| Cine MR imaging of myocardial contractile impairment in patients with hypertrophic cardiomyopathy attributable to Asp175Asn mutation in the alpha-tropomyosin gene. | |
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MedLine Citation:
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PMID: 16014439 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: To prospectively investigate the relationship between myocardial contractile impairment and left ventricular (LV) hypertrophy measured at cardiac magnetic resonance (MR) imaging in patients with hypertrophic cardiomyopathy (HCM) caused by the substitution of aspartic acid 175 with asparagine (ie, Asp175Asn mutation) in the alpha-tropomyosin gene (TPM1). MATERIALS AND METHODS: The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent. LV mass, maximal LV wall thickness, and myocardial fractional thickening during systole were measured at cine MR imaging in 24 subjects (11 male, 13 female; mean age, 42 years; age range, 17-68 years) with the Asp175Asn mutation in TPM1 and in 17 healthy volunteers (eight men, nine women; mean age, 38 years; age range, 23-60 years). The proportion of hypokinetic LV segments was calculated as the number of LV segments with fractional thickening of less than 30% divided by the total number of segments measured. Anthropometric and biochemical correlates of LV hypertrophy were determined. Univariate and multiple linear regression analyses were used to investigate the association of the proportion of hypokinetic segments and other correlates of LV hypertrophy with LV mass and maximal wall thickness. RESULTS: The proportion of hypokinetic segments was higher in patients with HCM than in control subjects (37% +/- 20 [standard deviation] vs 12% +/- 12, P < .001). In stepwise multiple regression analysis, the proportion of hypokinetic segments accounted for 42% (P < .001); the LV end-diastolic volume, for 24% (P = .003); and male sex, for 10% (P = .014) of the variability in LV mass in patients with HCM. The proportion of hypokinetic LV segments, which accounted for 48% of the variability in LV maximal wall thickness (P < .001), was the only variable significantly associated with maximal wall thickness. CONCLUSION: The extent of myocardial contractile impairment is strongly and independently related to LV mass and maximal wall thickness in patients with HCM attributable to the Asp175Asn mutation in TPM1. |
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Authors:
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Petri Sipola; Kirsi Lauerma; Pertti Jääskeläinen; Markku Laakso; Keijo Peuhkurinen; Hannu Manninen; Hannu J Aronen; Johanna Kuusisto |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2005-07-12 |
Journal Detail:
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Title: Radiology Volume: 236 ISSN: 0033-8419 ISO Abbreviation: Radiology Publication Date: 2005 Sep |
Date Detail:
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Created Date: 2005-08-24 Completed Date: 2005-10-04 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0401260 Medline TA: Radiology Country: United States |
Other Details:
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Languages: eng Pagination: 815-24 Citation Subset: AIM; IM |
Affiliation:
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Department of Clinical Radiology, Kuopio University Hospital, Puijonlaaksontie 2, Kuopio FIN-70210, Finland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aspartic Acid / genetics Cardiomyopathy, Hypertrophic / genetics*, physiopathology* Case-Control Studies Echocardiography Female Humans Hypertrophy, Left Ventricular / genetics*, physiopathology* Image Processing, Computer-Assisted Linear Models Magnetic Resonance Imaging, Cine* Male Middle Aged Mutation* Myocardial Contraction / physiology Prospective Studies Statistics, Nonparametric Tropomyosin / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Tropomyosin; 56-84-8/Aspartic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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