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Cardiac structure and function in patients with schizophrenia taking antipsychotic drugs: an MRI study

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Title: Cardiac structure and function in patients with schizophrenia taking antipsychotic drugs: an MRI study
Authors: Pillinger, T
Osimo, EF
De Marvao, A
Berry, MA
Whitehurst, T
Statton, B
Quinlan, M
Brugger, S
Vazir, A
Cook, SA
O'Regan, DP
Howes, OD
Item Type: Journal Article
Abstract: Cardiovascular disease (CVD) is a major cause of excess mortality in schizophrenia. Preclinical evidence shows antipsychotics can cause myocardial fibrosis and myocardial inflammation in murine models, but it is not known if this is the case in patients. We therefore set out to determine if there is evidence of cardiac fibrosis and/or inflammation using cardiac MRI in medicated patients with schizophrenia compared with matched healthy controls. Thirty-one participants (14 patients and 17 controls) underwent cardiac MRI assessing myocardial markers of fibrosis/inflammation, indexed by native myocardial T1 time, and cardiac structure (left ventricular (LV) mass) and function (left/right ventricular end-diastolic and end-systolic volumes, stroke volumes, and ejection fractions). Participants were physically fit, and matched for age, gender, smoking, blood pressure, BMI, HbA1c, ethnicity, and physical activity. Compared with controls, native myocardial T1 was significantly longer in patients with schizophrenia (effect size, d = 0.89; p = 0.02). Patients had significantly lower LV mass, and lower left/right ventricular end-diastolic and stroke volumes (effect sizes, d = 0.86-1.08; all p-values < 0.05). There were no significant differences in left/right end-systolic volumes and ejection fractions between groups (p > 0.05). These results suggest an early diffuse fibro-inflammatory myocardial process in patients that is independent of established CVD-risk factors and could contribute to the excess cardiovascular mortality associated with schizophrenia. Future studies are required to determine if this is due to antipsychotic treatment or is intrinsic to schizophrenia.
Issue Date: 7-Jun-2019
Date of Acceptance: 10-Apr-2019
URI: http://hdl.handle.net/10044/1/70586
DOI: https://dx.doi.org/10.1038/s41398-019-0502-x
ISSN: 2158-3188
Publisher: Nature Publishing Group
Journal / Book Title: Translational Psychiatry
Volume: 9
Issue: 1
Copyright Statement: © The Author(s) 2019. his article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution andreproductionin any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a linktotheCreativeCommons license,and indicate ifchanges were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicatedotherwise in a credit line to the material. Ifmaterial is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtainpermission directly from the copyright holder. To view a copy of this license, visithttp://creativecommons.org/licenses/by/4.0/.
Sponsor/Funder: The Academy of Medical Sciences
British Heart Foundation
Funder's Grant Number: nil
NH/17/1/32725
Publication Status: Published
Conference Place: United States
Open Access location: https://www.nature.com/articles/s41398-019-0502-x
Article Number: ARTN 163
Appears in Collections:Clinical Sciences
Imaging Sciences
National Heart and Lung Institute
Molecular Sciences



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