LITMIR.BIZ

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as a consequence of neointimal proliferation inside the BVS Unlike metallic stents, which are powerful light reflectors and induce posterior shadowing and blooming artifacts on the vessel surface, polymeric struts of BVS are transparent to the light so that scaffold integrity, apposition to the underlying wall, and changes in the strut characteristics over time can be easily studied. OCT also showed a very delayed and incomplete resorption of the PLLA stuts. The ABSORB II trial was also the first to report inferiority of ABSORB BVS: three year follow‐up was associated with a twofold greater risk of TLF in comparison with Xience V (10% vs 5%; p = 0.0425). ABSORB III trial demonstrated ABSORB BVS inferiority in terms of overall ST. Cumulative meta‐analyses embracing ABSORB II, ABSORB III, AIDA, EVERBIO II and TROFI II trials indicated higher target lesion failure and overall ST with BVS, especially in ACS and STEMI patients [113–116]. Several large registries, including two national trials (ABSORB JAPAN and ABSORB CHINA)[117–118] demonstrated better outcomes of ABSORB BVS when optimal lesion preparation was combined with final high pressure expansion guided by imaging, avoiding too small arteries. Still the meta‐analyses and the early results of the ABSORB IV trial determined the decision to interrupt production of ABSORB BVS in late 2017 [119]. OCT was instrumental in revealing rational mechanisms for their higher thrombogenicity, including higher strut profiles leading to turbulent flow and low radial strength leading to a smaller and more irregular final lumen areas. Occasionally, malapposed stuts were found to crush inside the lumen creating rare instances of late (up to 3 years) stent thrombosis (ScT). More recently a series of very late (5–7 years) follow‐up studies showed absence of ST at this time point and more consistent disappearance of the bioabsorbable stuts with OCT. Despite the failure of first generation BVS, newer BRS based on different technologies (magnesium) are under current examination with OCT liberally used to optimize initial results and confirm the absence of untoward late changes [120].

Near‐infrared spectroscopy

Atherosclerotic plaque formation is the consequence of inflammation and extracellular matrix formation as well as cholesterol deposition in the vasculature. Altered lipids attract proteolytic enzyme‐producing macrophages to their site, which engulf the lipids and leave behind a soft and unstable core that is highly abundant in foam cells and lipids. Cholesterol, whether esterified or unesterified, forms the major part of the lipid core. Histologic studies as well as studies with intravascular imaging have confirmed the association of the presence of lipid‐laden plaques with the risk of ACS and increased peri‐interventional complications. The ability to detect lipid‐rich plaques in patients is therefore of great clinical significance.

      Near‐infrared spectroscopy (NIRS) is widely used in many disciplines to identify the chemical composition of unknown substances. It utilizes the absorbance and reflectance of near‐infrared light from an illuminated targeted area to derive the presence of the target substance. This method is a simple quick technique that provides multiconstituent analysis, and requires no sample preparation or manipulation with hazardous agents [121]. Studies have documented the ability of NIRS to accurately identify lipid‐core atherosclerotic plaques in animal models or autopsy specimens and finally, after in vivo and ex vivo validation studies [122,123], an intraluminal spectroscopy catheter was developed and released for clinical use.

      System description

      Initially, intracoronary NIRS was developed as an independent imaging modality, but a major drawback was the inability to provide spatial orientation to match the lipid content alongside the plaque distribution. However, current co‐registered NIRS‐IVUS catheters (TVC Imaging System, InfraReDx Inc, Burlington, MA, USA) provide data regarding both the vessel structure and the plaque composition.

      After completion of an automatic pullback, data are processed displaying a two‐dimensional map of the vessel, revealing the probability of the presence of a lipid core plaque (LCP), with the pullback position in millimeters on the x‐axis and the circumferential position on the y‐axis. This display is known as the “chemogram.” For each pixel of 0.1 mm and 1°, length and angle respectively, the lipid core probability is calculated from the spectral data collected and semi‐quantitatively coded on a color scale from 0 for red and to 1 for yellow. Whenever a pixel lacks sufficient data, for instance the guidewire is shadowing, the pixel appears black.

      The block chemogram, also created from the NIRS images, combines the results for each 2‐mm section of the artery to create a “virtual block” that summarizes and reflects the probability of LCP intervals. The numeric value of each block produced is the 90th percentile of all pixel values obtained in the corresponding 2‐mm section of the artery in the chemogram. Here, the red coloration indicates a low probability of an LCP, whereas yellow coloration determines a higher probability of an LCP, alongside the intensity of the color reflecting the amount of cholesterol present. In isolation, the block chemogram specifically adapts a four‐color scale method of analysis (red (p < 0.57), orange (0.57 ≤ p < 0.84), tan (0.84 ≤ p < 0.98) and yellow (p ≥ 0.98)) that reflects the probability of the existence of an LCP in each 2‐mm block of pullback which aids the overall visual interpretation. Spectral data are paired with corresponding IVUS frames, overall displayed as a ring around the IVUS image. The lipid core burden index (LCBI) measures the portion of pixels that exceed an LCP probability of 0.6, in all viable pixels within the scanned region, multiplied by 1000. This is a quantitative measure of the intensity of yellow pixels present on the chemogram. The LCBI values vary from 0 to 1000 and the maximum value of LCBI for any of the 4‐mm segments along the analyzed segment is defined as the maxLCBI_4mm.

      Potential clinical uses

      Determination of high‐risk plaque

The necrotic core region has an abundance of lipid deposition and lacks mechanical stability due to the degradation of fibrous tissue and disappearance of cells. The size of the necrotic core has been significantly associated with the likelihood of plaque rupture. In a previous pathologic study of aortic plaques, ulceration, and thrombosis were characteristic of plaques with >40% of their volume occupied by extracellular lipids [124]. As the lipid core increases plaque vulnerability, the NIRS can potentially be used to identify high risk plaques (Figure 9.7). It has been shown that the target lesions responsible for ACS were in most cases lipid‐rich plaques; additionally, patients with ACS commonly harbored remote, nontarget lipid‐rich plaques [125]. In another study in patients with STEMI, maxLCBI_4mm > 400 in NIRS accurately distinguished culprit from non‐culprit segments within the artery and from the lipidrich plaque‐free autopsy histology segments [126]. In a recently published prospective observational study, NIRS imaging was performed in a non‐culprit coronary artery in 203 patients referred for angiography due to stable angina pectoris or ACS. It was shown that the one year cumulative incidence of a cardiovascular event in patients with an LCBI equal to or above the median value (43.0) was significantly higher than those with an LBCI value below the median [127].

Figure 9.7 A 39‐year‐old man was admitted with unstable angina. Angiography showed significant lesions in right and left anterior descending arteries. After post‐dilatation, near‐infrared spectroscopy–intravenous ultrasound (NIRS‐IVUS) imaging was performed, which revealed lipid core plaque in the mid‐ and distal left anterior descending (LAD) (b and c). Proximal segments were relatively disease free (a). Right coronary artery (RCA) also harbored lipid core plaques.

The Lipid Rich Plaque (LRP) study enrolled 1241 patients with stable or unstable angina and myocardial infarction and studied more than 5000 lesions assessed with NIRS‐IVUS. The study demonstrated that the identification of non‐critical, untreated, lipid‐rich plaques by NIRS imaging is associated with adverse events following PCI for de novo culprit lesions. NIRS allows the assessment of atherosclerotic plaques by the analysis of reflected spectrum of near infrared

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