Vulnerable Plaques and Patients: State-of-the-art

Mariusz Tomaniak; Yuki Katagiri; Rodrigo Modolo; Ranil de Silva; Ramzi Y. Khamis; Christos V. Bourantas; Ryo Torii; Jolanda J. Wentzel; Frank J.H. Gijsen; Gijs van Soest; Peter H. Stone; Nick E.J. West; Akiko Maehara; Amir Lerman; Antonius F.W. van der Steen; Thomas F. Lüscher; Renu Virmani; Wolfgang Koenig; Gregg W. Stone; James E. Muller; William Wijns; Patrick W. Serruys; Yoshinobu Onuma

Disclosures

Eur Heart J. 2020;41(31):2997-3004. 

In This Article

Abstract and Introduction

Abstract

Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term 'vulnerable plaque' was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of 'vulnerability' of a specific lesion to the more comprehensive goal of identifying patient 'cardiovascular vulnerability'. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and 'local' diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of 'high-risk' plaques occurring in 'vulnerable' patients.

Introduction

In the 1980s, Muller et al. studied coronary events triggered by morning awakening, anger, heavy exertion, and other stressors. The observation that a potential stressful trigger could be harmless on one day, yet lead to a cardiac event sometime later led to the concept of the 'vulnerable plaque', initially defined in 1989[1] as a plaque at increased risk of thrombosis (Supplementary material online, Table S1). Over the past three decades, the focus on 'vulnerable plaque'[1,2] (Supplementary material online, Figure S1) has evolved into a broader 'vulnerable patient and plaque' concept,[3,4] as the current evidence suggests that clinically silent plaque ruptures may occur[5] and that the coexistence of 'vulnerable plaques' in a 'vulnerable patient'—including the prothrombotic milieu of circulating blood—is likely needed to generate acute coronary events (Take home figure) (Supplementary material online, Appendix—Evolution of the concepts of 'vulnerable plaque' and 'vulnerable patient'). It has been also recognized that aside a thin-capped, lipid-rich plaque associated with culprit plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays,[4,6] by calcified nodule or by functional coronary alterations.

Some small-to-moderate sample size longitudinal imaging studies have suggested that atherosclerotic plaques of differing maturity frequently co-exist and their morphology may change over time, being able to both gain and lose the features of vulnerability;[8–14] even up to three quarters of vulnerable plaques might evolve towards a more stable phenotype while on a high-intensity statin therapy.[13]

At present, the clinical consequences of detecting the features of plaque vulnerability remain limited as the positive predictive value of current imaging modalities for the prediction of major adverse cardiac events (MACE) is too low for clinical relevance. However, such limitations have prompted a number of technical advances including both diagnostics and analytics. In 2003, Patrick W. Serruys, Antonio Colombo, and Christodoulos Stefanadis founded an annual international meeting of medical scientists studying the detection and treatment of vulnerable plaques and patients;[2] the expert discussions that have occurred over the course of the past 15 years form the basis for this state-of-the-art document aiming to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of high-risk plaques occurring in 'vulnerable' patients.

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