Key result
Review outlines evolving diagnostic pathways and emerging targeted therapies for wild-type transthyretin cardiac amyloidosis.
Why the study?
Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA) shares clinical features with other cardiac amyloidoses, but differences in pathophysiology, diagnosis, and management require clarification.
This review summarizes the pathophysiology, clinical presentation, diagnosis, and management of wild-type transthyretin cardiac amyloidosis compared to other forms of cardiac amyloidosis.
Refines ATTRwt-CA recognition in HFpEF; leaves open prospective validation of diagnostic algorithms.
Cardiac amyloidosis is thought to be a rare group of diseases caused by extracellular deposition of misfolded proteins in the extracellular cardiac matrix resulting in heart failure with preserved ejection fraction (HFpEF). This review focuses on the similarities and differences between the pathophysiology, clinical presentation and diagnostic tests of wild-type transthyretin cardiac amyloidosis (ATTRwt-CA) compared to immunoglobulin light chain amyloidosis and hereditary cardiac amyloidosis. We address some obstacles to timely diagnosis and opportunities for management of the clinical symptoms as well as possibility of future novel disease modifying therapies.
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Halatchev et al. (2018) conducted a review in Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA). This review outlines the pathophysiology, clinical presentation, diagnosis, and emerging therapies for wild-type transthyretin cardiac amyloidosis compared to other forms of cardiac amyloidosis.
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