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The myth of ‘stable’ coronary artery disease

Abstract

Patients with known cardiovascular disease who have not had a recent acute event are often referred to as having stable coronary artery disease (CAD). The concept of ‘stable’ CAD is misleading for two important reasons: the continuing risks of cardiovascular events over the longer term and the diverse spectrum of powerful risk characteristics. The risks of cardiovascular events are frequently underestimated and continue to exist, despite current standards of care for secondary prevention, including lifestyle changes, optimal medical therapy, myocardial revascularization and the use of antiplatelet agents to limit thrombosis. In dispelling the myth of ‘stable’ CAD, we explore the pathophysiology of the disease and the relative contribution of plaque and systemic factors to cardiovascular events. A broader concept of the vulnerable patient, not just the vulnerable plaque, takes into account the diversity and future risks of atherothrombotic events. We also evaluate new and ongoing research into medical therapies aimed at further reducing the risks of cardiovascular events in patients with chronic — but not stable — atherothrombotic disease.

Key points

  • The clinical label ‘stable’ coronary artery disease (CAD) needs to be reconsidered and be more clearly defined as chronic coronary vascular disease, including patient groups at substantial risk of future coronary events.

  • The risk of cardiovascular events in patients with chronic CAD is compounded by the presence of combined systemic and specific vascular risk factors.

  • Chronic CAD requires optimal medical therapy to mitigate the effect of modifiable risk factors and to reduce the risk of cardiovascular events (such as myocardial infarction, stroke and cardiovascular death).

  • Novel approaches might have the potential to reduce the risk of adverse events further, including profound lipid-lowering and inflammation-modifying agents and novel antithrombotic combinations.

  • The latest advances demonstrate that chronic vascular risk is modifiable and doing so has the potential to produce clinically worthwhile gains in the most susceptible patients.

  • The field will continue to evolve, with improved characterization of patients at the highest risk of vascular events.

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Fig. 1: Risks of death, MI or stroke in patients with ‘stable’ angina.
Fig. 2: Progression of atherothrombotic vascular disease.
Fig. 3: The persistent risk of MACE after a cardiovascular event.
Fig. 4: Residual risk of MACE and bleeding events in patients with chronic CAD treated with various antithrombotic regimens.
Fig. 5: Effect of different antithrombotic regimens in the context of proven secondary prevention regimens.

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Acknowledgements

The authors acknowledge H. Dawson (Chameleon Communications International), who provided editorial support with funding from Bayer and Janssen Scientific Affairs.

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All the authors researched data for the article, discussed its content and wrote the manuscript. K.A.A.F., M.M. and D.A. reviewed and edited the manuscript before submission.

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Correspondence to Keith A. A. Fox.

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Editorial support was funded by Bayer and Janssen Scientific Affairs. K.A.A.F. has received speaker honoraria and consulting fees from AstraZeneca, Bayer/Janssen, Sanofi/Regeneron and Verseon. M.M. has received speaker honoraria and consulting fees for his participation in executive committees, advisory boards or speeches from Amgen, Bayer, Fresenius, Novartis and Servier. J.M. has received speaker honoraria and consulting fees from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Merck Sharp & Dohme, Novartis and Servier. D.A. has received speaker honoraria and consulting fees from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb/Pfizer, Merck Sharp & Dohme and Novartis.

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GRACE ACS Risk and Mortality Calculator: https://www.mdcalc.com/grace-acs-risk-mortality-calculator

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Fox, K.A.A., Metra, M., Morais, J. et al. The myth of ‘stable’ coronary artery disease. Nat Rev Cardiol 17, 9–21 (2020). https://doi.org/10.1038/s41569-019-0233-y

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