Abstract

Acute coronary syndrome mostly arises from rupture or erosion of a vulnerable plaque. Vulnerable plaques typically appear as lipid-rich plaques with a thin cap, called thin-cap fibroatheromas. Various intracoronary imaging techniques can be used to detect vulnerable plaques, such as intravascular ultrasound (IVUS), optical coherence tomography (OCT) and near-infrared spectroscopy (NIRS), each visualizing different high-risk plaque characteristics. IVUS and its post-processing techniques, such as virtual histology IVUS, can primarily be used to identify calcified and soft plaques, while OCT is also able to quantitatively measure the cap thickness. The addition of NIRS allows the exact measurement of lipid content in the plaque. Non-invasive imaging techniques to identify vulnerable plaques, such as computed tomography, are less often used but are evolving and may be of additional diagnostic use, especially when prophylactic treatments for vulnerable plaques are further established. Pharmacological treatment with lipid-lowering or anti-inflammatory medication leads to plaque stabilization and reduction of cardiovascular events. Moreover, the implantation of a stent or scaffold for the local treatment of vulnerable plaques has been found to be safe and to stabilize high-risk plaque features. The use of drug-coated balloons to treat vulnerable plaques is the subject of ongoing research. Future studies should focus on non-invasive imaging techniques to adequately identify vulnerable plaques and further randomized clinical studies are necessary to find the most appropriate treatment strategy for vulnerable plaques.

Highlights

  • Since the introduction of percutaneous coronary intervention (PCI) in the 1970s, the mortality rates of chronic coronary syndrome (CCS) and acute coronary syndrome (ACS) have steadily decreased [1,2]

  • We describe the most commonly used intracoronary imaging techniques: intravascular ultrasound (IVUS), optical coherence tomography (OCT) and near-infrared spectroscopy (NIRS), which are summarized in Table 1 (Ref. [29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54])

  • In 2013, Madder et al [34] demonstrated that a maximum lipid core burden index (LCBI) per 4 mm segment of more than 400 adequately distinguished culprit segments causing ST-segment elevation myocardial infarction (MI) from control segments consisting of lipid-free autopsy specimen, which provided a sensitivity of 85% and specificity of 98%

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Summary

Introduction

Since the introduction of percutaneous coronary intervention (PCI) in the 1970s, the mortality rates of chronic coronary syndrome (CCS) and acute coronary syndrome (ACS) have steadily decreased [1,2]. The American Heart Association (AHA) estimated that ischemic heart disease, and ACS, accounts for around $150 billion health costs in the United States each year [4]. Even patients with prior PCI for ACS who are on guideline-directed secondary preventive therapy, have a significant residual risk for repeat coronary events. This risk is mainly driven by target-lesion related events (e.g., stent-related), while in the years succeeding the residual risk primarily arises from lesions in other coronary segments, which were often not considered rupture-prone during the initial PCI [5]. Early identification of these lesions responsible for (recurrent) coronary events could be of clinical significance and preventive treatment of these lesions might reduce disease burden and related health costs. In this review we provide a contemporary overview of (i) the morphology, (ii) the identification and (iii) possible treatment strategies of vulnerable plaques

The vulnerable plaque
Invasive imaging techniques to detect vulnerable plaques
Intravascular ultrasound
Optical coherence tomography
Near-infrared spectroscopy
Coronary angiography computed tomography
Cardiovascular magnetic resonance imaging
Nuclear imaging
Treatment of the lipid-rich plaque
Anti-inflammatory drugs
Local treatment
Findings
Conclusions
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