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Case Reports in Hematology
Volume 2017, Article ID 8795213, 3 pages
https://doi.org/10.1155/2017/8795213
Case Report

Systemic Amyloidosis and Cardiac Autonomic Neuropathy Associated with Waldenstrom’s Macroglobulinemia

Department of Internal Medicine, Monmouth Medical Center, 300 2nd Ave, Long Branch, NJ 07740, USA

Correspondence should be addressed to Aasems Jacob; moc.liamg@jsmesaa

Received 11 March 2017; Accepted 23 May 2017; Published 13 June 2017

Academic Editor: Marie-Christine Kyrtsonis

Copyright © 2017 Aasems Jacob et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A 73-year-old male with long-standing Waldenstrom’s macroglobulinemia complicated with systemic amyloidosis presented with a witnessed syncopal episode. He had complaints of orthostatic dizziness and palpitations for few months. Orthostatic hypotension and peripheral neuropathy were demonstrated on physical examination. EKG, 24-hour Holter monitoring, and 2D echocardiogram were unremarkable. MRI of the brain ruled out stroke. Patients with amyloidosis can develop cardiovascular disease through amyloid cardiomyopathy, small vessel disease, conduction defects, pericardial effusion, or autonomic denervation. After ruling out other life-threatening causes, Ewing’s battery of tests was done to rule out cardiac autonomic neuropathy. Two heart rate tests and one blood pressure test were abnormal which indicated severe cardiac autonomic neuropathy. Cardiac autonomic neuropathy can mask symptoms of acute coronary syndrome and hence early diagnosis using the simple bedside maneuver is beneficial. The test is also important for prognostication. Absence of augmentation of cardiac output from inadequate autonomic stimulation will lead to postural hypotension, exercise intolerance, and tachycardia. There may be no change in heart rate with Valsalva or deep breathing both of which increase parasympathetic tone. As the condition progresses, it may result in cardiac denervation which can result in silent myocardial infarction, syncope, and sudden death.