Cardiac amyloidosis and its electrophysiologic manifestations
Jose R. Martinez-Parachini, MD1, and Ansel P. Amaral, MD, PhD2
1Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
2Saint Francis Hospital and Heart Center, Roslyn, NY, USA
Address for Correspondence
1211 21st Avenue. Nashville, Tennessee 37232-8802.
Corresponding Author: Jose R. Martinez-Parachini, MD
Department of Medicine, Division of Cardiovascular Disease
Vanderbilt Heart and Vascular Institute, Medical Center East, South Tower
Amyloidosis is caused by deposition of abnormal amyloid fibrils with the feared consequence of end stage organ failure. Cardiac amyloidosis (CA) is an increasingly recognized antecedent of cardiomyopathy. CA is classified into transthyretin variants (ATTRwt – wild type and ATTRv – genetic variant) and a light chain variant (AL); each of these variants can be associated with unique electrophysiologic abnormalities. Pacing indications in current societal guidelines do not specify treatment options in infiltrative cardiac diseases, such as CA, and new disease modifying treatments are altering the landscape for intervention. Given the paucity of data, national and international groups have differing treatment options and recommendations. In this review, we aim to update and highlight the differing electrophysiologic changes seen in CA, their respective treatment course and suggest areas for future intervention.