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A Sensitive and Specific Quantitation Method for Determination of Serum Cardiac Myosin Binding Protein-C by Electrochemiluminescence Immunoassay
Published on: August 8, 2013
Cardiac and noncardiac, particularly neuromuscular, disease with troponin-T positivity
J Finsterer1, C Stöllberger, W Krugluger
1Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria. fifigsi@yahoo.de
Insights
Elevated cardiac troponin T levels often stem from non-cardiac conditions, particularly neuromuscular disorders. This study highlights the diverse causes of troponin T elevation beyond primary heart issues.
Area of Science:
- Cardiology
- Neurology
- Biochemistry
Background:
- Elevated cardiac troponin T (cTnT) is typically linked to myocardial damage.
- Non-cardiac conditions causing secondary myocardial damage are increasingly recognized.
- The association between cTnT elevation and neuromuscular disorders warrants further investigation.
Purpose of the Study:
- To retrospectively evaluate the frequency of primary and secondary cardiac causes of cTnT positivity.
- To determine the prevalence of cTnT positivity associated with neuromuscular disorders.
Main Methods:
- Retrospective analysis of 16,944 troponin T determinations over one year.
- Evaluation of 622 positive troponin T results.
- Correlation of troponin T positivity with creatine kinase levels, creatinine, and patient diagnoses.
Main Results:
- Troponin T was positive in 8.3% of determinations.
- Primary cardiac causes included myocardial ischemia (59%), atrial fibrillation (23%), and heart failure (22%).
- Secondary cardiac causes included renal insufficiency (22%), COPD (10%), and stroke (4%).
- Neuromuscular disorders were associated with cTnT positivity in 6.3% of cases.
Conclusions:
- Ischemic heart disease is the leading cause of cTnT elevation.
- Renal insufficiency and heart failure are significant contributors.
- cTnT positivity is frequently linked to neuromuscular disorders, suggesting cardiac involvement.
Objectives:
Although elevated cardiac troponin T is caused by myocardial damage in the vast majority of the cases (primary cardiac causes), noncardiac disease with secondary damage to the myocardium (secondary cardiac causes) is being increasingly recognised. The present study aimed to retrospectively evaluate the frequency of primary cardiac and secondary cardiac causes of troponin-T positivity, in particular how often troponin-T positivity is associated with neuromuscular disorders.
Results:
Of 16,944 troponin-T determinations in a secondary centre between April 2004 and April 2005, troponin T was positive in 1408 of them (8.3%). Of these, 622 were included for evaluation. Troponin-T positivity was associated with elevated creatine kinase in 54.5% and with creatinine >2 mg/dl (177 micromol/l) in 16.6% of the tests. The most frequent primary cardiac causes of troponin-T positivity were myocardial ischaemia (59%), atrial fibrillation (23%), and heart failure (22%). The most frequent secondary cardiac causes of troponin-T positivity were renal insufficiency (22%), chronic obstructive lung disease (10%), and acute stroke (4%). There was one cause for troponin-T positivity in 249 cases and more than one in 373 cases. A neurologist saw patients with troponin-T positivity in 9.5% of the cases. Troponin-T positivity was associated with a neuromuscular disorder in 6.3% of the cases. Causes of troponin-I positivity were also frequently causes of troponin-T positivity.
Conclusions:
Ischaemic heart disease is the most frequent cause of troponin-T positivity, followed by heart failure and renal insufficiency. Many causes previously described to be only responsible for troponin-I positivity also cause troponin-T elevation. Troponin-T positivity is frequently associated with neuromuscular disorders, most likely due to cardiac involvement of these conditions.
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