Septal wall thinning and systolic dysfunction in patients with hypertrophic cardiomyopathy caused by a cardiac troponin I gene mutation

Am Heart J. 2002 Apr;143(4):690-5. doi: 10.1067/mhj.2002.120291.

Abstract

Background: Lysine 183 deletion in the cardiac troponin I gene is 1 of the mutations that causes hypertrophic cardiomyopathy (HCM). However, the clinical course and determinants of poor prognosis in patients with this mutation have not been well established.

Methods and results: We analyzed 10 probands with HCM caused by this mutation and their family members. Forty-six of these 79 subjects were found to be carriers, and 33 were non-carriers. All non-carriers had a percent fractional shortening (%FS) of >25% at all ages. By contrast, 7 of 24 carriers >40 years of age had a %FS of <25%, and no carriers <40 years of age had a %FS of <25%. The change in interventricular septal thickness and the change in %FS were significantly correlated (R = 0.758; P =.0017).

Conclusion: These results suggest that about 30% of patients with HCM caused by a lysine 183 deletion mutation in the cardiac troponin I gene have systolic dysfunction develop after 40 years of age, and that patients with this mutation whose interventricular septal thickness shows a serial decrease should be followed-up closely for development of systolic dysfunction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age Factors
  • Aged
  • Cardiomyopathy, Hypertrophic / genetics*
  • Cardiomyopathy, Hypertrophic / pathology
  • Female
  • Heart Septum / pathology
  • Heterozygote
  • Humans
  • Male
  • Middle Aged
  • Point Mutation*
  • Prognosis
  • Regression Analysis
  • Systole
  • Troponin I / genetics*

Substances

  • Troponin I