Relationship between epicardial adipose tissue volume and coronary artery spasm.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 02 2021
Historique:
received: 04 07 2020
revised: 15 08 2020
accepted: 30 09 2020
pubmed: 6 10 2020
medline: 28 5 2021
entrez: 5 10 2020
Statut: ppublish

Résumé

Epicardial adipose tissue (EAT) is considered to play a critical role in vascular endothelial function. Coronary artery spasm has been postulated to be a causal factor in vascular endothelial abnormalities and atherosclerosis. This study aimed to investigate the relationship between coronary artery spasm and EAT volume, total abdominal adipose tissue (AAT) area, and abdominal visceral adipose tissue (AVAT) area. Among patients undergoing coronary computed tomography (CT) to evaluate coronary artery disease, we identified 110 patients who did not have significant coronary artery stenosis and underwent a coronary spasm provocation test with cardiac catheterization. They were divided into two groups according to the results of the spasm provocation test: spasm-positive and spasm-negative. EAT volume, total AAT area, and AVAT area were evaluated using CT images. Seventy-seven patients were included in the spasm-positive group and 33 patients in the spasm-negative group. There were no significant differences in baseline clinical characteristics between the two groups, except for the prevalence of current smoking (48% vs. 27%, p = 0.04). EAT volume was significantly higher in the spasm-positive group (108 ± 38 mL vs. 87 ± 34 mL, p = 0.007), while no significant difference was seen in total AAT area (280 ± 113 cm Our results suggest that EAT has a strong association with coronary artery spasm, while AAT may not.

Sections du résumé

BACKGROUND
Epicardial adipose tissue (EAT) is considered to play a critical role in vascular endothelial function. Coronary artery spasm has been postulated to be a causal factor in vascular endothelial abnormalities and atherosclerosis. This study aimed to investigate the relationship between coronary artery spasm and EAT volume, total abdominal adipose tissue (AAT) area, and abdominal visceral adipose tissue (AVAT) area.
METHOD
Among patients undergoing coronary computed tomography (CT) to evaluate coronary artery disease, we identified 110 patients who did not have significant coronary artery stenosis and underwent a coronary spasm provocation test with cardiac catheterization. They were divided into two groups according to the results of the spasm provocation test: spasm-positive and spasm-negative. EAT volume, total AAT area, and AVAT area were evaluated using CT images.
RESULTS
Seventy-seven patients were included in the spasm-positive group and 33 patients in the spasm-negative group. There were no significant differences in baseline clinical characteristics between the two groups, except for the prevalence of current smoking (48% vs. 27%, p = 0.04). EAT volume was significantly higher in the spasm-positive group (108 ± 38 mL vs. 87 ± 34 mL, p = 0.007), while no significant difference was seen in total AAT area (280 ± 113 cm
CONCLUSION
Our results suggest that EAT has a strong association with coronary artery spasm, while AAT may not.

Identifiants

pubmed: 33017629
pii: S0167-5273(20)33904-8
doi: 10.1016/j.ijcard.2020.09.074
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

8-12

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest H·I received lecture fees from Astellas Pharma Inc., Astrazeneca Inc., Daiichi-Sankyo Pharma Inc., and MSD K. K. T.A. received lecture fees from Astellas Pharma, AstraZeneca, Bayer, Daiichi Sankyo, and Bristol-Myers Squibb. T.M received lecture fees from Bayel Pharmaceutical Co., Ltd., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K. K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K. K., Pfizer Japan Inc., Sanofi-aventis K. K., and Takeda Pharmaceutical Co., Ltd. T.M received unrestricted research grant for Department of Cardiology, Nagoya University Graduate School of Medicine from Astellas Pharma Inc., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K. K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K. K., Otsuka Pharma Ltd., Pfizer Japan Inc., Sanofi-aventis K. K., Takeda Pharmaceutical Co., Ltd., and Teijin Pharma Ltd. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Takashi Kataoka (T)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Ken Harada (K)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Akihito Tanaka (A)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan. Electronic address: akihito17491194@gmail.com.

Tomohiro Onishi (T)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan; Department of Cardiology, Aichi Medical University Hospital, Nagakute, Japan.

Shun Matsunaga (S)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Hiroshi Funakubo (H)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Kazuhiro Harada (K)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Tomoyuki Nagao (T)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Norihiro Shinoda (N)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Nobuyuki Marui (N)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan.

Kiyoshi Niwa (K)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hiroshi Tashiro (H)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Yusuke Hitora (Y)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Kenji Furusawa (K)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hideki Ishii (H)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Department of Cardiology, Fujita Health University Bantane Hospital, Nagoya, Japan.

Tetsuya Amano (T)

Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan; Department of Cardiology, Aichi Medical University Hospital, Nagakute, Japan.

Toyoaki Murohara (T)

Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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