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Two recent papers published in Heart have evaluated the utility of advanced imaging modalities for the morphological detection and evaluation of high-risk atherosclerotic plaques.1 ,2 While these studies employed differing methodologies (CT angiography (CTA), optical coherence tomography (OCT) and optic angioscopy), the results are broadly concordant and of major potential clinical significance. Notably, when subjected to percutaneous coronary intervention (PCI), such high-risk plaques may embolise and release a slurry of lipid-rich necrotic debris to the distal circulation, with consequent myocardial damage. In addition, it has been proposed that PCI of lipid-rich plaques (LRP) with thin fibrous caps (<65 μm; thin-cap fibroatheroma (TCFA)) may be associated with lipid embolisation. However, since stable angina patients do not require urgent intervention, detailed assessment of target lesions may be feasible for the recognition and assessment of LRP before elective PCI.
Radiofrequency intravascular ultrasound (RF-IVUS) analysis is useful in defining the distribution, severity and composition of atherosclerotic plaques. Although RF-IVUS lacks the spatial resolution to directly measure fibrous cap thickness, it has been proposed that a necrotic core without overlying fibrous tissue (necrotic core abutting lumen) may represent TCFA. The presence of a thin cap, plaque burden of >70% and minimal lumen area (MLA) of <4.0 mm sq have been proposed as predictors of high-risk atherosclerotic plaques. In studies of stable coronary artery disease patients undergoing PCI of TCFA lesions, as detected by RF-IVUS, these patients appeared to suffer from increased myocardial damage.3 Similar to ultrasound, optical imaging has been extensively employed in the assessment of plaque composition; however, this technology may have niche applications due to its unique absorption and reflectance patterns of light. OCT produces high-resolution images allowing for direct fibrous cap thickness measurement. Detection of TCFA by OCT has been shown to predict PCI-related distal embolisation events in patients presenting with unstable angina,4 although this phenomenon has not been extensively studied in patients with stable coronary disease. Contrary to OCT, near infrared light spectroscopy (NIRS) cannot evaluate fibroatheroma cap thickness, but distinguishes between lipid and non-LRP. NIRS performed before and after stent implantation supports the hypothesis that PCI of LRP may frequently be associated with slow-reflow (figure 1). Furthermore, data from the COLOR Registry have revealed that PCI of lipid-rich regions is associated with elevations of cardiac biomarkers.5
Technological advances in CTA have allowed for the non-invasive characterisation of plaque composition. Although CTA does not have the spatial resolution to measure fibrous cap thickness, it has the ability to detect low attenuation plaques or LRP. In studies correlating CTA and OCT, the large size LRP with ring-like attenuation identified by CTA (the napkin-ring sign6) was mostly OCT-defined TCFA.4 Furthermore, as documented in at least four observational studies7–9 of 373 patients (table 1), PCI of such large sized CTA-verified LRP is associated with distal coronary embolisation. In addition, PCI of calcified plaques identified by CTA is another coronary substrate that has been linked with the slow-flow phenomenon.7 ,10
Although OCT, NIRS and CTA are able to recognise LRP, it is still unclear which of these available imaging tools is the most appropriate, or accurate, for the prediction of distal embolisation during PCI (table 2). We are also not certain if the incidence of lipid embolisation is high enough, or routinely of sufficient clinical consequence, to merit imaging in every patient. Even if there is a role for the assessment of LRP, it remains to be seen if the distal protection devices employed for thrombogenic debris may be as effective for lipid-rich emboli. The efficacy of these devices during native coronary PCI is currently being evaluated in the CANARY (NCT 01268319) trial wherein LRP is identified by NIRS. Nonetheless, until the dust settles, it is at least prudent that whenever we have an access to non-invasive CT angiographic results and LRP is identified, the initiation of aggressive lipid lowering therapy may help alter plaque composition, and presumably clinical outcomes. The recently reported YELLOW trial (Reduction in Yellow Plaque by Aggressive Lipid Lowering therapy) has demonstrated the efficacy of aggressive statin treatment in reducing NIRS-verified LRP content in lesions with decreased fractional flow reserve.11 A prospective randomised study of optimal medical therapy including statin treatment may be needed in stable patients with verified LRP to evaluate its impact on PCI outcomes.
Contributors I would like to undertake that the above mentioned manuscript has not been published elsewhere, accepted for publication elsewhere or under editorial review for publication elsewhere. There is no relationship with industry or any financial associations that might pose a conflict of interest in connection with the submitted article.
TR and WS contributed equally to the manuscript.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; internally peer reviewed.
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