MISC

2011年7月

Risk for atrial fibrillation in patients with hypertrophic cardiomyopathy: Association with insulin resistance

JOURNAL OF CARDIOLOGY
  • Yuji Shigematsu
  • ,
  • Mareomi Hamada
  • ,
  • Takayuki Nagai
  • ,
  • Kazuhisa Nishimura
  • ,
  • Katsuji Inoue
  • ,
  • Jun Suzuki
  • ,
  • Akiyoshi Ogimoto
  • ,
  • Jitsuo Higaki

58
1
開始ページ
18
終了ページ
25
記述言語
英語
掲載種別
DOI
10.1016/j.jjcc.2011.03.001
出版者・発行元
ELSEVIER IRELAND LTD

Background: We undertook a cross-sectional study to test the hypothesis that patients with hypertrophic cardiomyopathy (HCM) who have impaired left ventricular (LV) diastolic function are insulin resistant. We also evaluated the relation between the development of atrial fibrillation (AF) and insulin resistance (IR) in patients with HCM.
Methods and results: Eighty-eight patients with HCM (71 men, 17 women) were enrolled in the study. IR was estimated using the homeostasis model assessment (HOMA) index. Echocardiographically determined left atrial (LA) dimension was measured as a marker of LA size. The ratio of trasmitral early LV filling velocity to early diastolic mitral annulus velocity (E/e') was also measured as a marker of LV diastolic function. Twenty-seven patients (31%) had IR. Multivariate logistic regression analyses showed that independent determinants of AF were increased LA size [odds ratio (OR) 3.5, 95% confidence interval (CI) 1.2-9.8] and impaired LV diastolic function [OR 4.6, 95% CI 1.6-12.8]. The strongest determinant of LA size was the HOMA index (p = 0.0005). Similarly, the HOMA index (p = 0.0019) was an independent determinant of LV diastolic function.
Conclusion: IR is highly prevalent among non-diabetic patients with HCM. A possible mechanism by which IR affects the development of AF is mediated through its association with increased LA size or impaired LV diastolic function. IR may be an important underlying mechanism for the genesis of AF in HCM. (C) 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.jjcc.2011.03.001
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000292902500003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.jjcc.2011.03.001
  • ISSN : 0914-5087
  • Web of Science ID : WOS:000292902500003

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