Copyright
©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Transl Med. Jan 31, 2019; 8(1): 1-8
Published online Jan 31, 2019. doi: 10.5528/wjtm.v8.i1.1
Published online Jan 31, 2019. doi: 10.5528/wjtm.v8.i1.1
Inflammation and cardiovascular disease
Christina G Katsiari, Dimitrios P Bogdanos, Lazaros I Sakkas, Department of Rheumatology and Clinical Immunology, Division of Medicine, University of Thessaly, Larissa 41110, Greece
Author contributions: Katsiari CG, Bogdanos DP and Sakkas LI conceived the study and drafted the manuscript; all authors approved the final version of the article.
Conflict-of-interest statement: The authors have no conflict of interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Lazaros I Sakkas, Professor, FRCP (Hon), MD, PhD, Department of Rheumatology and Clinical Immunology, Division of Medicine, University of Thessaly, Panepistimiou 1, Larissa 41110, Greece. lsakkas@med.uth.gr
Telephone: +30-241-3502813
Received: August 4, 2018
Peer-review started: August 6, 2018
First decision: October 10, 2018
Revised: January 9, 2019
Accepted: January 28, 2019
Article in press: January 28, 2019
Published online: January 31, 2019
Peer-review started: August 6, 2018
First decision: October 10, 2018
Revised: January 9, 2019
Accepted: January 28, 2019
Article in press: January 28, 2019
Published online: January 31, 2019
Core Tip
Core tip: The association of inflammation with cardiovascular disease (CVD) has two aspects. The first is whether inflammation plays a pathogenic role in traditional risk factors-mediated CVD or it is just an epiphenomenon. The second is whether chronic inflammation caused by an inflammatory disease has any impact on CVD. Chronic inflammation exemplified by elevated high sensitivity C-reactive protein has been added for risk factors for CVD. How inflammation contributes to CVD is a topic of continuous research. A trial showing that anti-IL1b monoclonal-antibody reduced cardiovascular events is the best proof of the pathogenic contribution of inflammation in atherosclerosis and CVD.