Impact of circulating monocyte CD36 level on atrial fibrillation and subsequent catheter ablation

Yu Feng Hu; Hung I. Yeh; Hsuan Ming Tsao; Ching Tai Tai; Yenn Jiang Lin; Shih Lin Chang; Li Wei Lo; Ta Chuan Tuan; Cheng Hwai Tzeng; Sung Hao Huang; Yung Kuo Lin; Shih Ann Chen

doi:10.1016/j.hrthm.2010.12.036

Impact of circulating monocyte CD36 level on atrial fibrillation and subsequent catheter ablation

Yu Feng Hu, Hung I. Yeh, Hsuan Ming Tsao, Ching Tai Tai, Yenn Jiang Lin, Shih Lin Chang, Li Wei Lo, Ta Chuan Tuan, Cheng Hwai Tzeng, Sung Hao Huang, Yung Kuo Lin, Shih Ann Chen

Research output: Contribution to journal › Article › peer-review

20 Citations (Scopus)

Abstract

Background: Inflammation, an important mechanism in the pathogenesis of atrial fibrillation (AF), can be regulated by CD36 in monocytes. Objective: The purpose of this study was to test the hypothesis that CD36 in monocytes contributes to the pathogenesis of AF. Methods: A prospective study that enrolled 87 patients with AF and 70 without AF was conducted. Results: Compared to patients without AF, patients with AF had monocytes with a lower level of CD36 protein, which correlated with left atrial diameter, left atrial emptying fraction, and left atrial mean voltage. In AF patients after catheter ablation, Kaplan-Meier analysis showed that the sinus rhythm maintenance rate was higher in patients with high CD36 levels. Low CD36 level was an independent predictor of recurrence. After successful ablation, the CD36 level increased by 57%, reaching that of control patients. CD36 level was not correlated with the level of high-sensitivity C-reactive protein. Analysis of mRNA levels from a buffy coat revealed that AF patients had lower CD36 and interleukin-10 levels and higher peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels, with CD36 level positively correlated with interleukin-10 level but inversely correlated with peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels. Conclusion: Low CD36 levels in circulating monocytes were associated with AF occurrence and predicted recurrence after catheter ablation. The link between CD36 and AF identified a novel AF-related inflammatory pathway.

Original language	English
Pages (from-to)	650-656
Number of pages	7
Journal	Heart Rhythm
Volume	8
Issue number	5
DOIs	https://doi.org/10.1016/j.hrthm.2010.12.036
Publication status	Published - May 2011

Keywords

Atrial fibrillation
CD36
Inflammation
Mechanoelectrical function

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine
Physiology (medical)

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10.1016/j.hrthm.2010.12.036

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@article{f8ff3d7241244083979d395f60c42826,

title = "Impact of circulating monocyte CD36 level on atrial fibrillation and subsequent catheter ablation",

abstract = "Background: Inflammation, an important mechanism in the pathogenesis of atrial fibrillation (AF), can be regulated by CD36 in monocytes. Objective: The purpose of this study was to test the hypothesis that CD36 in monocytes contributes to the pathogenesis of AF. Methods: A prospective study that enrolled 87 patients with AF and 70 without AF was conducted. Results: Compared to patients without AF, patients with AF had monocytes with a lower level of CD36 protein, which correlated with left atrial diameter, left atrial emptying fraction, and left atrial mean voltage. In AF patients after catheter ablation, Kaplan-Meier analysis showed that the sinus rhythm maintenance rate was higher in patients with high CD36 levels. Low CD36 level was an independent predictor of recurrence. After successful ablation, the CD36 level increased by 57%, reaching that of control patients. CD36 level was not correlated with the level of high-sensitivity C-reactive protein. Analysis of mRNA levels from a buffy coat revealed that AF patients had lower CD36 and interleukin-10 levels and higher peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels, with CD36 level positively correlated with interleukin-10 level but inversely correlated with peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels. Conclusion: Low CD36 levels in circulating monocytes were associated with AF occurrence and predicted recurrence after catheter ablation. The link between CD36 and AF identified a novel AF-related inflammatory pathway.",

keywords = "Atrial fibrillation, CD36, Inflammation, Mechanoelectrical function",

author = "Hu, {Yu Feng} and Yeh, {Hung I.} and Tsao, {Hsuan Ming} and Tai, {Ching Tai} and Lin, {Yenn Jiang} and Chang, {Shih Lin} and Lo, {Li Wei} and Tuan, {Ta Chuan} and Tzeng, {Cheng Hwai} and Huang, {Sung Hao} and Lin, {Yung Kuo} and Chen, {Shih Ann}",

note = "Funding Information: This work was supported by research grants from the Taipei Veterans General Hospital ( V96C1-049 , V97C1-059 , V97A-097 , V96A-127 , V98C1-037 , V99C1-120 ), the National Scientific Council ( NSC95-2314-B-010-017 , NSC95-2314-B-010-025 , NSC96-2314-B-010-006 , NSC96-2628-B-010-036 , NSC97-2314-B-010-037-MY3 , NSC97-2314-B-010-038 , NSC98-2314-B-010-031-MY3 ), and the Research Foundation of Cardiovascular Medicine , ( RFCM 96-02-018 ). Dr. Yeh thanks Mackay Memorial Hospital for their support ( MMH-E 97003 ). Copyright: Copyright 2011 Elsevier B.V., All rights reserved.",

year = "2011",

month = may,

doi = "10.1016/j.hrthm.2010.12.036",

language = "English",

volume = "8",

pages = "650--656",

journal = "Heart Rhythm",

issn = "1547-5271",

publisher = "Elsevier",

number = "5",

}

TY - JOUR

T1 - Impact of circulating monocyte CD36 level on atrial fibrillation and subsequent catheter ablation

AU - Hu, Yu Feng

AU - Yeh, Hung I.

AU - Tsao, Hsuan Ming

AU - Tai, Ching Tai

AU - Lin, Yenn Jiang

AU - Chang, Shih Lin

AU - Lo, Li Wei

AU - Tuan, Ta Chuan

AU - Tzeng, Cheng Hwai

AU - Huang, Sung Hao

AU - Lin, Yung Kuo

AU - Chen, Shih Ann

N1 - Funding Information: This work was supported by research grants from the Taipei Veterans General Hospital ( V96C1-049 , V97C1-059 , V97A-097 , V96A-127 , V98C1-037 , V99C1-120 ), the National Scientific Council ( NSC95-2314-B-010-017 , NSC95-2314-B-010-025 , NSC96-2314-B-010-006 , NSC96-2628-B-010-036 , NSC97-2314-B-010-037-MY3 , NSC97-2314-B-010-038 , NSC98-2314-B-010-031-MY3 ), and the Research Foundation of Cardiovascular Medicine , ( RFCM 96-02-018 ). Dr. Yeh thanks Mackay Memorial Hospital for their support ( MMH-E 97003 ). Copyright: Copyright 2011 Elsevier B.V., All rights reserved.

PY - 2011/5

Y1 - 2011/5

N2 - Background: Inflammation, an important mechanism in the pathogenesis of atrial fibrillation (AF), can be regulated by CD36 in monocytes. Objective: The purpose of this study was to test the hypothesis that CD36 in monocytes contributes to the pathogenesis of AF. Methods: A prospective study that enrolled 87 patients with AF and 70 without AF was conducted. Results: Compared to patients without AF, patients with AF had monocytes with a lower level of CD36 protein, which correlated with left atrial diameter, left atrial emptying fraction, and left atrial mean voltage. In AF patients after catheter ablation, Kaplan-Meier analysis showed that the sinus rhythm maintenance rate was higher in patients with high CD36 levels. Low CD36 level was an independent predictor of recurrence. After successful ablation, the CD36 level increased by 57%, reaching that of control patients. CD36 level was not correlated with the level of high-sensitivity C-reactive protein. Analysis of mRNA levels from a buffy coat revealed that AF patients had lower CD36 and interleukin-10 levels and higher peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels, with CD36 level positively correlated with interleukin-10 level but inversely correlated with peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels. Conclusion: Low CD36 levels in circulating monocytes were associated with AF occurrence and predicted recurrence after catheter ablation. The link between CD36 and AF identified a novel AF-related inflammatory pathway.

AB - Background: Inflammation, an important mechanism in the pathogenesis of atrial fibrillation (AF), can be regulated by CD36 in monocytes. Objective: The purpose of this study was to test the hypothesis that CD36 in monocytes contributes to the pathogenesis of AF. Methods: A prospective study that enrolled 87 patients with AF and 70 without AF was conducted. Results: Compared to patients without AF, patients with AF had monocytes with a lower level of CD36 protein, which correlated with left atrial diameter, left atrial emptying fraction, and left atrial mean voltage. In AF patients after catheter ablation, Kaplan-Meier analysis showed that the sinus rhythm maintenance rate was higher in patients with high CD36 levels. Low CD36 level was an independent predictor of recurrence. After successful ablation, the CD36 level increased by 57%, reaching that of control patients. CD36 level was not correlated with the level of high-sensitivity C-reactive protein. Analysis of mRNA levels from a buffy coat revealed that AF patients had lower CD36 and interleukin-10 levels and higher peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels, with CD36 level positively correlated with interleukin-10 level but inversely correlated with peroxisome proliferator-activated receptor-γ and tumor necrosis factor-α levels. Conclusion: Low CD36 levels in circulating monocytes were associated with AF occurrence and predicted recurrence after catheter ablation. The link between CD36 and AF identified a novel AF-related inflammatory pathway.

KW - Atrial fibrillation

KW - CD36

KW - Inflammation

KW - Mechanoelectrical function

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ER -

Impact of circulating monocyte CD36 level on atrial fibrillation and subsequent catheter ablation

Abstract

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