Cardiac amyloidosis associated with a novel transthyretin aspartic acid-18 glutamic acid de novo mutation

Circ J. 2003 Nov;67(11):965-8. doi: 10.1253/circj.67.965.

Abstract

A 40-year-old man presented with initial symptoms of syncope caused by restrictive cardiomyopathy and autonomic nervous system impairment, but it was confirmed that he had a novel transthyretin (TTR) variant, aspartic acid-18 glutamic acid (Glu), and a de novo gene mutation. A polymerase chain reaction-induced mutation restriction analysis with a mismatched sense primer demonstrated that he was heterozygous for TTR Glu 18. Liver transplantation was not performed because of profound weakness and severe postural hypotension. Right-sided heart failure predominated in association with low output syndrome and a gradual decrease in total QRS voltage on electrocardiogram over 5 years of follow-up. Autonomic neuropathy developed and he eventually died of both-sided heart failure at the age of 45 years. Immunohistochemical and DNA studies are important to diagnose and treat TTR-related cardiac amyloidosis.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Amyloidosis / genetics*
  • Cardiomyopathy, Restrictive / etiology
  • Cardiomyopathy, Restrictive / genetics*
  • DNA Mutational Analysis
  • Fatal Outcome
  • Genetic Variation / physiology
  • Heart Failure
  • Heterozygote
  • Humans
  • Male
  • Mutation, Missense / physiology*
  • Prealbumin / genetics*

Substances

  • Prealbumin