Long-term outcome of 4 Korean families with hypertrophic cardiomyopathy caused by 4 different mutationsopen access
- Authors
- Choi J.-O.; Yu C.-W.; Nah J.C.; Park J.R.; Lee B.-S.; Choi Y.J.; Cho B.-R.; Lee S.-C.; Park S.W.; Kimura A.; Park J.E.
- Issue Date
- 2010
- Publisher
- John Wiley and Sons Inc.
- Citation
- Clinical Cardiology, v.33, no.7, pp 430 - 438
- Pages
- 9
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- Clinical Cardiology
- Volume
- 33
- Number
- 7
- Start Page
- 430
- End Page
- 438
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/15479
- DOI
- 10.1002/clc.20795
- ISSN
- 0160-9289
1932-8737
- Abstract
- Background: We sought to describe the long-term outcome of individuals in 4 Korean families with hypertrophic cardiomyopathy (HCM) with known mutations. Hypothesis: Long-term clinical features of familial HCM might be characterized according to the mutation causing HCM. Methods: We performed long-term (mean, 13.1 y) clinical evaluations on 46 subjects from 4 Korean families with different mutations. Results: Myosin light chain 3 gene (MYL3) mutation was associated with late-onset HCM with relatively poor prognosis; 1 sudden cardiac death and 2 cases of heart failure with atrial fibrillation occurred among 12 subjects with this mutation. Myosin binding protein C gene (MYBPC3) mutation was associated with 2 cases of sudden cardiac death and 3 cases of heart failure among 7 affected members. Cardiac troponin I type 3 gene (TNNI3) mutation was associated with 5 deaths related to atrial fibrillation and stroke among 12 mutation-positive members. Myosin heavy chain 7 gene (MYH7) mutation was associated with 11 deaths in 15 affected members. Conclusions: The clinical course was quite different for different HCM mutations. Even within the same family, individuals carrying the same mutation differed in disease expression and prognosis. © 2010 Wiley Periodicals, Inc.
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Collections - 2. Clinical Science > Department of Cardiology > 1. Journal Articles
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