An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Standard

An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction. / Hiram, Roddy; Xiong, Feng; Naud, Patrice; Xiao, Jiening; Sosnowski, Deanna K.; Le Quilliec, Ewen; Saljic, Arnela; Abu-Taha, Issam H.; Kamler, Markus; LeBlanc, Charles Alexandre; Al-UDatt, Doaa G.F.; Sirois, Martin G.; Hebert, Terence E.; Tanguay, Jean François; Tardif, Jean Claude; Dobrev, Dobromir; Nattel, Stanley.

I: Cardiovascular Research, Bind 120, Nr. 4, 2024, s. 345-359.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Hiram, R, Xiong, F, Naud, P, Xiao, J, Sosnowski, DK, Le Quilliec, E, Saljic, A, Abu-Taha, IH, Kamler, M, LeBlanc, CA, Al-UDatt, DGF, Sirois, MG, Hebert, TE, Tanguay, JF, Tardif, JC, Dobrev, D & Nattel, S 2024, 'An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction', Cardiovascular Research, bind 120, nr. 4, s. 345-359. https://doi.org/10.1093/cvr/cvad175

APA

Hiram, R., Xiong, F., Naud, P., Xiao, J., Sosnowski, D. K., Le Quilliec, E., Saljic, A., Abu-Taha, I. H., Kamler, M., LeBlanc, C. A., Al-UDatt, D. G. F., Sirois, M. G., Hebert, T. E., Tanguay, J. F., Tardif, J. C., Dobrev, D., & Nattel, S. (2024). An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction. Cardiovascular Research, 120(4), 345-359. https://doi.org/10.1093/cvr/cvad175

Vancouver

Hiram R, Xiong F, Naud P, Xiao J, Sosnowski DK, Le Quilliec E o.a. An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction. Cardiovascular Research. 2024;120(4):345-359. https://doi.org/10.1093/cvr/cvad175

Author

Hiram, Roddy ; Xiong, Feng ; Naud, Patrice ; Xiao, Jiening ; Sosnowski, Deanna K. ; Le Quilliec, Ewen ; Saljic, Arnela ; Abu-Taha, Issam H. ; Kamler, Markus ; LeBlanc, Charles Alexandre ; Al-UDatt, Doaa G.F. ; Sirois, Martin G. ; Hebert, Terence E. ; Tanguay, Jean François ; Tardif, Jean Claude ; Dobrev, Dobromir ; Nattel, Stanley. / An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction. I: Cardiovascular Research. 2024 ; Bind 120, Nr. 4. s. 345-359.

Bibtex

@article{ddcc8d4b0b0743f0ae12749aab5bd861,

title = "An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction",

abstract = "Aims Recent studies suggest that bioactive mediators called resolvins promote an active resolution of inflammation. Inflammatory signalling is involved in the development of the substrate for atrial fibrillation (AF). The aim of this study is to evaluate the effects of resolvin-D1 on atrial arrhythmogenic remodelling resulting from left ventricular (LV) dysfunction induced by myocardial infarction (MI) in rats. ......................................................................................................................................................................................................Methods MI was produced by left anterior descending coronary artery ligation. Intervention groups received daily intraperitoneal resolvin- and results D1, beginning before MI surgery (early-RvD1) or Day 7 post-MI (late-RvD1) and continued until Day 21 post-MI. AF vulnerability was evaluated by performing an electrophysiological study. Atrial conduction was analysed by using optical mapping. Fibrosis was quantified by Masson{\textquoteright}s trichrome staining and gene expression by quantitative polymerase chain reaction and RNA sequencing. Investigators were blinded to group identity. Early-RvD1 significantly reduced MI size (17 ± 6%, vs. 39 ± 6% in vehicle-MI) and preserved LV ejection fraction; these were unaffected by late-RvD1. Transoesophageal pacing induced atrial tachyarrhythmia in 2/18 (11%) sham-operated rats, vs. 18/18 (100%) MI-only rats, in 5/18 (28%, P < 0.001 vs. MI) early-RvD1 MI rats, and in 7/12 (58%, P < 0.01) late-RvD1 MI rats. Atrial conduction velocity significantly decreased post-MI, an effect suppressed by RvD1 treatment. Both early-RvD1 and late-RvD1 limited MI-induced atrial fibrosis and prevented MI-induced increases in the atrial expression of inflammation-related and fibrosis-related biomarkers and pathways. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Conclusions RvD1 suppressed MI-related atrial arrhythmogenic remodelling. Early-RvD1 had MI sparing and atrial remodelling suppressant effects, whereas late-RvD1 attenuated atrial remodelling and AF promotion without ventricular protection, revealing atrial-protective actions unrelated to ventricular function changes. These results point to inflammation resolution–promoting compounds as novel cardio-protective interventions with a particular interest in attenuating AF substrate development.",

author = "Roddy Hiram and Feng Xiong and Patrice Naud and Jiening Xiao and Sosnowski, {Deanna K.} and {Le Quilliec}, Ewen and Arnela Saljic and Abu-Taha, {Issam H.} and Markus Kamler and LeBlanc, {Charles Alexandre} and Al-UDatt, {Doaa G.F.} and Sirois, {Martin G.} and Hebert, {Terence E.} and Tanguay, {Jean Fran{\c c}ois} and Tardif, {Jean Claude} and Dobromir Dobrev and Stanley Nattel",

year = "2024",

doi = "10.1093/cvr/cvad175",

language = "English",

volume = "120",

pages = "345--359",

journal = "Cardiovascular Research",

issn = "0008-6363",

publisher = "Oxford University Press",

number = "4",

}

RIS

TY - JOUR

T1 - An inflammation resolution–promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction

AU - Hiram, Roddy

AU - Xiong, Feng

AU - Naud, Patrice

AU - Xiao, Jiening

AU - Sosnowski, Deanna K.

AU - Le Quilliec, Ewen

AU - Saljic, Arnela

AU - Abu-Taha, Issam H.

AU - Kamler, Markus

AU - LeBlanc, Charles Alexandre

AU - Al-UDatt, Doaa G.F.

AU - Sirois, Martin G.

AU - Hebert, Terence E.

AU - Tanguay, Jean François

AU - Tardif, Jean Claude

AU - Dobrev, Dobromir

AU - Nattel, Stanley

PY - 2024

Y1 - 2024

N2 - Aims Recent studies suggest that bioactive mediators called resolvins promote an active resolution of inflammation. Inflammatory signalling is involved in the development of the substrate for atrial fibrillation (AF). The aim of this study is to evaluate the effects of resolvin-D1 on atrial arrhythmogenic remodelling resulting from left ventricular (LV) dysfunction induced by myocardial infarction (MI) in rats. ......................................................................................................................................................................................................Methods MI was produced by left anterior descending coronary artery ligation. Intervention groups received daily intraperitoneal resolvin- and results D1, beginning before MI surgery (early-RvD1) or Day 7 post-MI (late-RvD1) and continued until Day 21 post-MI. AF vulnerability was evaluated by performing an electrophysiological study. Atrial conduction was analysed by using optical mapping. Fibrosis was quantified by Masson’s trichrome staining and gene expression by quantitative polymerase chain reaction and RNA sequencing. Investigators were blinded to group identity. Early-RvD1 significantly reduced MI size (17 ± 6%, vs. 39 ± 6% in vehicle-MI) and preserved LV ejection fraction; these were unaffected by late-RvD1. Transoesophageal pacing induced atrial tachyarrhythmia in 2/18 (11%) sham-operated rats, vs. 18/18 (100%) MI-only rats, in 5/18 (28%, P < 0.001 vs. MI) early-RvD1 MI rats, and in 7/12 (58%, P < 0.01) late-RvD1 MI rats. Atrial conduction velocity significantly decreased post-MI, an effect suppressed by RvD1 treatment. Both early-RvD1 and late-RvD1 limited MI-induced atrial fibrosis and prevented MI-induced increases in the atrial expression of inflammation-related and fibrosis-related biomarkers and pathways. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Conclusions RvD1 suppressed MI-related atrial arrhythmogenic remodelling. Early-RvD1 had MI sparing and atrial remodelling suppressant effects, whereas late-RvD1 attenuated atrial remodelling and AF promotion without ventricular protection, revealing atrial-protective actions unrelated to ventricular function changes. These results point to inflammation resolution–promoting compounds as novel cardio-protective interventions with a particular interest in attenuating AF substrate development.

AB - Aims Recent studies suggest that bioactive mediators called resolvins promote an active resolution of inflammation. Inflammatory signalling is involved in the development of the substrate for atrial fibrillation (AF). The aim of this study is to evaluate the effects of resolvin-D1 on atrial arrhythmogenic remodelling resulting from left ventricular (LV) dysfunction induced by myocardial infarction (MI) in rats. ......................................................................................................................................................................................................Methods MI was produced by left anterior descending coronary artery ligation. Intervention groups received daily intraperitoneal resolvin- and results D1, beginning before MI surgery (early-RvD1) or Day 7 post-MI (late-RvD1) and continued until Day 21 post-MI. AF vulnerability was evaluated by performing an electrophysiological study. Atrial conduction was analysed by using optical mapping. Fibrosis was quantified by Masson’s trichrome staining and gene expression by quantitative polymerase chain reaction and RNA sequencing. Investigators were blinded to group identity. Early-RvD1 significantly reduced MI size (17 ± 6%, vs. 39 ± 6% in vehicle-MI) and preserved LV ejection fraction; these were unaffected by late-RvD1. Transoesophageal pacing induced atrial tachyarrhythmia in 2/18 (11%) sham-operated rats, vs. 18/18 (100%) MI-only rats, in 5/18 (28%, P < 0.001 vs. MI) early-RvD1 MI rats, and in 7/12 (58%, P < 0.01) late-RvD1 MI rats. Atrial conduction velocity significantly decreased post-MI, an effect suppressed by RvD1 treatment. Both early-RvD1 and late-RvD1 limited MI-induced atrial fibrosis and prevented MI-induced increases in the atrial expression of inflammation-related and fibrosis-related biomarkers and pathways. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Conclusions RvD1 suppressed MI-related atrial arrhythmogenic remodelling. Early-RvD1 had MI sparing and atrial remodelling suppressant effects, whereas late-RvD1 attenuated atrial remodelling and AF promotion without ventricular protection, revealing atrial-protective actions unrelated to ventricular function changes. These results point to inflammation resolution–promoting compounds as novel cardio-protective interventions with a particular interest in attenuating AF substrate development.

U2 - 10.1093/cvr/cvad175

DO - 10.1093/cvr/cvad175

M3 - Journal article

C2 - 38091977

AN - SCOPUS:85182244709

VL - 120

SP - 345

EP - 359

JO - Cardiovascular Research

JF - Cardiovascular Research

SN - 0008-6363

IS - 4

ER -

ID: 388582520