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Role of biomechanical forces in the natural history of coronary atherosclerosis.

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

Brown, Adam J 
Evans, Paul C 
Gillard, Jonathan H 
Samady, Habib 

Abstract

Atherosclerosis remains a major cause of morbidity and mortality worldwide, and a thorough understanding of the underlying pathophysiological mechanisms is crucial for the development of new therapeutic strategies. Although atherosclerosis is a systemic inflammatory disease, coronary atherosclerotic plaques are not uniformly distributed in the vascular tree. Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis. Endothelial cell function is heavily influenced by changes in WSS, and longitudinal animal and human studies have shown that coronary regions with low WSS undergo increased plaque growth compared with high WSS regions. Local alterations in WSS might also promote transformation of stable to unstable plaque subtypes. Plaque rupture is determined by the balance between PSS and material strength, with plaque composition having a profound effect on PSS. Prospective clinical studies are required to ascertain whether integrating mechanical parameters with medical imaging can improve our ability to identify patients at highest risk of rapid disease progression or sudden cardiac events.

Description

Keywords

Animals, Biomechanical Phenomena, Coronary Artery Disease, Coronary Circulation, Coronary Vessels, Disease Progression, Humans, Plaque, Atherosclerotic, Prognosis, Rupture, Spontaneous, Signal Transduction, Stress, Mechanical

Journal Title

Nat Rev Cardiol

Conference Name

Journal ISSN

1759-5002
1759-5010

Volume Title

13

Publisher

Springer Science and Business Media LLC
Sponsorship
British Heart Foundation (None)
Medical Research Council (G1000847)
TCC (None)
British Heart Foundation (None)
British Heart Foundation (None)
European Commission (224297)
Medical Research Council (G0800784)
British Heart Foundation (FS/15/26/31441)
MRC (MC_PC_14116 v2)
National Institute for Health and Care Research (NIHR/CS/009/011)
This work was supported by the British Heart Foundation (FS/13/33/30168), Heart Research UK (RG2638/14/16), the Cambridge NIHR Biomedical Research Centre, and the BHF Cambridge Centre for Research Excellence.