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Is QTc-Interval Prolongation an Inherent Feature of Eating Disorders? A Cohort Study - 29/08/20

Doi : 10.1016/j.amjmed.2020.02.015 
Mori J. Krantz, MD a, b, , Dan V. Blalock, PhD c, d, Kundai Tanganyika, MD a, Morteza Farasat, MD a, b, Jennifer McBride, MD e, Philip S. Mehler, MD a, e
a Department of Medicine, University of Colorado Health Science Center, Aurora 
b Denver Health and Hospital Authority, Division of Cardiology, Denver, Colo 
c Center to Accelerate Discovery and Practice Transformation (ADAPT), Durham Veterans Affairs Medical Center, Durham, NC 
d Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC 
e Eating Recovery Center, Denver Colo 

Requests for reprints should be addressed to Mori J. Krantz, MD, 777 Bannock Street, MC 0960, Denver CO 80210.777 Bannock Street, MC 0960DenverCO80210

Abstract

Background

Anorexia nervosa is associated with a markedly increased risk of sudden cardiac death, but the mechanism has not been elucidated. Whether QT prolongation is an intrinsic feature of eating disorders is uncertain because previous studies are limited by small sample size, and extrinsic factors associated with QT prolongation were inconsistently reported. This study set to determine population-mean heart-rate–corrected QT interval (QTc) in an unselected cohort of patients with eating disorders.

Methods

Electrocardiogram (ECG) data from 1026 consecutive adults admitted into residential treatment were stratified by subtype: anorexia nervosa (caloric restriction only), anorexia nervosa binge-purge, and bulimia nervosa. Eating disorders not otherwise specified were excluded. Population-mean Fridericia-corrected QTc and categorical QTc threshold analysis were performed. Multivariable regression, controlling for age sex, duration of illness, body mass index (BMI), hypokalemia, QTc-prolonging drugs, purging behaviors, and laxatives was assessed.

Results

Among 906 patients, population-mean QTc (424 ± 25 standard deviation [SD]) was normal and lowest among patients with anorexia nervosa (417.3 ± 22.3, P <0.001 vs other subgroups). Only 1.2% (N = 11) had marked QTc prolongation (QTc >500 ms); all 11 patients had hypokalemia and were receiving QTc-prolonging medications or laxatives. After controlling for clinically relevant covariates, differences in mean QTc across eating disorder subtypes diminished yet persisted (P = 0.048).

Conclusions

In the largest study of patients with eating disorders, population-mean QTc was normal and varied by subtype. Marked QTc prolongation occurred solely in the presence of extrinsic factors, suggesting that QTc prolongation is not intrinsic to eating disorders. Therefore, further study is needed to define the etiology of sudden death in patients with eating disorders.

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Keywords : Anorexia nervosa, Bulimia, Eating disorders, QT prolongation, QTc interval


Esquema


 Funding: This study was funded by a Glassman endowment.
 Conflicts of Interest: None.
 Authorship: All authors had access to the data and a role in writing this manuscript.


© 2020  Elsevier Inc. Reservados todos los derechos.
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Vol 133 - N° 9

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