Role of inflammation in Atrial fibrillation pathophysiology and management

Masahide Harada, David R. Van Wagoner, Stanley Nattel

Research output: Contribution to journalReview article

106 Citations (Scopus)

Abstract

Atrial fibrillation (AF) is the most common clinically relevant arrhythmia, but the methods available for treating AF and its complications (of which the most important is thrombogenesis), as well as for assessing AF risk and underlying pathophysiology, are largely limited. Emerging evidence suggests a significant role of inflammation in the pathogenesis of AF. That evidence includes elevated serum levels of inflammatory biomarkers in AF subjects, the expression of inflammatory markers in cardiac tissues of AF patients and animal models of AF, and beneficial effects of anti-inflammatory drugs in experimental AF paradigms. Inflammation is suggested to be linked to various pathological processes, such as oxidative stress, apoptosis, and fibrosis, that promote AF substrate formation. Inflammation has also been associated with endothelial dysfunction, platelet activation, and coagulation cascade activation, leading to thrombogenesis. Thus, inflammation may contribute to both the occurrence/maintenance of AF and its thromboembolic complications. Here, we review the evidence for a role of inflammation and inflammatory biomarkers in the risk management and treatment of AF. We also summarize the current knowledge of inflammationdependent cellular and molecular mechanisms in AF pathophysiology and their potential as therapeutic targets.

Original languageEnglish
Pages (from-to)495-502
Number of pages8
JournalCirculation Journal
Volume79
Issue number3
DOIs
Publication statusPublished - 01-01-2015

Fingerprint

Atrial Fibrillation
Inflammation
Biomarkers
Platelet Activation
Risk Management
Pathologic Processes
Cardiac Arrhythmias
Oxidative Stress
Fibrosis
Anti-Inflammatory Agents
Animal Models
Maintenance
Apoptosis

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Harada, Masahide ; Van Wagoner, David R. ; Nattel, Stanley. / Role of inflammation in Atrial fibrillation pathophysiology and management. In: Circulation Journal. 2015 ; Vol. 79, No. 3. pp. 495-502.
@article{a42dc9633b8a450bbbaf7462c99a5d56,
title = "Role of inflammation in Atrial fibrillation pathophysiology and management",
abstract = "Atrial fibrillation (AF) is the most common clinically relevant arrhythmia, but the methods available for treating AF and its complications (of which the most important is thrombogenesis), as well as for assessing AF risk and underlying pathophysiology, are largely limited. Emerging evidence suggests a significant role of inflammation in the pathogenesis of AF. That evidence includes elevated serum levels of inflammatory biomarkers in AF subjects, the expression of inflammatory markers in cardiac tissues of AF patients and animal models of AF, and beneficial effects of anti-inflammatory drugs in experimental AF paradigms. Inflammation is suggested to be linked to various pathological processes, such as oxidative stress, apoptosis, and fibrosis, that promote AF substrate formation. Inflammation has also been associated with endothelial dysfunction, platelet activation, and coagulation cascade activation, leading to thrombogenesis. Thus, inflammation may contribute to both the occurrence/maintenance of AF and its thromboembolic complications. Here, we review the evidence for a role of inflammation and inflammatory biomarkers in the risk management and treatment of AF. We also summarize the current knowledge of inflammationdependent cellular and molecular mechanisms in AF pathophysiology and their potential as therapeutic targets.",
author = "Masahide Harada and {Van Wagoner}, {David R.} and Stanley Nattel",
year = "2015",
month = "1",
day = "1",
doi = "10.1253/circj.CJ-15-0138",
language = "English",
volume = "79",
pages = "495--502",
journal = "Circulation Journal",
issn = "1346-9843",
publisher = "Japanese Circulation Society",
number = "3",

}

Role of inflammation in Atrial fibrillation pathophysiology and management. / Harada, Masahide; Van Wagoner, David R.; Nattel, Stanley.

In: Circulation Journal, Vol. 79, No. 3, 01.01.2015, p. 495-502.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Role of inflammation in Atrial fibrillation pathophysiology and management

AU - Harada, Masahide

AU - Van Wagoner, David R.

AU - Nattel, Stanley

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Atrial fibrillation (AF) is the most common clinically relevant arrhythmia, but the methods available for treating AF and its complications (of which the most important is thrombogenesis), as well as for assessing AF risk and underlying pathophysiology, are largely limited. Emerging evidence suggests a significant role of inflammation in the pathogenesis of AF. That evidence includes elevated serum levels of inflammatory biomarkers in AF subjects, the expression of inflammatory markers in cardiac tissues of AF patients and animal models of AF, and beneficial effects of anti-inflammatory drugs in experimental AF paradigms. Inflammation is suggested to be linked to various pathological processes, such as oxidative stress, apoptosis, and fibrosis, that promote AF substrate formation. Inflammation has also been associated with endothelial dysfunction, platelet activation, and coagulation cascade activation, leading to thrombogenesis. Thus, inflammation may contribute to both the occurrence/maintenance of AF and its thromboembolic complications. Here, we review the evidence for a role of inflammation and inflammatory biomarkers in the risk management and treatment of AF. We also summarize the current knowledge of inflammationdependent cellular and molecular mechanisms in AF pathophysiology and their potential as therapeutic targets.

AB - Atrial fibrillation (AF) is the most common clinically relevant arrhythmia, but the methods available for treating AF and its complications (of which the most important is thrombogenesis), as well as for assessing AF risk and underlying pathophysiology, are largely limited. Emerging evidence suggests a significant role of inflammation in the pathogenesis of AF. That evidence includes elevated serum levels of inflammatory biomarkers in AF subjects, the expression of inflammatory markers in cardiac tissues of AF patients and animal models of AF, and beneficial effects of anti-inflammatory drugs in experimental AF paradigms. Inflammation is suggested to be linked to various pathological processes, such as oxidative stress, apoptosis, and fibrosis, that promote AF substrate formation. Inflammation has also been associated with endothelial dysfunction, platelet activation, and coagulation cascade activation, leading to thrombogenesis. Thus, inflammation may contribute to both the occurrence/maintenance of AF and its thromboembolic complications. Here, we review the evidence for a role of inflammation and inflammatory biomarkers in the risk management and treatment of AF. We also summarize the current knowledge of inflammationdependent cellular and molecular mechanisms in AF pathophysiology and their potential as therapeutic targets.

UR - http://www.scopus.com/inward/record.url?scp=84923465521&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84923465521&partnerID=8YFLogxK

U2 - 10.1253/circj.CJ-15-0138

DO - 10.1253/circj.CJ-15-0138

M3 - Review article

C2 - 25746525

AN - SCOPUS:84923465521

VL - 79

SP - 495

EP - 502

JO - Circulation Journal

JF - Circulation Journal

SN - 1346-9843

IS - 3

ER -