Concurrent Waldenstrom Macroglobulinemia and Mutant Transthyretin Cardiac Amyloidosis

Xiaoxiao Qian; Hooman Bakhshi; Rakesh Biswas; Raghav Gattani; Jamie L Kennedy

doi:10.55729/2000-9666.1117

Concurrent Waldenstrom Macroglobulinemia and Mutant Transthyretin Cardiac Amyloidosis

J Community Hosp Intern Med Perspect. 2022 Nov 7;12(6):95-99. doi: 10.55729/2000-9666.1117. eCollection 2022.

Authors

Xiaoxiao Qian¹, Hooman Bakhshi¹, Rakesh Biswas², Raghav Gattani¹, Jamie L Kennedy³

Affiliations

¹ Departemt of Cardiology, Inova Heart and Vascular Institute, Falls Church, VA, USA.
² Departemt of Hematology and Oncology, Inova Fairfax Hospital, Falls Church, VA, USA.
³ Department of Advanced Heart Failure and Transplant, Inova Heart and Vascular Institute, Falls Church, VA, USA.

Abstract

Cardiac amyloidosis is caused by abnormal deposit of amyloid in the myocardium and can be divided into light chain (AL) amyloidosis and transthyretin (ATTR) amyloidosis. ATTR amyloidosis can be further divided into wild-type and mutant type based on genetic mutation. Differentiation between AL, wild-type, and mutant type ATTR amyloidosis has significant prognostic and therapeutic implications.

Keywords: Cardiac amyloidosis; Endomyocardial biopsy; Waldenstrom macroglobulinemia.

Publication types

Case Reports