Author + information
- Received April 13, 2017
- Revision received August 7, 2017
- Accepted August 15, 2017
- Published online December 18, 2017.
- Thomas J. Ford, MBChB (Hons)a,b,
- Colin Berry, MBChB, PhDa,
- Bernard De Bruyne, MD, PhDc,
- Andy S.C. Yong, MBBS, PhDd,e,
- Peter Barlis, MBBS, MPH, PhDf,
- William F. Fearon, MDg and
- Martin K.C. Ng, MBBS (Hons), PhDe,h,∗ ()
- aBritish Heart Foundation Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom
- bUniversity of New South Wales, Sydney, Australia
- cCardiovascular Center Aalst, Onze-Lieve-Vrouw Clinic, Aalst, Belgium
- dDepartment of Cardiology, Concord Hospital, Sydney, Australia
- eSydney Medical School, The University of Sydney, Sydney, Australia
- fFaculty of Medicine, University of Melbourne, Melbourne, Australia
- gDepartment of Cardiovascular Medicine, Stanford University Medical Center, Stanford, California
- hDepartment of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia
- ↵∗Address for correspondence:
Prof. Martin K.C. Ng, Royal Prince Alfred Hospital, Department of Cardiology, Missenden Road, Camperdown, NSW 2050, Australia.
In this review, the authors explore the evolving evidence linking physiological assessment of coronary artery disease with plaque progression and vulnerability. Reducing adverse clinical events remains the ultimate goal for diagnostic tests, and this review highlights evidence supporting the prognostic value of physiological metrics in predicting outcomes. Historical and contemporary studies support synergy among lesion severity, ischemia, plaque vulnerability, and patient prognosis. Ischemia contributes to clinical events through association with plaque burden, but this review addresses the emerging concept that it associates with atherothrombosis via disturbed lesion hemodynamics. Biomechanical pathophysiological forces including endothelial shear stress—the frictional force generated by blood flow on the vessel wall—are increasingly linked with atherogenesis, vulnerable plaque morphology, and platelet and leukocyte activation. The authors conclude by transitioning from the model of the vulnerable plaque to the concept of the “vulnerable patient,” looking more broadly at physiological contributors to Virchow’s triad underpinning acute coronary syndrome.
- acute coronary syndromes(s)
- coronary physiology
- endothelial shear stress
- mechanisms of atherosclerosis
- plaque vulnerability
Drs. Ford and Berry have received research support from the British Heart Foundation (grant RE-13-5-30177). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received April 13, 2017.
- Revision received August 7, 2017.
- Accepted August 15, 2017.
- 2017 American College of Cardiology Foundation
- Central Illustration
- Ischemia Based on Anatomic Evaluation (Invasive Coronary Angiography)
- Ischemia Based on Functional Evaluation
- Biomechanical Pathophysiological Forces Including ESS
- Future Directions: Natural History of Plaques, Inflammation, and Plaque Vulnerability