CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Allan S. Jaffe, MD*,
Luciano Babuin, MD and
Fred S. Apple, PhD
* Cardiovascular Division, Gonda 5, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905 (Email: jaffe.allan{at}mayo.edu).
Drs. Fye, Nagajothi, and Trivedi raise important issues that we are pleased to address.
One that many of us have tried to reinforce for years is that elevations of biomarkers of cardiac injury are not synonymous with myocardial infarction (1). This is especially important for cardiac troponin which, because it is more sensitive than creatine kinase MB (CKMB), detects cardiac injury in many situations which are not due to primary coronary abnormalities. Thus, many patients with elevations do not require the extensive workups Dr. Fye correctly indicates can occur if one obviates common sense. Some may need an evaluation for pulmonary embolism or myocarditis and some only watchful waiting. Some of this can occur in the outpatient setting in our view, but we often see cardiologists assume that once the patient is discharged that they can forget about elevations. Neglecting such a potent risk factor for mortality is not good common sense either. Regardless of the etiology, elevations of troponin are indicative of significant cardiovascular disease and usually are associated with an adverse prognosis in the short term (2) and over time once recovery occurs (3) and in those who are more compensated (4). When such elevations occur in critically ill individuals, first efforts should be focused on the primary disease process which very often is the stimulus for the cardiac injury. Additional work is necessary to distinguish when we as cardiologists should address cardiac issues acutely over and above treating the underlying disease state. Many of us are actively involved in trying to define such subsets at present. Whether or not acute intervention is needed, it is clear from most studies that elevations of troponin also predict adverse long term events (3,4). Thus, those who were critically ill and recover and those in whom "incidental" elevations of troponin were detected, require careful evaluation. That could mean an evaluation for ischemic heart disease but as Dr. Fye suggests, it is prudent to consider other etiologies for elevations as well.
It is also good common sense to upgrade our clinical judgment periodically. It is thus prudent in considering the possibility in a given patient of ischemic heart disease to take note of information concerning the lack of perfection of the angiogram, (5) differences in the way in which women present with infarction, (6) and the recent article in the Journal of the American College of Cardiology suggesting the high frequency of unrecognized myocardial infarctions detected in older individuals by MRI (7).
The issue of reinfarction is one where we have used common sense. The state of the art and guidelines are not the same. The later are often much more conservative. It was presumed in the initial studies, that increases in CKMB post-infarction were indicative of reinfarction. There was no independent validation of that. There has been no validation of the use of increases on the down slope at all and those criteria are likely very insensitive. We now know that reinfarction is easily detected with troponin by the presence of a rising pattern of values (8). In the vast majority of patients, changes in troponin, presuming sensitive assays and recommended cut off values, occur rapidly, obviating the delay in the occasional patient in whom decision making might depend on the values (9). Because troponin is more sensitive, it should provide a clearer signal on the down slope than CKMB and several groups are considering a recommendation of a 20% to 25% change in that situation. Those criteria too will likely be insensitive but will prevent false-positive diagnoses as well. Once one starts to rely on troponin values, the ease with which they can be used becomes easily appreciated and their use becomes part of good common sense. Hanging onto the past adds costs and retards the ability of clinicians to learn how easily many of these issues can be resolved.
The issue Dr. Fye highlights is that we need to be smarter about how we respond to elevations of troponin both acutely and longer term. Troponin elevations should never trump common sense, but we must also be open to the possibility that at times, especially in a busy world, we may need to allow our common sense to evolve as the science of our discipline improves and to acknowledge a responsibility to work up patients with abnormal troponin values as outpatients when appropriate rather than ignore such elevations. All of that would be good common sense.
 |
References
|
|---|
1. Jaffe AS, Babuin L, Apple FS. Biomarkers in acute cardiac disease: the present and the future J Am Coll Cardiol 2006;48:1-11.[Abstract/Free Full Text]2. Waxman DA, Hetch S, Schappert J, Husk G. A model for troponin I as a quantitative predictor of in hospital mortality J Am Coll Cardiol 2006;48:1755-1762.[Abstract/Free Full Text] 3. Babuin DA, Rio Perez JA, Alegria JR, Afessa B, Jaffe AS. Elevated troponin is an independent predictor of short- and long-term mortality in medical intensive care unit patients Eur Heart J 2006;27(Suppl 1):217-218.[Free Full Text] 4. Landesberg G, Shatz V, Akopnik I, et al. Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery J Am Coll Cardiol 2003;42:47-54.[Abstract/Free Full Text] 5. Topol EJ, Nissen SE. Our preoccupation with coronary luminologyThe dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333-2342. 6. Nabel EG, Selker HP, Califf RM, et al. National Heart, Lung and Blood Institute, American College of Cardiology FoundationWomen’s Ischemic Syndrome Evaluation: current status and future research directions: report of the National Heart, Lung and Blood Institute workshop: October 2–4, 2002: Section 3: diagnosis and treatment of acute cardiac ischemia: gender issues. Circulation 2004;109:e50-e52. 7. Barbier CE, Bjerner T, Johansson L, Lind L, Ahlström H. Myocardial scars more frequent than expected: magnetic resonance imaging detects potential risk group J Am Coll Cardiol 2006;48:765-771.[Abstract/Free Full Text] 8. Apple FS, Murakami MM. Cardiac troponin and creatine kinase MB monitoring during in-hospital myocardial reinfarction Clin Chem 2005;51:460-463.[Free Full Text] 9. MacRae AR, Kavsak PA, Lustig V, et al. Assessing the requirement for the six-hour interval between specimens in the American Heart Association classification of Myocardial Infarction in Epidemiology and Clinical Research Studies Clin Chem 2006;52:812-818.[Abstract/Free Full Text]
Related Articles
-
Biomarkers in Acute Cardiac Disease
- Nagapradeep Nagajothi and Atul Trivedi
J. Am. Coll. Cardiol. 2006 48: 2358.
[Full Text]
[PDF]
-
Troponin Trumps Common Sense
- W. Bruce Fye
J. Am. Coll. Cardiol. 2006 48: 2357-2358.
[Full Text]
[PDF]
|
Top
References