A long time ago in a land far away I trained to become a cardiologist.  However, in the last few years it seems my skills as a cardiologist have not been needed as much as my ability to interpret serum troponin levels.  Hence I think I have become a troponinologist

 Most physicians practicing today were educated about and have become familiar with serum biomarkers and their relationship to the diagnosis of acute myocardial infarction or acute coronary syndromes (unstable angina/non Q wave myocardial infarction).  For years the gold standard was the documentation of either normal or abnormal levels of MB CPK on serial blood tests.  However, the gold standard is not necessarily golden.  The detection of MB CPK in the serum is indicative of myocardial cell necrosis with a few exceptions.  But time and medical research marches on and we have now entered the era of serum troponin measurements and it is important that practicing physicians who order troponin levels understand some of the differences between troponin and CPK-MB levels. 

Serum troponin levels are more sensitive and more specific for myocardial injury compared with CPK levels.  Like CPK levels the troponin measurements will rise in the first 6-12 hours of an acute myocardial event but unlike CPK levels which then drop over the next 24 -48 hours, troponin levels will remain elevated for 10 to 14 days.    This is sometimes helpful in determining if someone had a myocardial infarction several days ago where the CPK levels may have already returned to normal.  Serum myoglobin levels are drawn in many hospital settings, but they are not as specific for myocardial injury compared to troponin levels. Also myoglobin levels rise and fall more quickly compared with CPK and troponin levels.  

There is a huge financial interest in cardiac biomarkers.  Laboratory medicine specialists, cardiologists, and emergency room physicians all have a tremendous stake in the accurate measurement and interpretation of these tests.  Billions of health care dollars are being spent in the United States each year on patients admitted to the hospital with troponin elevations which reflexively trigger consultations with cardiologists and subsequent imaging studies. 

 Experts in the field have had lengthy discussions and published guidelines on what determines an abnormal troponin level.     Currently the cut off is above the 99 percentile of a referenced population. Many labs will include a 10% coefficient of variation strategy which raises the abnormal level somewhat higher.  Troponin levels in acute coronary syndrome should demonstrate a significant elevation with an appropriate rise or fall over time.  A mild elevation which is flat is not suggestive of an acute coronary syndrome.     

 It is this group of patients who exceed the 99 percentile but have no signs or symptoms of myocardial infarction or myocardial ischemia that cause most problems for the practicing physician.   What is not well understood by many clinicians is that while troponin is very sensitive for myocardial necrosis, it is not specific for myocardial infarction.  An elevated troponin level does not mean a myocardial infarction. 

 Troponin is specific to the myocardium and unless there is myocardial necrosis no troponin should be detectable in the blood stream.  But there are many reasons to have troponins detected in the blood besides myocardial infarction or acute coronary syndromes.  Some of these include myocarditis, renal failure, congestive heart failure, pulmonary embolism, and even transient tachycardias such as atrial fibrillation. 

 Of equal importance is education about when not to order troponin levels.  The assay was never intended to be used for all emergency room patients and obtaining a troponin level with someone in a low pretest likelihood of acute coronary syndrome may lead to trouble in terms of false positive results. 

 As we move forward with improved biomarker assays, it is incumbent on the laboratory medicine specialists to ensure high quality and reproducibility.  But even more important will be the education of the clinician on the use and abuse of biomarker measurements and how to interpret the results.  Some laboratories are considering an explanation with the results reporting correlation with established guidelines such as from the European Society of Cardiology/American College of Cardiology/American Heart Association criteria for acute myocardial infarction.  Such explanations may also need to include the fact that there are multiple causes of troponin elevations and interpretation must be taken in context with the patient’s clinical circumstances. 

 Troponin measurements have become the work horse of cardiac biomarkers and will remain so for the foreseeable future.  It is incumbent on the clinician to understand the interpretation of an abnormal troponin level and realize that elevations may be due to a number of etiologies besides coronary atherosclerosis with ischemia.  Clinical conditions that cause stress on the myocardium in the absence of coronary artery disease may cause the troponin level to elevate such as pulmonary embolism, sepsis, congestive heart failure and tachycardia.  There is still no substitute for taking a careful history and physical exam and interpreting the laboratory studies along with what is found at the bedside.