Is more rapid diagnosis of heart attack worthwhile?

Is more rapid diagnosis of heart attack worthwhile? – Editorial

Allan Jaffe

The article by Chesebro[1] on the use of serum markers for the more rapid diagnosis of myocardial infarction provides important information about the relative kinetics of a variety of markers of myocardial injury. Most of the substances currently measured are proteins rather than enzymes. Thus, the more appropriate term is “biomarkers” and not “enzymes.” Recently, substantial importance has been placed on making a diagnosis of acute myocardial infarction earlier and more rapidly.[2] Indeed, although not discussed extensively by Chesebro, the need for this type of approach is an area of substantial controversy.[3]

At present, there are adequate diagnostic criteria that do not require biochemical confirmation of the types of myocardial infarctions that require aggressive interventions, whether one believes in the primacy of thrombolysis or primary angioplasty. Indeed, a delay caused by the routine measurement of biomarkers is, in my opinion, inappropriate. Furthermore, patients who present very early (e.g., during the first two hours) after the onset of clinical symptoms are unlikely to have elevation of any of the biomarkers. Thus, with the exception of an occasional patient in whom the diagnosis of acute myocardial infarction is in question, biomarkers for myocardial infarction, no matter how rapid this information can be obtained, are unlikely to be helpful.

Although not mentioned by Chesebro, the use of biomarkers has been recommended by some for making a definitive decision on whether the patient can safely return home or whether the patient needs to be hospitalized.[3] However, patients with unstable angina in the absence of evidence of myocardial injury still can be at risk for sudden death or subsequent ischemic events.[4] Thus, although biomarkers may provide potentially helpful information, caution is recommended from placing too much emphasis on this indication.

Finally, in the interest of cost-containment, the triage of patients who are more or less likely to have complications associated with acute ischemic heart disease might be valuable. Certainly, patients with an element of myocardial injury would be at greater risk, and it has been argued that these individuals might be admitted to an intensive care unit, whereas others could be hospitalized in less intensive-care facilities. However, the incremental value of biomarkers over and above electrocardiographic findings and clinical presentation has never been studied adequately.[5] Thus, the key issue not addressed by Chesebro in her review is not whether we can make an earlier and more rapid diagnosis but whether or not we should.

In my opinion, the predominant reasons for increasing the rapidity of diagnosis are related to the increased rapidity with which patients are being seen in our facilities. Physicians wish to discharge individuals who are admitted to the hospital more rapidly (often in less than 24 hours) or wish to discharge those who are being evaluated in the emergency department predominantly for logistic reasons. However, as indicated by Chesebro, there is a trade-off between the high levels of specificity that can be accomplished with markers that rise somewhat later and the increased rapidity of diagnosis with markers that tend to be elevated earlier.

Thus, is it better to spend only six hours on the work-up and have a less accurate diagnosis (in particular if elevations of biomarkers are present) or is it better to spend nine to 12 hours and have definitive diagnosis using measurement of troponin and/or the MB fraction of creatine kinase (CK-MB)? I believe that the difference in timing is not critical once one has decided that the patient will either be admitted to the hospital or kept in an observation unit for some number of hours. Therefore, the most cost-effective approach might well be to use just one marker and to make the diagnosis definitively. However, others may disagree,[6] and it is for this reason that Chesebro has presented the alternative strategies that might be used if one wants a more rapid diagnosis.

With regard to the article by Chesebro, I would add the following comments:

1. The fact that the CK-MB peak rises three to four hours later than myoglobin, CK-MB isoforms or fatty acid binding protein (not discussed by the article) does not make it a “retrospective sign of infarction.”

2. Determining infarct size is possible utilizing peak, total creatine kinase or CK-MB as long as one is careful to compare patients treated similarly. Thus, what may be suggested by the authors is that infarct sizing is unreliable when patients treated with reperfusion are compared with those who are not reperfused. However, when similar therapy is used, there are good data confirming the reliability of CK infarct size compared to pathology.[7]

3. There is a rapid assay for cardiac troponin I (c-TnI). The assay done in a laboratory takes approximately seven minutes. What the authors may be alluding to is another concept that many have linked to the early diagnosis of acute infarction: the use of point of care testing. This approach allows for the bedside determination of biomarker values, increasing the rapidity of evaluation by removing the need to transport samples to the laboratory. The increased rapidity is counterbalanced in part by the semiquantitative nature of the measurements and the difficulty with quality control. This point may be what the authors are trying to make when they suggest that the assay for c-TnI takes time.

In the final analyses, the question is not if we can but if we should make the diagnosis of acute myocardial infarction more rapid.


[1.] Chesebro MJ. Using serum markers in the early diagnosis of myocardial infarction. Am Fam Physician 1997;55:2667-74.

[2.] Guest TM, Jaffe AS. Rapid diagnosis of acute myocardial infarction. Cardiol Clin 1995;13:283-94.

[3.] Jaffe AS. More rapid biochemical diagnosis of myocardial infarction: necessary? prudent? cost-effective? [editorial] Clin Chem 1993;39:1567-9.

[4.] Antman EM, Tanasijevic MJ, Thompson B, Schactman M, McCabe CH, Cannon CP, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;335:1342-9.

[5.] Brush JE Jr, Brand DA, Acampora D, Chalmer B, Wackers FJ. Use of the initial electocardiogram to predict in-hospital complications of acute myocardial infarction. N Engl J Med 1985;312:1137-41.

[6.] Newby LK, Gibler WB, Ohman EM, Christenson RH. Biochemical markers in suspected acute myocardial infarction: The need for early assessment [editorial]. Clin Chem 1995;41:1263-5.

[7.] Hackel DB, Reimer KA Ideker RE, Mikat EM, Hartwell TD, Parker CB, et al. Comparison of enzymatic and anatomic estimates of myocardial infarct size in man. Circulation 1984; 70:824-35.

Dr. Jaffe is professor of medicine, vice chairman for academic affairs and chief of the cardiovascular division at the State University of New York Health Science Center, Syracuse.

COPYRIGHT 1997 American Academy of Family Physicians

COPYRIGHT 2004 Gale Group