Cardiac Troponin as a Key Biomarker in Light Chain and Transthyretin Amyloidosis

Cardiac amyloidosis (CA), caused by the deposition of amyloid fibrils in the myocardium, is increasingly recognized as a cause of heart failure with preserved ejection fraction. The two most frequent types are light chain (AL) amyloidosis and transthyretin (ATTR) amyloidosis, with distinct pathophysiological mechanisms but convergent cardiac consequences.

Cardiac troponin (cTn), particularly high-sensitivity assays (hs-cTnT, hs-cTnI), is consistently elevated in CA and serves as the biomarker of choice for detecting myocardial injury. Multiple mechanisms contribute to troponin release in CA, including direct cytotoxicity of amyloid precursors, interstitial fibril infiltration, coronary microvascular dysfunction, diastolic dysfunction, and acute-on-chronic myocardial injury.

Clinically, cTn has diagnostic, prognostic, and therapeutic monitoring roles.

• In AL amyloidosis, cTn thresholds are incorporated into the Mayo Clinic 2004 and 2012 staging systems, alongside NT-proBNP and serum free light chains, to stratify survival and guide therapy.
• In ATTR amyloidosis, cTn (mainly cTnT) is a validated prognostic marker, often used in staging systems together with NT-proBNP and estimated glomerular filtration rate.
• For both AL and ATTR, dynamic changes in cTn during treatment provide insights into cardiac response and disease progression.

The review emphasizes that cTn, integrated with imaging and other biomarkers, not only refines staging but also improves monitoring of therapeutic efficacy, particularly as effective therapies like tafamidis (for ATTR) and chemotherapy (for AL) become available. Future directions include assay harmonization and validation of hs-cTnI thresholds in CA.

#CardiacAmyloidosis #Troponin #Biomarkers #CardioOncology #HeartFailure

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