Impact of Carpal Tunnel Syndrome Surgery on Early Diagnosis and Treatment of Transthyretin Cardiac Amyloidosis.

Background and Objectives: Cardiac amyloidosis is an infiltrative, progressive, and restrictive cardiomyopathy that leads to heart failure, reduces life quality, and causes death. This is a multisystem disorder caused by mutations of the transthyretin protein and is associated not only with cardiac diseases or carpal tunnel syndrome but also with nerve, liver, lung, gastrointestinal tract, kidney, or eye pathologies. Carpal tunnel syndrome is an early red-flag symptom of transthyretin (TTR) cardiac amyloidosis; therefore, screening for unsuspected cardiac amyloidosis can be performed through histological testing of flexor retinaculum specimens gathered during carpal tunnel release surgery. Our case highlights that early detection and accurate diagnosis of a disease are important factors for improving clinical outcomes in patients with TTR amyloidosis. Case Summary: We report the case of a 71-year-old man who presented with bilateral carpal tunnel syndrome. Amyloid deposits were detected after carpal tunnel release surgery through histological testing of the synovial tissue. The patient was sent for a cardiological evaluation. Physical examination, laboratory tests, and the ECG revealed no significant changes. The diagnosis of amyloidosis was confirmed with multimodality imaging in the early stage, which helped to start specific medicamental treatment with the transthyretin stabilizer tafamidis. Conclusions: Our objective is to highlight the early recognition and specific medicamental treatment of cardiac amyloidosis for better patient prognosis and outcomes.

Reactive Oxygen Species Induced Pathways in Heart Failure Pathogenesis and Potential Therapeutic Strategies.

With respect to structural and functional cardiac disorders, heart failure (HF) is divided into HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Oxidative stress contributes to the development of both HFrEF and HFpEF. Identification of a broad spectrum of reactive oxygen species (ROS)-induced pathways in preclinical models has provided new insights about the importance of ROS in HFrEF and HFpEF development. While current treatment strategies mostly concern neuroendocrine inhibition, recent data on ROS-induced metabolic pathways in cardiomyocytes may offer additional treatment strategies and targets for both of the HF forms. The purpose of this article is to summarize the results achieved in the fields of: (1) ROS importance in HFrEF and HFpEF pathophysiology, and (2) treatments for inhibiting ROS-induced pathways in HFrEF and HFpEF patients. ROS-producing pathways in cardiomyocytes, ROS-activated pathways in different HF forms, and treatment options to inhibit their action are also discussed.