacks specificity for the heart. Serum concentrations are elevated after injury to a variety of tissues (especially skeletal muscle) or recent cocaine use and in patients with impaired renal function due to decreased clearance. Because of these limitations and lack of apparent advantage over troponins and CK-MB, serum myoglobin is not routinely measured in patients with suspected MI.

So it seems that until a more specific serum myoglobin test is found, CK-MB and troponins continue to be the standard of measure cardiac damage.

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  • Nick

    I just finished two months in Emergency and this topic was of some interest for me. Right now the conservative ED attendings (ie, most of them) admit almost everyone with a reasonable story of chest pain — even if they’re young, healthy, and the first set of enzymes and EKG is normal. 12-24 hours of observation plus a stress test is a hassle for everyone (including the patient), but the risk of sending someone home with an MI is too great to ignore. And, as recent US and UK studies show, that still happens 2-4% of the time.

    But one estimate of the cost-per-life-saved of admitting low-probability patients is US$1 million.

    What to do? The problem with myoglobin, as you and UTD state, is it’s nonspecific. In fact, many of the same young, low-risk patients coming in with chest pain are manual laborers who could easily have high myoglobin from skeletal muscle damage.

    More hospitals are setting up Chest Pain centers, where “rule outs” can be sent for observation without clogging up the rest of the emergency department. It should I haven’t seen one of these places yet but I hear should cost less, be easier on the patient, and make everyone more comfortable about doing the appropriate workup.

  • Anonymous

    I WORK IN A SMALL HOSPITAL CLOSE TO LEXINGTON, KY. THEY ARE DOING THE 24 HOUR OBSERVATION FOR PATIENTS PRESENTING WITH CHEST PAIN AND THE FIRST SET OF ENZYMES ARE NEGATIVE. I HAVE SEEN FIRST HAND OVER THE PAST 6 MONTHS , AT LEAST ONCE OR TWICE A WEEK, ONE OF THE OBSERVATION PATIENTS BEING POSITIVE BEFORE THE SECOND SET OF ENZYMES. SEVERAL OF THESE PATIENTS HAVE BEEN IN THEIR 30′S AND 40′S. ONE YOUNG WOMAN WAS COMPLAINING OF SHOULDER PAIN. HER TROPONIN WAS EXTREMLY HIGH THE SECOND SET OF ENZYMES. WE HAD ALREADY STARTED RETAVASE BASED ON EKG CHANGES. SHE WAS TAKEN STRAIGHT TO THE CATH LAB AND HAD STENTS PLACED. SHE SAID WE SAVED HER LIFE.

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