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Editor's Correspondence
February 25, 2008

Are Guideline-Based Therapies for Myocardial Infarction Generalizable to Troponin-Only Positive Patients?

Author Affiliations

Copyright 2008 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2008

Arch Intern Med. 2008;168(4):436-437. doi:10.1001/archinternmed.2007.118

Shah et al1 have analyzed troponin-only positive “myocardial infarctions” (MIs) with regard to guideline-based management and report that guideline-based therapies are underused. I am not certain their analysis is correct. When the criteria for MI were revised to include troponin-only positive MIs, I was concerned that we were not looking at a homogeneous population when compared with patients who presented with electrocardiographic changes and elevated creatine phosphokinase of muscle band (CPK-MB) level. When I expressed my concern to a member of the committee who revised the definition, I was told not to worry about it, that it would be better for the hospital because we would get more reimbursement for all these new MIs. Recently, in my own cardiology practice I have seen elevated troponin levels in cases of diabetic ketoacidosis (cardiac catheterization showed normal coronary arteries), urosepsis, acidosis, pneumonia, sepsis, severe chronic obstructive pulmonary disease, pulmonary embolus, disseminated intravascular coagulation, and many other conditions. It is not clear to me that this represents the same pathology that is seen with a traditional MI with chest pain, electrocardiographic changes, and an elevated CPK-MB level (coronary atherosclerosis, unstable plaque, and plaque rupture). If the pathology is different, I do not think that we can assume that therapies that were tested for that type of MI are necessarily beneficial for elevated troponin level in settings of severe myocardial stress without likely plaque instability. For instance, despite inclusion in the article, positive troponin status by itself is not an indication for either lytic therapy or primary percutaneous coronary intervention. Having participated in a moderate number of multicenter clinical trials in cardiology, I can think of none in which a patient with elevated troponin but normal CPK and CPK-MB levels, with severe comorbidities such as sepsis, diabetic ketoacidosis, disseminated intravascular coagulation, chronic obstructive pulmonary disease requiring intubation, or pulmonary embolism, would be considered an appropriate candidate for inclusion.

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