Troponin, an important biomarker in the diagnosis of heart attacks
We spoke to Dr Jacobus Ungerer, chemical pathologist at Pathology Queensland, to discuss troponin testing in relation to myocardial infarction.
Myocardial infarction (MI), or heart attack, is an important cause of death worldwide. It is caused by a decrease in oxygen supply to the heart muscle, resulting in cell death. Early diagnosis and treatment is critical. However, the clinical presentation is variable and non-specific; electrocardiograph (ECG) changes may sometimes be absent. Cardiac troponin is a biomarker that is released from injured cardiac muscle cells and can be measured in blood. Cardiac troponin is such a relatively specific and sensitive marker for cardiac injury that cardiac troponin testing now forms the basis for the diagnosis of MI.
Earlier this year the Fourth Universal Definition of Myocardial Infarction Consensus Document was published. In the document the role of troponin testing is clearly described.
“Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are components of the contractile apparatus of heart cells and are only found in heart muscle. Levels of these troponins in the blood can be used as a specific marker for heart muscle (myocardial) damage. Damage to cardiac muscle will result in a release of cTnI and cTnT into the blood, therefore measuring the concentration of troponin in the blood is an accurate and specific indicator of the degree of damage.” said Dr Ungerer.
Cardiac troponin tests are mainly used to assist in the diagnosis of acute MI. However, cardiac troponin is also a marker for all myocardial damage, irrespective of the cause. Other causes of myocardial injury (not due to acute MI) include, heart failure, myocarditis (inflammation of the heart muscle), chemotherapy and pulmonary embolism (blood clot in the lung).
If myocardial ischaemia (reduced blood flow, and therefore oxygen to the heart) is present clinically (e.g., chest pain) or detected by ECG changes together with a rising and/or falling pattern of cardiac troponin values, then a diagnosis of acute MI is likely. If there are no symptoms of myocardial ischemia, then elevated cardiac troponin levels may indicate acute myocardial injury (not related to MI) if the pattern of values is rising and/or falling, or may be related to more chronic ongoing myocardial injury if the pattern is unchanging.
“According to guidelines, the term MI should be used when there is clinical evidence of acute myocardial ischemia with an increase in troponin, as well as an acute rise and/or fall in levels. The increase in troponin is evidence of heart muscle injury. To summarise, in the appropriate clinical context, an increased cardiac troponin result, together with an acute change in concentration, is indicative of a myocardial infarction.
“The upper reference level of troponin is defined as the level below which 99 percent of healthy individuals would be. Any troponin value above this cut-off is assumed to be increased,” said Dr Ungerer.
Due to the clinical importance of troponin, accurate measurement is needed. Cardiac troponin levels in healthy individuals are extremely low – only a few nanograms per litre – which makes measuring it technically challenging. However, troponin assays are continuously improving and the latest assays have the ability to measure troponin with high precision at low levels, even in healthy individuals.
“Early diagnosis of myocardial infarction is important. In practice however, the diagnosis is often difficult. Patients usually present with chest pain symptoms that is not specific for MI. In fact, only about 10% of patients presenting to an emergency department with these symptoms will be diagnosed with MI. With the introduction of cTnI and cTnT testing, it is now possible to diagnose MI accurately within a few hours after presentation.” concluded Dr Ungerer.
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This article appeared in the October 2018 Edition of ePathWay which is an online magazine produced by the Royal College of Pathologists of Australasia (http://www.rcpa.edu.au/Library/Publications/ePathway).
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