Inflammation in coronary atherosclerosis: diagnosis and treatment
- PMID: 40139681
- DOI: 10.1136/heartjnl-2024-325408
Inflammation in coronary atherosclerosis: diagnosis and treatment
Abstract
Coronary atherosclerosis is a chronic condition characterised by the development of an atherosclerotic plaque in the inner layer of the coronary artery, mainly associated with cholesterol accumulation and favoured by endothelial dysfunction related to other cardiovascular risk factors, such as smoking, diabetes and hypertension. A key actor in this process is the systemic inflammatory response, which can make plaques either grow slowly over the course of years (like a 'mountain'), obstructing coronary flow, and causing stable coronary artery disease, or make them explode (like a 'volcano') with subsequent abrupt thrombosis causing an acute coronary syndrome. This central role of inflammation in coronary atherosclerosis has led to its consideration as a modifiable cardiovascular risk factor and a therapeutic target. Classic anti-inflammatory drugs have been tested in clinical trials with some encouraging results, and new drugs specifically designed to tackle inflammation are currently being under investigation in ongoing trials. The objectives of this review are to (1) summarise the role of inflammatory biomarkers and imaging techniques to detect inflammation at each stage of plaque progression, and (2) explore currently available and upcoming anti-inflammatory therapies.
Keywords: Acute Coronary Syndrome; Cardiovascular Diseases; Coronary Artery Disease; Diagnostic Imaging; Inflammation.
© Author(s) (or their employer(s)) 2025. No commercial re-use. See rights and permissions. Published by BMJ Group.
Conflict of interest statement
Competing interests: SB has received speaker’s fees from Abbott Vascular, General Electric, iVascular, Medis, and Siemens, outside the present work. He has received consulting fees from Boston Scientific, Insight Lifetech, Novo Nordisk and Zoll, outside the present work. His institution has received research grants from Abbott Vascular. AA has served as a consultant for Cardiol Therapeutics, Kiniksa, Implicit Biosciences, Merck, Novartis, Novo Nordisk, Olatec, Sanofi and Swedish Orphan Biovitrum. GBZ declares that he has consulted for Abiomed, Amarin, Balmed, Cardionovum, Crannmedical, Endocore Lab, Eukon, Guidotti, Innovheart, Meditrial, Microport, Opsens Medical, Terumo and Translumina. DJA declares that he has received consulting fees or honoraria from Abbott, Amgen, AstraZeneca, Bayer, Biosensors, Boehringer Ingelheim, Bristol-Myers Squibb, Chiesi, CSL-Behring, Daiichi-Sankyo, Eli Lilly, Faraday, Haemonetics, Janssen, Merck, Novartis, Novo Nordisk, PhaseBio, PLx Pharma, Pfizer, Sanofi and Vectura, outside the present work; DA declares that he has received consulting fees or honoraria from Abbott, Amgen, AstraZeneca, Bayer, Biosensors, Boehringer Ingelheim, Bristol-Myers Squibb, Chiesi, CSL-Behring, Daiichi-Sankyo, Eli Lilly, Faraday, Haemonetics, Janssen, Merck, Novartis, Novo Nordisk, PhaseBio, PLx Pharma, Pfizer, Sanofi and Vectura, outside the present work; DA also declares that his institution has received research grants from Amgen, AstraZeneca, Bayer, Biosensors, CeloNova, CSL Behring, Daiichi-Sankyo, Eisai, Eli Lilly, Faraday, Gilead, Janssen, Matsutani Chemical Industry Co, Merck, Novartis, Osprey Medical, Renal Guard Solutions and the Scott R. MacKenzie Foundation. All other authors have no disclosure to declare.
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