Summary of different spectroscopic methods.
Abstract
Acute coronary syndrome (ACS) arising from plaque rupture is the leading cause of mortality worldwide. Near-infrared spectroscopy (NIRS) combined with intravascular ultrasound (NIRS-IVUS) is a novel catheter-based intravascular imaging modality that provides a chemogram of the coronary artery wall, which enables the detection of lipid core and specific quantification of lipid accumulation measured as the lipid-core burden index (LCBI) in patients undergoing coronary angiography. Recent studies have shown that NIRS-IVUS can identify vulnerable plaques and vulnerable patients associated with increased risk of adverse cardiovascular events, whereas an increased coronary plaque LCBI may predict a higher risk of future cardiovascular events and periprocedural events. NIRS is a promising tool for the detection of vulnerable plaques in CAD patients, PCI-guidance procedures, and assessment of lipid-lowering therapies. Previous trials have evaluated the impact of statin therapy on coronary NIRS defined lipid cores, whereas NIRS could further be used as a surrogate end point of future ACS in phase II clinical trials evaluating novel anti-atheromatous drug therapies. Multiple ongoing studies address the different potential clinical applications of NIRS-IVUS imaging as a valuable tool for coronary plaque characterization and predictor of future coronary events in CAD patients.
Keywords
- near-infrared spectroscopy (NIRS)
- intravascular ultrasound (IVUS)
- thin-cap fibroatheroma (TCFA)
- acute coronary syndrome (ACS)
- vulnerable plaque
1. Introduction
Coronary artery disease (CAD) is the leading cause of global mortality and the rupture of an unstable atherosclerotic plaque precedes the majority of acute coronary syndromes (ACS) [1, 2]. Autopsy studies have shown that the putative substrate for most ACS and many cases of sudden cardiac death (SCD) is the rupture of a thin-cap fibroatheroma (TCFA), the so-called “
Near-infrared spectroscopy (NIRS) is a novel intravascular-imaging modality that provides chemical assessment related to the presence of cholesterol esters in lipid cores and can generate spectra that distinguishes cholesterol from collagen in coronary plaques through their unique spectroscopic fingerprints [10]. NIRS was first used in 1993 for the detection of lipid content in an experimental animal model [11], followed by subsequent
2. Near-infrared spectroscopy system
2.1. Principles of diffuse reflectance NIRS
Spectroscopy is based on the analysis of electromagnetic spectra induced by near-infrared light and provides direct evaluation of plaque composition, which could yield information on plaque vulnerability [13]. Several spectroscopic methods have been investigated for the purpose of identifying atherosclerotic plaque composition, although the commercially available catheter uses diffuse reflectance NIRS [13, 25]. The principle of NIRS relies on the interaction of light in the form of photons with different functional groups of organic molecules in a tissue, which results in reflected light in the NIR region from molecular vibrational energy in the form of oscillations of atoms within their chemical bonds. Photons can be absorbed or scattered by tissue, which determines the amount of light that is detected by the spectrometer. The wavelengths of light in NIRS are approximately in the 800–2500 nm range. Unique combinations of carbon-hydrogen (C-H), nitrogen-hydrogen (N-H), and oxygen-hydrogen (O-H) bonds are responsible for the major absorption of NIR light, whereas each functional group of large complex molecules yields absorption patterns at specific wavelengths, known as the
Diffuse reflectance NIR spectroscopy has many features that enable
Raman NIRS | Fluorescence spectroscopy | Diffuse reflectance NIRS | Nuclear magnetic resonance (NMR) spectroscopy | |
---|---|---|---|---|
Principle | Raman shift from the scattering of a photon upon interaction with matter, generating a near-infrared wavelength forming the Raman spectra | Absorbance of energy from a tissue exposed to ultraviolet light, which in turns releases energy in the form of light | Reflected light from a tissue detected by the spectrometer at a wavelength, generating a NIR spectrum | Chemical shift from chemical groups exposed to an oscillating electromagnetic field and frequencies decoded by the Fourier transform to generate NMR spectrum |
Plaque characterization | Cholesterol esters, collagen, phospholipids, triglycerides, calcium | Collagen, elastin fibers, lipoproteins, calcium, macrophages, foam cells | Lipid-core plaques | Unsaturated and polyunsaturated fatty acids, cholesterol esters, phospholipids, triglycerides |
Validation studies |
|
|
|
13-Carbon NMR used in |
Advantages | Evaluates the chemical composition of living tissues Signal more specific but weaker than diffuse reflectance NIRS (difficult to detect signal |
Strong fluorescence in arterial tissue, enabling rapid time acquisitions | Evaluates the chemical composition of living tissues, NIR light can penetrate blood and acquire signals from structures several millimeters deep relative to tissue surface | Lack of ionizing radiation (less radioactivity with carbon-13), noninvasive modality, enables to study several biological processes with metabolic, physiologic, and anatomic data combined to imaging |
Availability | In development—fiber optics catheter-based system for PCI applications under investigation | No |
Catheter-based NIRS-IVUS system used as a clinical application | Costly, preclinical research |
2.2. NIRS-IVUS-combined catheter system
Spectroscopy has a strong fundamental basis for compositional measurement and is a highly efficient method for the identification of chemical components of unknown organic molecules. A single NIRS modality catheter system, the LipiscanTM (InfraRedx Inc., Burlington, MA, USA), was first developed for invasive detection of LCP [26]. In order to obtain anatomical information on the vessel and optimal plaque characterization, a hybrid technology (TVC Imaging SystemTM, InfraRedx Inc.) combining near-infrared spectroscopy(NIRS) and intravascular imaging (IVUS) was further developed, which allows simultaneous, co-registered acquisition of structural and compositional data of coronary artery plaques. Thus, combining the two complementary technologies enables a complete assessment of patient’s arteries, including vessel size and structure, plaque volume, area, and composition [26, 35].
The commercially available NIRS-IVUS imaging system consists of a 3.2-French (F) rapid-exchange catheter compatible with 6F-guiding catheters, a pullback and rotation device, and a console that houses the scanning NIR laser, the computer that processes the spectral signal and two monitors [10, 26, 36]. Within the catheter body is a rotating core of optical fibers that deliver near-infrared light and measure the proportion of light reflected back over the range of optical wavelength (800–2500 nm) in the form of an imaging spectrum. The catheter-imaging core enables to collect data rapidly by rotating at 960 rpm with synchronized pullback at an automated speed of 0.5 mm/s. The system acquires >30,000 spectra per 100 mm. IVUS images are simultaneously acquired by a transducer at a frequency of 40 MHz and with an axial resolution of 100 μm, together with co-registered NIRS measurements, with a maximum imaging length of 12 cm and a depth of 1 mm or less. Thus, the NIRS spectra data are mapped and paired with corresponding cross-sectional IVUS frames, presented as a ring around the IVUS image [26, 27, 35, 36]. An upgrade version of the TVC catheter Imaging SystemTM was released by the company in 2015, which uses an extended bandwidth transducer that generates IVUS images at frequencies between 30 and 70 MHz, thus increasing the resolution and depth-to-field of the images [36].
2.3. Interpretation of NIRS data
Upon completion of the automated pullback scan, spectral data are automatically analyzed by a computer-based algorithm that transforms NIR spectra into a probability of LCP presence. The probability is mapped to a color pixel that will generate a digital two-dimensional color map of the artery called the NIRS chemogram, which represents the probability of the presence of LCP over the scanned segment of a vessel (
Figure 3
). On the longitudinal chemogram, the
Chemometrics is the methodology applied by NIRS technology to analyze lipid content in atherosclerotic arteries [37]. The NIRS system was used in an extensive
The lipid-core burden index (LCBI) is a measure of the lipid burden within the scanned region, calculated by dividing the number of yellow pixels that exceed an LCP probability of 0.6 per million by the total number of valid pixels in the segment, then multiplied by a factor of 1000 (LCBI range: 0–1000). Other measures can be computed on the chemogram image, such as the LCBI of a region of interest (ROI) and the maximum LCBI of the 4-mm region within the highest lipid burden within the ROI (maxLCBI4mm) [26, 27, 35, 36, 39]. It has been shown that a high LCBI detected in coronary plaques is associated with an increased risk of future cardiovascular events and periprocedural complications (see Section 2.6), which suggests that LCBI could be a useful biomarker for risk assessment and therapeutic efficacy in future clinical trials.
2.4. Validation of the NIRS-imaging system
2.4.1. Preclinical and autopsy studies
Autopsy, animal, and human studies have been carried out to test the utility and safety of NIRS for the purpose of eventually bringing this technology to patients in the catheterization laboratory. Cassis and Lodder first demonstrated the ability of NIRS to accurately identify low-density lipoprotein (LDL)
The first study to test the hypothesis that NIR spectroscopy could identify plaque composition and features associated with plaque vulnerability, defined by histology as the presence of lipid pool, thin fibrous cap (<65 μm by ocular micrometry), and inflammatory cell infiltration, was performed in 199 human aortic samples obtained at the time of autopsy [43]. An algorithm was constructed using NIR spectra obtained from 50% of the samples (calibration set) and was then tested on unknown samples (validation set) to determine its ability to identify high-risk features as determined by histology. Spectra associated with each of the three histological features of interest were defined by the results obtained from the calibration set. The main findings of this study were that NIRS could identify histology features associated with plaque vulnerability in human plaques
Since the intention of inventers of the NIRS system was to commercialize a catheter-based instrument that could assess plaques in coronary arteries
2.4.2. Autopsy calibration and validation studies
The catheter-based system was improved with the addition of an automated pullback and rotation device allowing the system to circumferentially scan the length of a vessel. Calibration and validation studies of NIRS for the detection of LCP were first performed in human autopsy specimens of coronary arteries [16, 35]. The largest
2.4.3. Clinical validation studies
The first use of the NIRS system in coronary arteries of living humans was performed in six patients undergoing elective PCI for stable angina using an early prototype (2001; Lahey Clinic, Burlington, MA) [13, 16, 40]. No device-related adverse events occurred, showing the safety and feasibility of the system to distinguish spectra measured through blood. However, significant motion artifacts were present due to slow-signal acquisition time (2.5 s). In August 2005, an improved ultrafast NIR system prototype was developed with a faster scanning laser and was later used in a feasibility study of 10 patients in 2006 (Lahey Clinic, Burlington, MA). The trial confirmed the safety of the newer improved device and showed its ability to discriminate between signals obtained in the artery and those from blood alone, with no measurable artifacts of motion [16, 40].
A subsequent pivotal study, the SPECTACL (SPECTroscopic Assessment of Coronary Lipid) clinical study, was performed to validate the accuracy of LCP-detected NIRS signals collected in coronary arteries of 106 patients [10]. The study met its primary end point of demonstrating that spectral data could be safely acquired in coronary arteries of patients with the intravascular NIRS system and that the spectra were equivalent to those gathered from autopsy specimens (success rate of 0.83; 95% confidence interval (CI): 0.70–0.93). Thus, this study supported the feasibility of LCP detection in living patients. Subsequent studies showed intra- and inter-catheter reproducibility of automated interpretation of NIR spectra signals [50, 51].
2.5. Comparison with other intravascular imaging modalities for plaque characterization
The most common cause of acute coronary syndromes (ACS) is believed to be coronary artery thrombosis due to the rupture of lipid-rich “
2.5.1. Intravascular ultrasound (IVUS) imaging
Intravascular ultrasound imaging (IVUS) produces cross-sectional images of the lumen and the artery wall
Spatial resolution (μm) | Depth (mm) | Energy source | Remodeling | Plaque composition | Calcium | Fibrous cap | Lipid core | Thrombus | Macrophages | Neovessels | |
---|---|---|---|---|---|---|---|---|---|---|---|
IVUS | 100–150 | 10 | Ultrasound | ++ | − | ++ | ± | + | ± | − | − |
RF-IVUS | 100 | 10 | Ultrasound | − | + | ++ | + | + | − | − | − |
OCT | 10 | 2–3 | Near-infrared light | − | + | ++ | ++ | + | ++ | + | + |
NIRS | 1000 | _ | Near-infrared light | − | − | − | − | ++ | − | − | − |
NIRS-IVUS | 100–150 | 10 | Near-infrared light + ultrasound | ++ | − | ++ | ± | ++ | ± | − | − |
2.5.2. Virtual histology (VH) imaging
As compared to conventional invasive ultrasound techniques, radiofrequency (RF) IVUS provides additional information on plaque composition and morphology by spectral analysis of ultrasound backscatter [60]. A color-coded map allows the distinction of different components of atherosclerotic plaques, such as calcification (white), lipid/fibrofatty (light-green), fibrous (green) tissue, and necrotic core (red) [61]. Virtual histology (VH)-IVUS spectral analysis correlates with histopathology studies of plaques and can identify the four plaque components with sensitivity, specificity, and predictive accuracy ranging from 80 to 92% [54, 62, 63]. VH-IVUS detection of LCPs has been associated with higher incidence of clinical events [64, 65] and periprocedural complications during PCI [66–68]. Prospective assessment of vulnerable plaques was performed in the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) trial, a multicenter multimodality study that prospectively analyzed by IVUS and IVUS-VH imaging the coronary arteries of 697 ACS patients [64]. Their findings suggested that the presence of TCFA defined by VH-IVUS (hazard ratio (HR), 3.35; 95% CI, 1.77–6.36;
2.5.3. Optical coherence tomography (OCT)
Optical coherence tomography is an invasive catheter-based imaging modality that measures the intensity and echo time delay of reflected near-infrared light from internal structures in tissues [71]. This technique provides a resolution of 10–20 μm
2.5.4. Near-infrared spectroscopy (NIRS)
In contrast to IVUS, RF-IVUS, and OCT, which collect structural information, NIRS is unique for its ability to directly identify the chemical composition of the arterial wall and assess the presence of the LCP. NIRS detects unequivocal fingerprints from lipid core that is not affected by signal loss behind calcium due to acoustic shadowing, as it can occasionally preclude grayscale IVUS analysis, and the validation of NIRS included both calcified and non-calcified lipid cores in the definition of LCP [38]. NIRS alone does not provide information about structural anatomic parameters, such as vessel remodeling, plaque thickness, lumen area, and calcification [77]. However, as previously mentioned, the combined NIRS-IVUS-imaging catheter allows co-registration of both IVUS and NIRS data, which gives information on both plaque composition and morphology. NIRS-IVUS has shown to improve LCP detection, by comparison to IVUS, in calcified plaques as well as in lesions with small plaque burden [78]. The combined measures of plaque burden and LCBI improved the accuracy of fibroatheroma detection as compared with plaque burden alone by grayscale IVUS. Indeed, Puri et al. [79] conducted an
Several studies have compared NIRS with other intravascular-imaging modalities for LCP detection. It was previously shown that large plaque area measured by grayscale IVUS was more often associated with lipid accumulation/LCP detected by NIRS [19, 80]. However, Brugaletta et al. [80] found a weak correlation between the VH necrotic core content of the plaque and the block chemogram probability values (
In summary, there are important differences in LCP detection between different intravascular-imaging modalities, owing to their different imaging properties and limitations. As previously mentioned, OCT has the highest resolution but the weakest tissue penetration, limiting assessment of plaque burden and overall plaque volume [84]. While IVUS-VH and OCT require image interpretation for the detection of LCP, NIRS provides automated LCP detection without the need for manual imaging processing, facilitating its use in the catheterization laboratory and enabling rapid ad hoc clinical decision making during procedures. Moreover, OCT and NIRS can image through calcified lesions, whereas IVUS cannot. VH-IVUS can incorrectly misclassify intracoronary stents as calcium surrounded by necrotic core, a major limitation that is not found with OCT and NIRS imaging [84]. From the strengths and weaknesses of each individual imaging modality, it appears that the combination of two or more imaging technologies could improve LCP and vulnerable plaque detection [85].
2.6. NIRS-IVUS clinical applications
There is growing evidence from multiple studies of the clinical applications and value of the NIRS-IVUS imaging modality, including identifying the culprit lesion in ACS, optimizing PCI procedure, identifying plaques at high risk of periprocedural complications, for risk stratification, monitoring lipid-lowering therapy, and assessing plaque vulnerability (e.g., Table 3 ) [86].
Setting | Study or authors | Publishing year |
|
Clinical end point(s) | Results, references |
---|---|---|---|---|---|
LCP detection and |
SPECTACL | 2009 | 106 | (1) Evaluate the similarities of NIRS spectra obtained in patients to spectra previously obtained and validated by histology in autopsy specimens;(2) to assess the safety of the device; and (3) to quantify the presence of LCP at target and non-target sites | NIRS system enables to safely obtain spectral data in patients that were similar to those from autopsy specimens and results demonstrated the feasibility of invasive detection of coronary LCP [10] |
Plaque characterization | Brugaletta et al. | 2011 | 31 | Compare the findings of NIRS, IVUS-VH and IVUS grayscale obtained in matched coronary vessel segments of patients undergoing coronary angiography | Larger plaque area by grayscale IVUS was more often associated with either elevated percentage of VH derived-necrotic core (NC) or LCP by NIRS; correlation between LCP detected by NIRS and NC by VH was weak [80] |
Pu et al. | 2012 | 66 | Evaluate NIRS combined with IVUS to provide novel information on human coronary plaque characterization | Combining NIRS and IVUS contributes to plaque characterization |
|
Vulnerable plaque | ATHEROREMO-NIRS | 2014 | 203 | Determine the long-term prognostic value of intracoronary NIRS as assessed in a nonculprit vessel in patients with CAD | CAD patients with an LCBI ≥ 43.0 had a fourfold risk of MACE during 1-year follow-up [92] |
Madder et al. | 2016 | 121 | Evaluate the association between large lipid-rich plaques (LRP) detected by NIRS at non-stented sites in a target artery and subsequent MACCE | Detection of large LRP by NIRS (maxLCBI4mm ≥400) at non-stented sites in a target vessel was associated with an increased risk of future MACCE [93] | |
Acute coronary syndrome | Madder et al. | 2012 | 60 | Determine the frequency of LCP at target and remote sites in ACS vs. stable angina patients | Target lesions responsible for ACS were frequently composed of LCP; LCP in culprit and non culprit lesions were more common in patients with ACS vs. stable angina patients [77] |
Madder et al. | 2013 | 20 | To describe NIRS findings in culprits lesions of STEMI patients | maxLCBI4mm > 400 detected in vivo by NIRS is a threshold for identification of STEMI culprit plaques [17] | |
Madder et al. | 2015 | 81 | Assess the lipid burden of culprit lesions in NSTEMI and UA patients | LCP similar to those detected at STEMI culprit sites were detected at culprit sites of NSTEMI and UA patients [18] | |
Periprocedural MI | COLOR registry | 2011 | 62 | Analyse the relationship between the presence of large LCP detected by NIRS and periprocedural MI | NIRS provides a rapid and automated detection of extensive LCPs that are associated with a high risk of periprocedural MI [20] |
Raghunathan et al. | 2011 | 30 | Evaluate if an association between the presence and extend of LCP detected by NIRS before PCI and periprocedural MI | PCI of LCP detected lesions by NIRS is associated with increased risk of MI after PCI [21] | |
Maini et al. | 2013 | 77 | Evaluation of LCP modification with coronary revascularization and its correlation with periprocedural MI | Plaque modification can be performed by interventional methods and evaluated with NIRS; axial plaque shifting is an acute prognostic marker for postprocedural MI [124] | |
PCI optimization | Dixon et al. | 2012 | 69 | Compare the target lesions length using NIRS combined with angiography vs. angiography alone | Patients undergoing stent implantation could have LCP extended beyond angiographic margins of the initial target lesion using QCA alone [97] |
Hanson et al. | 2015 | 58 | Assess the prevalence of plaque burden and LCP extended beyond angiographic borders of target lesions | NIRS-IVUS imaging demonstrates that target lesion length is commonly underestimated by angiography alone [98] | |
Ali et al. | 2013 | 65 | Characterize neointimal composition of in-stent restenosis in both BMS and DES using a multimodality approach with OCT and NIRS-IVUS | In-stent thin-cap neoatherosclerosis is more prevalent, more diffusely distributed across stented segment and is associated with increased periprocedural MI in DES compared with BMS [108] | |
Madder et al. | 2016 | 120 | Evaluate NIRS-IVUS system findings of increased lipid signals in pre-existing stents, speculated to indicate neoatherosclerosis, and compare with a control group of freshly implanted stents, in which any lipid signal originates from fibroatheroma under the stent | Detection of LCP in pre-existing stents by NIRS alone is not reliable evidence of neoatherosclerosis, as the lipid signal may originate from fibroatheroma under the stent [109] | |
Monitoring lipid-lowering therapies | YELLOW | 2013 | 87 | Determine the impact of short-term intensive statin therapy (Rosuvastatin 40 mg OD) on intracoronary plaque content | Short-term intensive treatment with statin was associated with a significant reduction in LCBI / lipid content compared to standard therapy [22] |
Prevention of PCI complications | Brilakis et al. | 2012 | 9 | Investigate whether the use of a distal embolic protection device might prevent complications of LCP interventions | The use of a distal protection device frequently resulted in embolized material retrieval after stenting of native coronary artery lesions with large LCP [123] |
CANARY | 2015 | 85 | Evaluate if a distal protection device reduce postprocedural MI for PCI of LCP lesions | Distal protection device dis not reduce postprocedural MI [125] | |
Erlinge et al. | 2015 | 18 | Evaluate if aspiration thrombectomy reduces the lipid content of culprit plaques by NIRS-IVUS in ACS patients assessed | Thrombus aspiration resulted in a 28% reduction in lipid content by performing aspiration thrombectomy in culprit lesion [129] |
2.6.1. In vivo detection of culprit lesions in ACS
Several studies have evaluated NIRS detection of LCP, shown by an increased LCBI, at the site of culprit lesions associated with coronary events. Madder et al. [17] performed NIRS imaging in culprit vessels of 20 patients with acute ST-segment elevation myocardial infarction (STEMI) and compared their findings with spectra analysis in nonculprit segments of the artery and with autopsy control segments. The maxLCBI4mm was 5.8-fold higher in STEMI culprit segments than in 87 nonculprit segments of the STEMI culprit vessel (median (interquartile range (IQR)): 523 [445 to 821] vs. 90 [6 to 265];
Similar NIRS findings of lipid burden were observed in culprit lesions of patients in non-ST segment elevation myocardial infarction (NSTEMI) [18, 77]. LCPs are more common in patients with ACS compared to stable angina patients. From the 81 NSTEMI and unstable angina (UA) patients who underwent culprit vessel NIRS imaging prior to stenting, non-STEMI culprit segments had a 3.4-fold greater maxLCBI4mm than nonculprit segments (448 ± 229 vs. 132 ± 154,
2.6.2. Association with cardiovascular risk factors
A recent clinical study has evaluated the association between clinical risk factors and blood characteristics of vascular inflammation and lipid content/LCP visualized by NIRS. de Boer et al. [19] reported the use of NIRS in a nonculprit coronary artery in 208 patients undergoing percutaneous coronary intervention or invasive diagnostic coronary exploration for various indications. It was found that male gender, hypercholesterolemia, and the presence of multivessel CAD were modestly associated with higher LCBI values on NIRS. A history of peripheral vascular disease and/or cerebral disease and the use of beta-blockers were positively associated with LCBI, while biomarkers such as blood lipids and high-sensitivity C-reactive protein were not. All clinical characteristics reflecting patients with high CAD risk explained only 23% of the variability in LCBI. Moreover, the LCBI on NIRS and the percentage area of plaque burden determined by IVUS were modestly correlated (
2.6.3. Assessing plaque vulnerability and risk stratification
Retrospective autopsy studies have revealed specific histological culprit lesion morphologies in patients suffering from an ACS, which has created an enthusiasm in the use of intravascular coronary artery imaging in search of the “
The first prospective human study, published in 2014, has evaluated the association of high LCP by NIRS and cardiovascular events. The ATHEROREMO-NIRS (The European Collaborative Project on Inflammation and Vascular Wall Remodeling in Atherosclerosis—Near-Infrared Spectroscopy) trial is a prospective, observational study that aimed to evaluate the prognostic value of NIRS in a nonculprit coronary artery from 203 patients referred for angiography due to stable angina or ACS [92]. The results showed that the 1-year cumulative incidence of all-cause mortality, non-fatal ACS, stroke, and unplanned coronary revascularization was 4-fold increased in patients with an LCBI equal or above to the median value of 43.0 compared to those with an LCBI value below the median (adjusted HR: 4.04; 95% CI: 1.33–12.29;
The detection of fibroatheroma could help to identify culprit lesions in ACS patients, predict lesions subject to periprocedural complications, could allow optimal stent selection, and reduce the rate of stent restenosis. Whether the detection of fibroatheroma using NIRS-IVUS will prevent future events is currently being studied in several trials, including the Lipid-Rich Plaque study (LCP; Clinical Trials.org Identifier: NCT02033694), PROSPECT II ABSORB trial (A Multicentre Prospective Natural History Study Using Multimodality Imaging in Patients With acute Coronary Syndromes; Clinical Trials.org Identifier: NCT02171065), and ORACLE-NIRS trial (Lipid cORe Plaque Association With CLinical Events: a Near-InfraRed Spectroscopy Study; Clinical Trials.org Identifier: NCT02265146).
2.6.4. Optimizing percutaneous coronary intervention procedures
Visual estimation of a coronary stenosis on a two-dimensional (2D) angiography or quantitative coronary angiography (QCA) of lesion lengths is often misleading from image foreshortening and underestimation of plaque burden. IVUS offers accurate length measurement during automated pullback, proximal and distal reference diameter of a vessel, and enables to evaluate the presence and extent of calcifications [26]. The ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) study, a prospective, multicenter, nonrandomized “all-comers” registry of 8583 consecutive patients, showed that IVUS-guidance PCI, performed in 39% of patients, was associated with reduced 1-year rates of MACE (3.1% vs. 4.7%; adjusted HR, 0.70; 95% CI: 0.55–0.88;
The use of combined NIRS-IVUS imaging may further optimize stent implantation by accurate identification of lipid margins, and thus cover all the segments with high lipid burden. Dixon et al. [97] analyzed 75 lesions with NIRS imaging and demonstrated that lipid-core plaque extended beyond the angiographic margins of the initial target lesion in 16% of cases. Hanson et al. [98] showed that atheroma, defined as plaque burden >40% or LCP, extended beyond angiographic margins in 52 of the 58 lesions analyzed with NIRS-IVUS (90% of lesions), with a mean lesion length that was significantly longer when assessed by NIRS-IVUS as compared with angiography alone (19.8 ± 7.0 vs. 13.4 ± 5.9 mm;
Detection of lipid core in a lesion has also been used as one of the factors to consider in the decision to implant a bare metal stent (BMS) or a drug-eluting stent (DES). Several studies have demonstrated a greater frequency of stent thrombosis after DES implantation when struts were penetrating into a lipid-rich necrotic core plaque rather than in a non-yellow (fibrous) plaque [103, 104]. The absence of struts coverage by the formation of a neointima layer during vessel’s healing process was seen with both DES and BMS implantation in lipid-rich plaques, which is likely the underlying mechanism of stent thrombosis seen in those patients [105, 106]. Neoatherosclerosis is an important contributor to late-stent thrombosis with newer generation DES, as well as late in-stent restenosis. Histologically, neoatherosclerosis is characterized by the accumulation of lipid-laden macrophages within the neointima with or without necrotic core formation and/or calcification and can occur months to years following stent placement [107]. Originally described in postmortem studies, neoatherosclerosis has more recently been detected by intracoronary imaging. Ali et al. [108] used NIRS and OCT to assess the development of neoatherosclerosis in 65 consecutive patients with symptomatic in-stent restenosis. The prevalence of LCP within neointimal hyperplasia segments was 89% using NIRS versus 62% using OCT. Neoatherosclerosis was associated with significantly reduced minimal cap thickness with plaque rupture occurring exclusively in those patients. Moreover, DES had a higher prevalence and earlier occurrence of neoatherosclerosis, thinner cap, and more lipid burden and density. However, LCP identified by NIRS alone was not associated with periprocedural MI during treatment for in-stent restenosis, which reflects the limited ability of NIRS to differentiate lipid located within the neointimal tissue from a lipid core located underneath stent struts. Nevertheless, postmortem imaging and subsequent histology analysis showed that NIRS could correctly characterize lipid despite the presence of metal struts. Similar findings were reported in a study published by Madder et al. [109], whereas NIRS was not reliable for neoatherosclerosis detection when used as the sole imaging modality for LCP detection. The NIRS lipid signal could not distinguish neoatherosclerosis from fibroatheroma underlying the stent. No doubt that NIRS can detect coronary LCP, but it seems unlikely suitable as a standalone technique for accurate neoatherosclerosis detection and that the adjunction of IVUS or OCT will be required to determine the position of NIRS lipid signal relative to the underlying stent struts [110].
It was proposed that the growth of neointima tissue on the top of a vulnerable plaque might increase the thickness of the fibrous cap [103, 110, 111]. Brugaletta et al. [112] reported the ability of bioresorbable vascular scaffold (BVS) implantation to promote the growth of neointimal tissue, which acts as a barrier to isolate vulnerable plaques. An ongoing trial, the PROSPECT II ABSORB sub-study trial (Clinical Trials.org Identifier: NCT021711065), will randomize patients with plaques at high risk of causing future coronary events (plaque burden ≥70%) to receive an AbsorbTM BVS (Abbott Vascular, IL, USA) with optimal medical therapy (OMT) versus OMT alone. This sub-study aims to evaluate the changes in the plaque at 2 years follow-up. Clinically, large LCPs have been shown to be associated with MACE, especially periprocedural myocardial infarction [21]. Whether lipid burden influences long-term outcomes following stent implantation remains elusive.
2.6.5. Prevention of periprocedural complications
Approximately 3–15% of percutaneous coronary interventions are complicated by periprocedural myocardial infarction (PPMI) and no-reflow, in part by distal embolization of intraluminal thrombus and/or lipid-core plaque content, which is associated with adverse long-term outcomes [113, 114]. It was reported that periprocedural MIs are associated with increased atherosclerotic burden and large LCPs [115–118]. Indeed, embolization of the lipid core after stent implantation in a plaque with high lipid content has been identified as an important cause of periprocedural no-reflow and MI with and without the presence of intracoronary thrombus [118–120]. A pilot study performed in nine patients using an embolic protection device showed that embolized material consisted in fibrin and platelet aggregates, which reflects the highly thrombogenic content of necrotic core of large atheroma plaques and LCP [98, 120, 121]. In a sub-study of the COLOR (Chemometric Observation of Lipid-Core Plaques of Interest in Native Coronary Arteries) registry, a prospective multicenter observational study aiming to determine a relationship between NIRS-defined high LCBI and periprocedural MI, Goldstein et al. [20] analyzed the cardiac biomarkers of 62 stable patients undergoing PCI. The main findings were that periprocedural MI, defined in the study as a postprocedural elevation above three times the upper limit of normal (ULN) for either creatine kinase-MB (CK-MB) or cTnI measured 4–24 h after PCI, occurred in nine patients (14.5%) and was more common among patients with a maxLCBI4mm ≥ 500 (7 of 14 patients, 50%) versus patients with a maxLCBI4mm < 500 (2 of 48 patients, 4.2%). The authors concluded that a high LCP, defined as a maxLCBI4mm ≥ 500, was associated with periprocedural events. These results are concordant with the registry study conducted by Raghunathan et al. [21], in which the analysis of 30 patients who underwent pre-procedure NIRS imaging showed a postprocedural increase of CK-MB more than three times the UNL in 27% of patients with a ≥1 yellow blocks (
Distal embolization, as an important mechanism of periprocedural MI, was further supported by several studies that have demonstrated a significant decrease in the size of LCP after stenting [122–124]. Stone et al. showed in the CANARY trial that LCP measured as LCBI by NIRS in the stented vessels reduces with PCI treatment, with a significant reduction of median LCBI from 143.2 before PCI to 17.9 after PCI (
In order to prevent periprocedural MI during PCI, several strategies were proposed during stenting procedures, including aspiration thrombectomy, embolization distal-protection devices, vasodilators, intensive anticoagulation, and antiplatelet therapies. The CANARY (Coronary Assessment by NIR of Atherosclerotic Rupture-Prone Yellow) trial randomized 85 stable angina patients undergoing stent implantation of a single native coronary lesion and pre-procedure NIRS-defined maxLCBI4mm ≥ 600 to PCI with or without distal-protection filter [125]. Among the 31 randomized cases with a maxLCBI4mm≥ 600, there was no difference in the rates of periprocedural MI with or without the use of distal-protection filter (35.7 vs. 23.5%, respectively; relative risk 1.52; 95% CI: 0.50–4.60,
Thrombectomy is often used to aspirate thrombus and restore blood flow in the culprit vessel during primary PCI in STEMI patients. The clinical benefits of routine thrombus aspiration remain a matter of debate, since the TAPAS (Thrombus Aspiration during Percutaneous Coronary Intervention in Acute Myocardial Infarction) study demonstrated a reduction of mortality while larger studies such as TASTE (Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia) and TOTAL (Trial of Routine Aspiration Thrombectomy with PCI versus PCI Alone in Patients with STEMI) did not show a reduction of cardiovascular mortality, with an increased rate of stroke at a 30-day follow-up in the TOTAL trial [126–128]. Erlinge et al. [129] performed NIRS-IVUS imaging in 18 ACS patients to examine if aspiration thrombectomy reduced the lipid content of ACS culprit plaques. The culprit lipid content was quantified by NIRS-IVUS before and after thrombectomy as the lipid-core burden index (LCBI), and aspirates were examined by histological staining for lipids, calcium, and macrophages. Culprit lesions were found to have high lipid content prior to thrombectomy, which resulted in a 28% reduction in culprit lesion lipid content (pre-aspiration LCBI 466 ± 141 vs. post-aspiration 335 ± 117,
As aforementioned, the use of intracoronary NIRS-IVUS imaging for accurate identification of LCP lesions prone to embolize, as well as different treatment strategies, for periprocedural MI prevention are attractive approaches, however their clinical benefits on myocardial salvage and prevention of embolization remains to be demonstrated in future studies.
2.6.6. Monitoring effects of lipid-lowering therapies
It is well known that statin therapy reduces rates of cardiovascular events in secondary prevention. The pharmacological effects of specific lipid-reducing agents that reduce free and esterified cholesterol could be evaluated with NIRS, as it informs on the lipid content of coronary artery plaques over time. The demonstration of markedly reduced LCBI values in a patient after 1 year of high-dose rosuvastatin therapy was the first indication that NIRS-IVUS could be used to evaluate the effect of systemic anti-atherosclerotic medical therapy [130]. In the YELLOW (Reduction in Yellow Plaque by Aggressive Lipid-Lowering Therapy) trial, Kini et al. [22] prospectively randomized 87 patients with multivessel coronary artery disease undergoing PCI with one culprit and one nonculprit hemodynamically significant lesions, defined by fractional flow reserve (FFR <0.80), to receive intensive statin therapy (rosuvastatin of 40 mg daily) or standard lipid-lowering therapy. The nonculprit lesions had a baseline assessment by NIRS-IVUS and FFR, prior to randomization. Rosuvastatin therapy resulted in a significant reduction in the plaque lipid content/maxLCBI4mm compared to standard therapy. The significant reduction in maxLCBI4mm associated with intensive statin therapy was observed across subgroups of the study population, based on age, gender, presence of diabetes, and baseline lipid profile. However, no significant changes were observed for the maxLCBI4mm and LCBI measurements at the lesion site in the standard lipid treatment group at follow-up. Although baseline LCBI was significantly higher in patients randomly allocated to intensive versus standard therapy, the YELLOW trial highlights that LCP measured by NIRS was associated with CAD and that it could be a potential tool to monitor regression of the disease in phase II clinical trials evaluating novel anti-atheromatous therapies.
A similar study of the effect of rosuvastatin treatment on the coronary plaque composition and necrotic core, the IBIS-3 (Integrated Biomarker and Imaging Study 3) trial, failed to demonstrate a significant reduction of necrotic core volume or LCBI under intensive rosuvastatin therapy for 1 year [131]. The effects of high-dose statin therapy are being further investigated in the YELLLOW II trial (Clinical Trials.org Identifier: NCT01837823), a phase II clinical study, that aims to assess the regression of plaque lipid content and changes in plaque morphology from atherosclerotic lesions after 8–12 weeks of high-dose statin therapy by utilizing NIRS, IVUS, and OCT imaging modalities in the coronary arteries.
2.7. Limitations of the technology
Near-infrared spectroscopy (NIRS) identifies the chemical signature of the lipid component, specifically lipid core-containing coronary plaque (LCP). The main limitations of NIRS technology are the lack of information regarding the lumen, plaque anatomy, and status of the fibrous cap or its attenuation. Although NIRS may be one of the most sensitive modalities to detect lipid-core plaques, it cannot provide information on the depth of the lipid core. Moreover, the accurate measurement of lipid volume/burden with NIRS has not been validated [132]. To overcome these pitfalls, a new combined imaging catheter adding intravascular ultrasound (IVUS) imaging was developed. However, since intravascular ultrasound has a low sensitivity to visualize lipid inside a plaque, the additional value of this new system will require further evaluation [26].
The clinical relevance of imaging specific features of the vulnerable plaque for risk stratification and clinical decision making remains unclear. Higher-resolution imaging modalities, such as OCT, better assessed determinants of vulnerable plaques than NIRS; however, there is currently no commercialized system combining OCT and NIRS modalities. The prognostic utility and incremental value of NIRS when associated with biomarkers of plaque vulnerability assessed by IVUS (plaque burden, MLA, and remodeling) remains to be investigated [26, 133]. Many studies have brought evidence that IVUS-guided PCI achieves superior outcomes compared to angiography guidance alone [134]. The potential value of adding NIRS for lipid-rich plaques at risk of embolization and for a complete coverage of LCPs remains to be investigated. NIRS-IVUS-imaging modality is an invasive diagnostic modality that targets patients in the setting of secondary prevention, thus precluding its utilization for primary prevention, along with other invasive imaging technologies.
2.8. Future trials and perspective
NIRS-IVUS-imaging technology is improving and should become a sensitive modality for coronary plaque characterization. A new algorithm for collagen detection has been developed using the same spectroscopy signal, which enables to detect the amount of fibrous tissue over the LCP (thin or thick fibrous cap) [15]. This technology will be further optimized by adding a recently developed, but not yet available, high-resolution IVUS, which will allow to accurately differentiate between thin and thick fibrous caps. Co-registration of NIRS with other imaging modalities is also being developed. The use of combined OCT-NIRS catheters has been recently demonstrated as a proof of concept [15].
NIRS-IVUS has also been used in the carotid arteries to detect LCP, which could represent a suitable imaging modality to determine the risk of stroke or the risk of complications during carotid stent placement or endarterectomy. However, this new clinical application remains to be validated in future studies [15].
Multiple prospective outcome studies are currently ongoing to evaluate the ability of NIRS-IVUS imaging to detect vulnerable plaques that are likely to cause future adverse events. Among those studies are the LRP trial (Lipid-rich Plaque Study; Clinical Trial.org Identifier: NCT02033694), the PROSPECT II ABSORB trial (Providing Regional Observations to Study Predictors of Events in the Coronary Tree II; Clinical Trial.org Identifier: NCT02171065), and the ORACLE-NIRS trial (Lipid-core plaque association with clinical events: a near-infrared spectroscopy study; Clinical Trial.org Identifier: NCT02265146). The YELLOW II trial (NCT01837823), which aims to evaluate the effects of rosuvastatin treatment on lipid content after 8–10 weeks of treatment regimen, has completed patient enrolment but results are still pending. Another trial has been completed and awaiting for results publication, the NIRS-TICAGRELOR trial (Clinical Trial.org Identifier: NCT02282332), which aims to evaluate the effect of the P2Y12 inhibitor ticagrelor (AstraZeneca, Cambridge, England) on plaque stabilization and reduction of inflammation by NIRS-defined reduction of LCBI in patients on long-term statin therapy undergoing non-urgent PCI.
3. Conclusion
NIRS is a promising tool for the detection of vulnerable plaques in CAD patients, PCI-guidance procedures, and assessment of lipid-lowering therapies. NIRS-IVUS has been shown to be a reliable and reproducible modality for the detection of intracoronary LCPs, with validation using the current gold-standard, histology. It has already been shown that this imaging modality is highly specific for identifying NSTEMI and STEMI culprit plaques, that it can be used to follow the progression of vulnerable plaques over time, and to evaluate the effect of lipid-lowering therapies and intracoronary devices. Moreover, preliminary data have shown that NIRS-IVUS-imaging technology can identify vulnerable patients. Multiple ongoing clinical trials will hopefully validate this tool for vulnerable plaque and patient detection, as well as for treatment management and follow-up of patients with CAD.
Abbreviations
Acute coronary syndrome
Bare-metal stent
Bioresorbable vascular scaffold
Coronary artery disease
Coronary artery bypass graft
Conventional coronary angiography
Creatine kinase-MB
Cardiac troponin I
Drug-eluting stent
French
Fibroatheroma
US Food and Drug Administration
Frequency-domain optical coherence tomography
Fractional flow reserve
Intravascular ultrasound
Lipid-core burden index
Lipid-core plaque
Low-density lipoprotein
Lipid-rich plaque
Major adverse cardiac events
Major adverse cardiac and cerebrovascular events
Maximum lipid-core burden index in 4-mm region
Myocardial infarction
Minimal lumen area
Necrotic core
Near-infrared spectroscopy
Non-ST segment elevation myocardial infarction
Optical coherence tomography
Optical frequency domain imaging
Optimal medical therapy
Percutaneous coronary intervention
Periprocedural myocardial infarction
Quantitative coronary angiography
Region of interest
Sudden cardiac death
ST-segment elevation myocardial infarction
Thin-cap fibroatheroma
Unstable angina
Upper limit of normal
Virtual histology
References
- 1.
White HD, Chew DP. Acute myocardial infarction. Lancet. 2008;372:570–584. DOI: 10.1016/S0140-6736(08)61237-4 - 2.
Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014;114:1852–66. DOI: 10.1161/CIRCRESAHA.114.302721 - 3.
Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation. 1989;79:733–743. DOI: 10.1161/01.CIR.79.4.733 - 4.
Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–1275. DOI: 10.1161/01.ATV.20.5.1262 - 5.
Chamuleau SA, van Eck-Smit BL, Meuwissen M, Piek JJ. Adequate patient selection for coronary revascularization: an overview of current methods used in daily clinical practice. Int J Cardiovasc Imaging 2002;18:5–15. DOI: 10.1023/A:1014372125457 - 6.
Mintz GS, Painter JA, Pichard AD, Kent KM, Satler LF, Popma JJ, Chuang YC, Bucher TA, Sokolowicz LE, Leon MB. Atherosclerosis in angiographically “normal” coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:1479–1485. DOI: 10.1016/0735-1097(95)00088-L - 7.
Glagov S, Weisenberg E, Zarins C, Stankunavicius R, Kolletis G. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:1371–1375. DOI: 10.1056/NEJM198705283162204. - 8.
Goldstein JA. Angiographic plaque complexity: the tip of the unstable plaque iceberg. J Am Coll Cardiol. 2002;39:1464–1467. DOI: 10.1016/S0735-1097(02)01772-2 - 9.
Tardif JC, Lesage F, Harel F, Romeo P, Pressacco J. Imaging biomarkers in atherosclerosis trials. Circ Cardiovasc Imaging. 2011;4:319–333. DOI: 10.1161/CIRCIMAGING.110.962001 - 10.
Waxman S, Dixon SR, L’Allier P, Moses JW, Peterson JL, Cutlip D, Tardif JC, Nesto RW, Muller JE, Hendricks MJ, Sum ST, Gardner CM, Goldstein JA, Stone GW, Krucoff MW. In vivo validation of a catheter-based near-infrared spectroscopy system for detection of lipid core coronary plaques: initial results of the SPECTACL study. JACC Cardiovasc Imaging. 2009;2:858–868. DOI: 10.1016/l.jcmg.2009.05.001 - 11.
Cassis LA, Lodder RA. Near-IR imaging of atheromas in living arterial tissue. Anal Chem. 1993;65:1247–1256. DOI: 10.1021/ac00057a023 - 12.
Wang J, Geng YJ, Guo B, Klima T, Lal BN, et al. Near-infrared spectroscopic characterization of human advanced atherosclerotic plaques. J Am Coll Cardiol. 2002;39:1305–1313. DOI: 10.1016/S0735-1097(02)01767-9 - 13.
Moreno PR, Muller JE. Identification of high-risk atherosclerotic plaques: a survey of spectroscopic methods. Curr Opin Cardiol. 2002;17:638–647. ISSN: 0268-4705 - 14.
Jaguszewski M, Klingerberg R. Intracoronary near-infrared spectroscopy (NIRS) imaging for detection of lipid content of coronary plaques: current experience and future perspectives. Curr Cardiovasc Imaging Rep. 2013;6:426–430. DOI:10.1007/s12410-013-9224-2 - 15.
Erlinge D. Near-infrared spectroscopy for intracoronary detection of lipid-rich plaques to understand atherosclerotic plaque biology in man and guide clinical therapy. J Intern Med. 2015;278:110–125. DOI: 10.1111/joim.12381 - 16.
Caplan JD, Waxman S, Nesto RW, Muller JE. Near-infrared spectroscopy for the detection of vulnerable coronary artery plaques. J Am Coll Cardiol. 2006;47:C92–96. DOI: 10.1016/j.jacc.2005.12.045 - 17.
Madder RD, Goldstein JA, Madden SP, Puri R, Wolski K, Hendricks M, Sum ST, Kini A, Sharma S, Rizik D, Brilakis ES, Shunk KA, Petersen J, Weisz G, Virmani R, Nicholls SJ, Maehara A, Mintz GS, Stone GW, Muller JE. Detection by near-infrared spectroscopy of large lipid core plaques at culprit sites in patients with acute ST-segment elevation myocardial infarction. JACC Cardiovasc Interv. 2013;6:838–846. DOI:10.1016/j.jcin.2013.04.012 - 18.
Madder RD, Husaini M, Davis AT, Van Oosterhout S, Harnek J, Götberg M, Erlinge D. Detection by near-infrared spectroscopy of large lipid cores at culprit sites in patients with non-ST-segment elevation myocardial infarction and unstable angina. Catheter Cardiovasc Interv. 2015;86:1014–1021. DOI: 10.1002/ccd.25754 - 19.
de Boer SPM, Brugaletta S, Garcia-Garcia HM, Simsek C, Heo JH, Lenzen MJ, Schultz C, Regar E, Zijlstra F, Boersma E, Serruys PW. Determinants of high cardiovascular risk in relation to plaque-composition of a non-culprit coronary segment visualized by near-infrared spectroscopy in patients undergoing percutaneous coronary intervention. Eur Heart J. 2014;35:282–289. DOI: 10.1093/eurheartj/eht378 - 20.
Goldstein JA, Maini B, Dixon SR, Brilakis ES, Grines CL, Rizik DG, Powers ER, Steinberg DH, Shunk KA, Weisz G, Moreno PR, Kini A, Sharma SK, Hendricks MJ, Sum ST, Madden SP, Muller JE, Stone GW, Kern MJ. Detection of lipid-core plaques by intracoronary near-infrared spectroscopy identifies high risk of periprocedural myocardial infarction. Circ Cardiovasc Interv. 2011;4:429–437. DOI: 10.1161/CIRCINTERVENTIONS.111.963264 - 21.
Raghunathan D, Abdel-Karim A-RR, Papayannis AC, daSilva M, Jeroudi OM, Rangan BV, Banerjee S, Brilakis ES. Relation between the presence and extent of coronary lipid core plaques detected by near-infrared spectroscopy with postpercutaneous coronary intervention myocardial infarction. Am J Cardiol. 2011;107:1613–1618. DOI: 10.1016/j.amjcard.2011.01.044 - 22.
Kini AS, Baber U, Kovacic JC, Limaye A, Ali ZA, Sweeny J, et al. Changes in plaque lipid content after short-term intensive versus standard statin therapy: the YELLOW trial (reduction in yellow plaque by aggressive lipid-lowering therapy). J Am Coll Cardiol. 2013;62:21–29. DOI: 10.1016/j.jacc.2013.03.058 - 23.
Oemrawsingh RM, Cheng JM, Garcia-Garcia HM, van Geuns R-J, de Boer SPM, Simsek C, et al. Near-infrared spectroscopy predicts cardiovascular outcome in patients with coronary artery disease. J Am Coll Cardiol. 2014;64:2510–2518. DOI: 10.1016/j.jacc.2014.07.998 - 24.
Jang IK. Near infrared spectroscopy: another toy or indispensable diagnostic tool? Circ Cardiovasc Interv. 2012;5:10–11.DOI: 10.1161/CIRCINTERVENTIONS.111.967935 - 25.
Jaffer FA, Verjans JW. Molecular imaging of atherosclerosis: clinical state-of-the-art. Heart 2014;100:1469–1477. DOI: 10.1136/heartjnl-2011-301370 - 26.
Kilic ID, Caiazzo G, Fabris E, Serdoz R, Abou-Sherif S, Madden S, Moreno PR, Goldstein J, Di Mario C. Near-infrared spectroscopy-intravascular ultrasound: scientific basis and clinical applications. Eur Heart J. 2015;16:1299–1306. DOI:10.1093/ehjci/jev208 - 27.
Dempsey RJ, Davis DG, Buice RG, Lodder RA. Biological and medical applications of near-infrared spectroscopy. Appl Spectrosc OSA. 1996;50:18A–34A. DOI: 10.1366/0003702963906537 - 28.
Downes A, Elfick A. Raman spectroscopy and related techniques in biomedicine. Sensors. 2010;10:1871–89. DOI: 10.3390/s100301871. - 29.
Hanlon EB, Manoharan R, Koo TW, Shafer KE, Motz JT, Fitzmaurice M, Kramer JR, Itzkan I, Dasari RR, Feld MS. Prospects for in vivo Raman spectroscopy. Phys Med Biol. 2000;45:R1–59. DOI: 10.1088/0031-9155/45/2/201 - 30.
de Lima CJ, Sathaiah S, Silveira L, Zângaro RA, Pacheco MT. Development of catheters with low fiber background signals for Raman spectroscopic diagnosis applications. Artif Organs. 2000;24:231–234. DOI: 10.1046/j.1525-1594.2000.06525.x - 31.
Marcu L, Fishbein MC, Maarek JM, Grundfest WS. Discrimination of human coronary artery atherosclerotic lipid-rich lesions by time-resolved laser-induced fluorescence spectroscopy. Arterioscler Thromb Vasc Biol. 2002;21:1244–1250. DOI: 10.1161/hq0701.092091 - 32.
Toussaint JF, Southern JF, Fuster V, Kantor HL.13C-NMR spectroscopy of human atherosclerotic lesions. Relation between fatty acid saturation, cholesteryl ester content, and luminal obstruction. Arterioscler Thromb. 1994;14:1951–1957. DOI: 10.1161/01.ATV.14.12.1951 - 33.
Peng S, Guo W, Morrisett JD, Johnstone MT, Hamilton JA. Quantification of cholesteryl esters in human and rabbit atherosclerotic plaques by magic-angle spinning 13C-NMR. Arterioscler Thromb Vasc Biol. 2000;20:2682–2688. DOI: 10.1161/01.ATV.20.12.2682 - 34.
Trouart TP, Altbach Mi, Hunter GC, Eskelson CD, Gmitro AF. MRI and NMR spectroscopy of the lipids of atherosclerotic plaque in rabbits and humans. Magn Res Med. 1997;38:19–26. DOI: 10.1002/mrm.1910380105 - 35.
Shydo B, Hendricks M, Frazier G. Imaging of plaque composition and structure with the TVC Imaging SystemTM and TVC InsightTM catheter. J Invasive Cardiol. 2013;25:5A–8A. ISSN: 1557-2501 - 36.
Negi SI, Didier R, Ota H, Magalhaes MA, Popma CJ, Kollmer MR, Spad M-A, Torguson R, Suddath W, Satler LF, Pichard A, Waksman R. Role of near-infrared spectroscopy in intravascular coronary imaging. Cardiovasc Revasc Med. 2015;16:299–305. DOI: 10.1016/j.carrev.2015.06.001 - 37.
Lavine BK, Workman J. Chemometrics. Anal Chem. 2013;85:705–714. DOI: 10.1021/ac303193j - 38.
Gardner CM, Tan H, Hull EL, Lisauskas JB, Sum ST, Meese TM, Jiang C, Madden SP, Caplan JD, Burke AP, Virmani R, Goldstein J, Muller JE. Detection of lipid core coronary plaques in autopsy specimens with a novel catheter-based near-infrared spectroscopy system. JACC Cardiovasc Imaging. 2008;1:638–648. DOI: 10.1016/j.jcmg.2008.06.001 - 39.
Danek BA, Karatasakis A, Madder RD, Muller JE, Madden S, Banerjee S, Brilakis ES. Experience with the multimodality near-infrared spectroscopy/intravascular ultrasound coronary imaging system: principles, clinical experience, and ongoing studies. Curr Cardiovasc Imaging Rep. 2016;9:7. DOI: 10.1007/s12410-015-9369-2 - 40.
Sum ST, Madden SP, Hendricks MJ, Chartier SJ, Muller JE. Near-infrared spectroscopy for the detection of lipid core coronary plaques. Curr Cardiovasc Imaging Rep. 2009;2:307–415. DOI: 10.1007/s12410-009-0036-3 - 41.
Lodder RA, Cassis L, Ciurczak EW. Arterial analysis with a novel near-IR fiber-optic probe. Spectroscopy. 1990;5:12–17. - 42.
Jarros W, Neumeister V, Lattke P, Schuh D. Determination of cholesterol in atherosclerotic plaques using near infrared diffuse reflection spectroscopy. Atherosclerosis. 1999;147:327–337. DOI: 10.1016/S0021-9150(99)00203-8 - 43.
Moreno PR, Lodder RA, Purushothaman KR, Charash WE, O’Connor WN, Muller JE. Detection of lipid pool, thin fibrous cap, and inflammatory cells in human aortic atherosclerotic plaques by near-infrared spectroscopy. Circulation 2002;105:923–927. DOI:10.1161/hc0802.104291 - 44.
Moreno PR, Ryan SE, Hopkins D, Wise B, Purushothaman KR, Charash WE, O’Connor W, Muller JE. Identification of lipid-rich plaques in human coronary artery autopsy specimens by near-infrared spectroscopy. J Am Coll Cardiol. 2001;37:356A. DOI: 10.1016/S0735-1097(01)80005-X - 45.
Moreno PR, Ryan SE, Hopkins D. Identification of lipid-rich aortic atherosclerotic plaques in living rabbit with a near infrared spectroscopy catheter. J Am Coll Cardiol. 2001;37:3A. DOI: 10.1016/S0735-1097(01)80001-2 - 46.
Marshik B, Tan H, Tang J, Lindquist A, Zuluaga A. Discrimination of lipid-rich plaques in human aorta specimens with NIR spectroscopy through whole blood. Am J Cardiol. 2002;90:129H. DOI: 10.1016/S0002-9149(02)02727-3 - 47.
Marshik B, Tan H, Tang J, Lindquist A, Zuluaga A. Detection of thin-capped fibroatheromas in human aorta tissue with near infrared spectroscopy through blood. J Am Coll Cardiol. 2003;41:42. DOI :10.1016/S0735-1097(03)80181-X - 48.
Waxman S, Tang J, Marshik BJ, Tan H, Khabbaz KR, Connolly RJ, Dunn TA, Zuluaga AF, DeJesus S, Caplan JD, Muller EJ. In vivo detection of a coronary artificial target with a near infrared spectroscopy catheter.Am J Cardiol. 2004;94:141E. DOI: 10.1016/j.amjcard.2004.07.055 - 49.
Waxman S, Khabba K, Connolly R. Intravascular imaging of atherosclerotic human coronaries in a porcine model: a feasibility study. Int J Cardiovasc Imaging. 2008;24:37–44. DOI: 10.1007/s10554-007-9227-7 - 50.
Garcia BA, Wood F, Cipher D, Banerjee S, Brilakis ES. Reproducibility of near-infrared spectroscopy for the detection of lipid core coronary plaques and observed changes after coronary stent implantation. Catheter Cardiovasc Interv. 2010; 76:359–365. DOI: 10.1002/ccd.22500 - 51.
Abdel-Karim A-RR, Rangan B V, Banerjee S, Brilakis ES. Intercatheter reproducibility of near-infrared spectroscopy for the in vivo detection of coronary lipid core plaques.Catheter Cardiovasc Interv. 2011; 77:657–661. DOI: 10.1002/ccd.22763 - 52.
Kolodgie FD, Burke AP, Farb A, Gold HK, Yuan J, Narula J, Finn AV, Virmani R. The thin-cap fibroatheroma: a type of vulnerable plaque: the major precursor lesion to acute coronary syndromes. Curr Opin Cardiol. 2001;16:285–292. ISSN: 0268-4705 - 53.
Rizik D, Goldstein JA. NIRS-IVUS imaging to characterize the composition and structure of coronary plaques. J Invasive Cardiol. 2013;25:2A–4A. ISSN: 1557-2501 - 54.
Garcia-Garcia HM, Serruys PW. Advances in the invasive diagnosis and treatment of vulnerable coronary plaques. Eur Cardiol Rev 2008;4:105–110. ISSN: 0268-4705 - 55.
Nissen SE. Halting the progression of atherosclerosis with intensive lipid lowering: results from the Reversal of Atherosclerosis with Aggressive lipid Lowering (REVERSAL) trial. Am J Med. 2005;118:22–27. DOI: 10.1016/j.amjmed.2005.09.020 - 56.
Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, Davignon J, Erbel R, Fruchart JC, Tardif JC, Schoenhagen P, Crowe T, Cain V, Wolski K, Goormastic M, Tuzcu EM. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: The asteroid trial. JAMA. 2006;295:1556–65. DOI: 10.1001/jama.295.13.jpc60002 - 57.
Nicholls SJ, Ballantyne CM, Barter PJ, Chapman J, Erbel RM, Libby P, Raichlen JS, Uno K, Borgman M, Wolski K, Nissen SE. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med. 2011;365:2078–2087. DOI: 10.1056/NEJMoa1110874 - 58.
Lee SY, Mintz GS, Kim SY, Hong YJ, Kim SW, Okabe T, Pichard AD, Satler LF, Kent KM, Suddath WO, Waksman R, Weissman NJ. Attenuated plaque detected by intravascular ultrasound clinical, angiographic, and morphologic features and post-percutaneous coronary intervention complications in patients with acute coronary syndromes. JACC Cardiovasc Interv. 2009;2:65–72. DOI: 10.1016/j.jcin.2008.08.022 - 59.
Guedes A, Tardif JC. Intravascular ultrasound assessment of atherosclerosis. Curr Atheroscler Rep. 2004;6:219–224. DOI: 10.1007/s11883-004-0035-4 - 60.
Vince DG, Dixon KJ, Cothren RM, Cornhill JF. Comparison of texture analysis methods for the characterization of coronary plaques in intravascular ultrasound imaging.Comput Med Imaging Graph 2000;24:221–229. DOI: 10.1016/S0895-6111(00)00011-2 - 61.
Kawasaki M, Takatsu M, Noda T, Ito Y, Kunishima A, Arai M, Nishigaki K, Takemura G, Morita N, Minatoguchi S, Fujiwara H. Noninvasive quantitative tissue characterization and two-dimensional color-coded map of human atherosclerotic lesions using ultrasound integrated backscatter: comparison between histology and integrated backscatter images. J Am Coll Cardiol. 2001;38:486–492. DOI: 10.1016/S0735-1097(01)01393-6 - 62.
Nasu K, Tsuchikane E, Katoh O, Vince G, Virmani R, Surmely JF, Murata A, Takeda Y, Ito T, Ehara M, Matsubara T, Terashima M, Suzuki T. Accuracy of in vivo coronary plaque morphology assessment: a validation study of in vivo virtual histology compared with in vitro histopathology. J Am Coll Cardiol. 2006;47:2405–2412. DOI: 10.1016/j.jacc.2006.02.044 - 63.
Van Herck G, De Meyer G, Ennekens G, Van Herck P, Herman A, Vrints C. Validation of in vivo plaque characterisation by virtual histology in a rabbit model of atherosclerosis. EuroIntervention 2009;5:149–156. - 64.
Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS, Mehran R, McPherson J, Farhat N, Marso SP, Parise H, Templin B, White R, Zhang Z, Serruys PW. A prospective natural-history study of coronary atherosclerosis. N Engl J Med 2011;364:226–235. DOI: 10.1056/NEJMoa1002358 - 65.
Calvert PA, Obaid DR, O’Sullivan M, Shapiro LM, McNab D, Densem CG, Schofield PM, Braganza D, Clarke SC, Ray KK, West NE, Bennett MR. Association between IVUS finding and adverse outcomes in patients with coronary artery disease. The VIVA (VH-IVUS in vulnerable atherosclerosis) study. J Am Coll Cardiol Imaging 2011;8:894–901. DOI: 10.1016/j.jcmg.2011.05.005 - 66.
Kawaguchi R, Oshima S, Jingu M, Tsurugaya H, Toyama T, Hoshizaki H, Taniguchi K. Usefulness of virtual histology intravascular ultrasound to predict distal embolization for ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1641–1646. DOI: 10.1016/j.jacc.2007.06.051 - 67.
Claessen BE, Maehara A, Fahi M, Xu K, Stone GW, Mintz GS. Plaque composition by intravascular ultrasound and distal embolization after percutaneous coronary intervention. JACC Cardiovasc Imaging. 2012;S111–S118. DOI: 10.1016/j.jcmg.2011.11.018 - 68.
Jang JS, Jin HY, Seo JS, Yang TH, Kim DK, Park YA, Cho KI, Park YH, Kim DS. Meta-analysis of plaque composition by intravascular ultrasound and its relation to distal embolization after percutaneous coronary intervention. Am J Cardiol. 2013;111:968–972. DOI: 10.1016/j.amjcard.2012.12.016 - 69.
Stone PH, Saito S, Takahashi S, Makita Y, Nakamura S, Kawasaki T, Takahashi A, Katsuki T, Nakamura S, Namiki A, Hirohata A, Matsumura T, Yamazaki S, Yokoi H, Tanaka S, Otsuji S, Yoshimachi F, Honye J, Harwood D, Reitman M, Coskun AU, Papafaklis MI, Feldman CL. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION study. Circulation. 2012;126:172–181. DOI: 10.1161/CIRCULATIONAHA.112.096438 - 70.
Cheng JM, Garcia-Garcia HM, de Boer SP, Kardys I, Heo JM, Akkerhuis KM, Oemrawsingh RM, van Domburg RT, Ligthart J, Witberg KT, Regar E, Serruy PW, van Geuns RJ, Boersma E. In vivo detection of high-risk coronary plaques by radiofrequency intravascular ultrasound and cardiovascular outcome: results of the ATHEROREMO-IVUS study. Eur Heart J. 2014;35:639–647. DOI: 10.1093/eurheartj/eht484 - 71.
Huang D, Swanson EA, Lin CP, Schuman JS, Stinson WG, Chang W, Hee MR, Flotte T, Gregory K, Puliafito CA, et al. Optical coherence tomography. Science. 1991;254:1178–1181. DOI: 10.1126/science.1957169 - 72.
Prati F, Regar E, Mintz GS, Arbustini E, Di Mario C, Jang IK, Akasaka T, Costa M, Guagliumi G, Grube E, Ozaki Y, Pinto F, Serruys PW. Expert review document on methodology, terminology, and clinical applications of optical coherence tomography: physical principles, methodology of image acquisition, and clinical application for assessment of coronary arteries and atherosclerosis. Eur Heart J. 2010;31:401–415. DOI: 101093/eurheartj/ehp433 - 73.
Ozaki Y, Okumura M, Ismail TF, Naruse H, Hattori K, Kan S, Ishikawa M, Kawai T, Takagi Y, Ishii J, Prati F, Serruys PW. The fate of incomplete stent apposition with drug-eluting stents: an optical coherence tomography-based natural history study. Eur Heart J. 2010;31:1470–1476. DOI: 10.1093/eurheartj/ehq066 - 74.
Onuma Y, Serruys PW, Perkins LE, Okamura T, Gonzalo N, Garcia-Garcia HM, Regar E, Kamberi M, Powers JC, Rapoza R, van Beusekom H, van der Giessen W, Virmani R. Intracoronary optical coherence tomography and histology at 1 month and 2, 3, and 4 years after implantation of everolimus-eluting bioresorbable vascular scaffolds in a porcine coronary artery model: an attempt to decipher the human optical coherence tomography images in the ABSORB trial. Circulation. 2010;122:2288–2300. DOI: 10.1161/CIRCULATIONAHA.109.921528 - 75.
Radu MD, Falk E - 76.
Takarada S, Imanishi T, Liu Y, Ikejima H, Tsujioka H, Kuroi A, Ishibashi K, Komukai K, Tanimoto T, Ino Y, Kitabata H, Kubo T, Nakamura N, Hirata K, Tanaka A, Mizukoshi M, Akasaka T. Advantage of next-generation frequency-domain optical coherence tomography compared with conventional time-domain system in the assessment of coronary lesion. Catheter Cardiovasc Interv. 2010;75:202–206. DOI: 10.1002/ccd.22273 - 77.
Madder RD, Smith JL, Dixon SR, Goldstein JA. Composition of target lesions by near-infrared spectroscopy in patients with acute coronary syndrome versus stable angina. Circ Cardiovasc Interv. 2012;5:55–61. DOI: 10.1161/CIRCINTERVENTIONS.111.963934 - 78.
Brilakis ES, Banerjee S. How to detect and treat coronary fibroatheroma: the synergy between IVUS and NIRS. JACC Cardiovasc Imaging. 2015;8:195–197. DOI: 10.1016/j.jcmg.2014.11.009 - 79.
Puri R, Madder RD, Madden SP, Sum ST, Wolski K, Muller JE, Andrews J, King KL, Kiyoko K, Uno K, Kapadia SR, Tuzcu EM, Nissen SE, Virmani R, Maehara A, Mintz GS, Nicholls SJ. Near-infrared spectroscopy enhances intravascular ultrasound assessment of vulnerable coronary plaque. A combined pathological and in vivo study. Arterioscler Thromb Vasc Biol. 2015;35:2423–2431. DOI: 10.1161/ATVBAHA.115.306118 - 80.
Brugaletta S, Garcia-Garcia HM, Serruys PW, de Boer S, Ligthart J, Gomez-Lara J, Witberg K, Diletti R, Wykrzykowska J, van Geuns RJ, Schultz C, Regar E, Duckers HJ, van Mieghem N, de Jaegere P, Madden SP, Muller JE, van der Steen AF, van der Giessen WJ, Boersma E. NIRS and IVUS for characterization of atherosclerosis in patients undergoing coronary angiography. JACC Cardiovasc Imaging. 2011;4:647–655. DOI: 10.1016/j.jcmg.2011.03.013 - 81.
Pu J, Mintz GS, Brilakis ES, Banerjee S, Abdel-Karim A-RR, Maini B, Biro S, Lee JB, Stone GW, Weisz G, Maehara A. In vivo characterization of coronary plaques: novel findings from comparing greyscale and virtual histology intravascular ultrasound and near-infrared spectroscopy. Eur Heart J. 2012; 33:372–383. DOI: 10.1093/eurheartj/ehr387 - 82.
Yonetsu T, Suh W, Abtahian F, Kato K, Vergallo R, Kim SJ, Jia H, McNulty I, Lee H, Jang IK. Comparison of near-infrared spectroscopy and optical coherence tomography for detection of lipid. Catheter Cardiovasc Interv. 2014;84:710–717. DOI: 10.1002/ccd.25084 - 83.
Roleder T, Kovacic JC, Ali Z, Sharma R, Cristea E, Moreno P, Sharma SK, Narula J, Kini AS. Combined NIRS and IVUS imaging detects vulnerable plaque using a single catheter system: a head-to-head comparison with OCT. EuroIntervention. 2014;10:303–311. DOI: 10.4244/EIJV1013A53 - 84.
Fur E, Brilakis ES. Comparative intravascular imaging for lipid core plaque: VH-IVUS vs OCT vs NIRS. J Invasive Cardiol. 2013;25:9A–13A. ISSN: 1557-2501 - 85.
Bourantas CV, Garcia-Garcia HM, Naka KK, Sakellarios A, Athanasiou L, Fotiadis DI, Michalis LK, Serruys PW. Hybrid intravascular imaging, current applications and prospective potential in the study of coronary atherosclerosis. J Am Coll Cardiol. 2013;61:1369–1378. DOI: 10.1016/j.jacc.2012.10.057 - 86.
Madder RD, Steinberg DH, Anderson D. Multimodality direct coronary imaging with combined near-infrared spectroscopy and intravascular ultrasound: initial US experience. Catheter Cardiovasc Interv. 2013;81:551–557. DOI: 10.1002/ccd.23358 - 87.
Madder RD, Wohns DH, Muller JE.Detection by intracoronary near-infrared spectroscopy of lipid core plaque at culprit sites in survivors of cardiac arrest. J Invasive Cardiol. 2014;26:78–79. DOI: - 88.
Gebhard C, L’Allier PL, Tardif JC. Near-infrared spectroscopy for cardiovascular risk assessment? Not ready for primetime. Eur Heart J. 2014;35:263–265. DOI: 10.1093/eurheartj/eht361 - 89.
Narula J, Nakano M, Virmani R, Kolodgie FD, Petersen R, Newcomb R, Malik S, Fuster V, Finn AV. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol. 2013; 61:1041–1051. DOI: 10.1016/j.jacc.2012.10.054 - 90.
Patel D, Hamamdzic D, Llano R, Patel D, Cheng L, Fenning RS, Bannan K, Wilensky RL. Subsequent development of fibroatheromas with inflamed fibrous caps can be predicted by intracoronary near infrared spectroscopy. Arterioscler Thromb Vasc Biol. 2013; 33:347–353. DOI: 10.1016/ATVBAHA.112.300710 - 91.
Kang SJ, Mintz GS, Pu J, Sum ST, Madden SP, Burke AP, Xu K, Goldstein JA, Stone GW, Muller JE, Virmani R, Maehara A. JACC Cardiovasc Imaging. 2015;8:184–194. DOI: 10.1016/j.jcmg.2014.09.021 - 92.
Oemrawsingh RM, Cheng JM, García-García HM, van Geuns R-J, de Boer SPM, Simsek C, Kardys I, Lenzen MJ, van Domburg RT, Regar E, Serruys PW, Akkerhuis KM, Boersma E. Near-infrared spectroscopy predicts cardiovascular outcome in patients with coronary artery disease. J Am Coll Cardiol. 2014; 64:2510–2518. DOI: 10.1016/j.jacc.2014.07.998 - 93.
Madder RD, Husaini M, Davis AT, VanOosterhout S, Kan M, Wohns D, McNamara RF, Wolschleger K, Gribar J, Collins JS, Jacoby M, Decker JM, Hendricks M, Sum ST, Madden S, Ware JH, Muller JE. Large lipid-rich coronary plaques detected by near-infrared spectroscopy at non-stented sites in the target artery identify patients likely to experience future major adverse cardiovascular events. Eur Heart J. 2016;17:393–399. - 94.
Witzenbichler B, Maehara A, Weisz G, Neumann FJ, Rinaldi MJ, Metzger DC, Henry TD, Cox DA, Duffy PL, Brodie BR, Stuckey TD, Mazzaferri EL, Xu K, Parise H, Mehran R, Mintz GS, Stone GW. Relationship between intravascular ultrasound guidance and clinical outcomes after drug-eluting stents: the assessment of dual antiplatelet therapy with drug-eluting stents (ADAPT-DES) study. Circulation. 2014;129:463–470. DOI : 10.1161/CIRCULATIONAHA.113.003942 - 95.
Jang JS, Song YJ, Kang W, Jin HY, Seo JS, Yang TH, Kim DK, Cho KI, Kim BH, Park YH, Je HG, Kim DS. Intravascular ultrasound-guided implantation of drug-eluting stents to improve outcome: a meta-analysis. JACC Cardiovasc Interv. 2014;7:233–243. DOI: 10.1016/j.jcin.2013.09.013 - 96.
Ahn JM, Kang SJ, Yoon SH, Park HW, Kang SM, Lee JY, Lee SW, Kim YH, Lee CW, Park SW, Mintz GS, Park SJ. Meta-analysis of outcomes after intravascular ultrasound-guided versus angiography-guided drug-eluting stent implantation in 26,503 patients enrolled in three randomized trials and 14 observational studies. Am J Cardiol. 2012;109:60–66. DOI: 10.1016/j.amjcard.2013.12.043 - 97.
Dixon SR, Grines CL, Munir A, Madder RD, Safian RD, Hanzel GS, Pica MC, Goldstein JA. Analysis of target lesion length before coronary artery stenting using angiography and near-infrared spectroscopy versus angiography alone. Am J Cardiol. 2012;109:60–66. DOI: 10.1016/j.amjcard.2011.07.068 - 98.
Hanson ID, Goldstein JA, Dixon SR, Stone GW. Comparison of coronary artery lesion length by NIRS-IVUS versus angiography alone. Coron Artery Dis. 2015;26:484–489. DOI: 10.1097/MCA.0000000000000263 - 99.
Saeed B, Banerjee S, Brilakis ES. Slow flow after stenting of a coronary lesion with a large lipid core plaque detected by near-infrared spectroscopy. EuroIntervention. 2010;6:545. - 100.
Awata M, Kotani J, Uematsu M, Morozumi T, Watanabe T, Onishi T, Iida O, Sera F, Nanto S, Hori M, Nagata S. Serial angiographic evidence of incomplete neointimal coverage after sirolimus-eluting stent implantation: comparison with bare-metal stents. Circulation. 2007;116:910–916. DOI: 10.1161/CIRCULATIONAHA.105.6609057 - 101.
Waxman S, Freilich MI, Stuer MJ, Shishkov M, Bilazarian S, Virmani R, Bouma BE, Tearney GJ. A case of lipid core plaque progression and rupture at the edge of a coronary stent: elucidating the mechanisms of drug-eluting stent failure. Circ Cardiovasc Interv. 2010;3:193–196. DOI: 10.1161/CIRCINTERVENTIONS.109.917955 - 102.
Stouffer GA.The use of near-infrared spectroscopy to optimize stent length.J Invasive Cardiol. 2013;25:5A–8A. ISSN: 1557-2501 - 103.
Joner M, Finn AV, Farb A, Mont EK, Kolodgie FD, Ladich E, Kutys R, Skorija K, Gold HK, Virmani R. Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk. J Am Coll Cardiol. 2006;48:193–202. DOI: 10.1016/j.jacc.2006.03.042 - 104.
Oyabu J, Ueda Y, Ogasawara N, Okada K, Hirayama, Kodama K. Angioscopic evaluation of neointima coverage: sirolimus drug-eluting stent versus bare metal stent. Am Heart J. 2006;152:1168–1174. DOI: 10.1016/j.ahj.2006.07.025 - 105.
Finn AV, Nakazawa G, Ladich E, Kolodgie FD, Virmani R. Does underlying plaque morphology play a role in vessel healing after drug-eluting stent implantation. JACC Cardiovasc Imaging. 2008;1:1485–1488. DOI: 10.1016/j.jcmg.2008.04.007 - 106.
Nakazawa G, Finn AV, Joner M, Ladich E, Kutys R, Mont EK, Gold HK, Burke AP, Kolodgie FD, Virmani R. Delayed arterial healing and increased late stent thrombosis at culprit sites after drug-eluting stent placement for acute myocardial infarction patients: an autopsy study. Circulation. 2008;118:1138–1145. DOI: 10.1161/CIRCULATIONAHA.107.762047 - 107.
Otsuka F, Byrne RA, Yahagi K, Mori H, Ladich E, Fowler DR, Kutys R, Xhepa E, Kastrati A, Virmani R, Joner M. Neoatherosclerosis: overview of histopathologic findings and implications for intravascular imaging assessment. Eur Heart J. 2015;36:2147–2159. DOI: 10.1093/eurheartj/ehv205 - 108.
Ali ZA, Roleder T, Narula J, Mohanty BD, Baber U, Kovacic JC, et al. Increased thin-cap neoatheroma and periprocedural myocardial infarction in drug-eluting stent restenosis: multimodality intravascular imaging of drug-eluting and bare-metal stents. Circ Cardiovasc Interv. 2013; 6:507–517. DOI: 10.1161/CIRCINTERVENTIONS.112.000248 - 109.
Madder RD, Khan M, Husaini M, Chi M, Dionne S, VanOosterhout S, Borgman A, Collins JS, Jacoby M. Combined near-infrared spectroscopy and intravascular ultrasound imaging of pre-existing coronary artery stents. Can near-infrared spectroscopy reliably detect neoatherosclerosis? Circ Cardiovasc Imaging. 2016;9:e003576. DOI: 10.1161/CIRCIMAGING.115.003576 - 110.
Ramcharitar S, Gonzalo N, van Geuns RJ, Garcia-Garcia HM, Wykrzykowska JJ, Ligthart JM. First case of stenting of a vulnerable plaque in the SECRIIT I trial-the dawn of a new era? Nat Rev Cardiol. 2009;6:374–378. DOI: 10.1038/nrcardio.2009.34 - 111.
Finn AV, Joner M, Nakazawa G, Kolodgie F, Newell J, John MC, et al. Pathological correlates of late drug-eluting stent thrombosis: strut coverage as a marker of endothelialization. Circulation. 2007;115:2435–2441. DOI: 10.1161/CIRCULATIONAHA.107.693739 - 112.
Brugaletta S, Radu MD, Garcia-Garcia HM, Heo JH, Farooq V, Girasis C, et al. Circumferential evaluation of the neointima by optical coherence tomography after ABSORB bioresorbable vascular scaffold implantation: can the scaffold cap the plaque? Atherosclerosis. 2012;221:106–112. DOI: 10.1016/j.atherosclerosis.2011.12.008 - 113.
Heusch G, Kleinbongard P, Böse D, Levkau B, Haude M, Schulz R, Erbel R. Coronary microembolization: From bedside to bench and back to bedside. Circulation. 2009;120:1822–1836. DOI:10.1161/CIRCULATIONAHA.109.888784 - 114.
Prasad A, Singh M, Lerman A, Lennon RJ, Holmes DR Jr, Rihal CS. Isolated elevation in troponin T after percutaneous coronary intervention is associated with higher long-term mortality. J Am Coll Cardiol. 2006;48:1765–1770. DOI: 10.1016/j.jacc.2006.04.102 - 115.
Tanaka A, Kawarabayashi T, Nishibori Y, Sano T, Nishida Y, Fukuda D, Shimada K, Yoshikawa J. No-reflow phenomenon and lesion morphology in patients with acute myocardial infarction. Circulation. 2002;105:2148–2152. DOI: 10.1016/01.CIR.0000015697.59592.07 - 116.
Limbruno U, De Carolo M, Pistolesi S, Micheli A, Petronio AS, Camacci T, Fontanini G, Balbarini A, Mariani M, De Caterina R. Distal embolization during primary angioplasty: histopathologic features and predictability. Am Heart J. 2005;150:102–108. DOI: 10.1016/j.ahj.2005.01.016 - 117.
Kotani J, Nanto S, Mintz GS, Kitakaze M, Ohara T, Morozumi T, Nagata S, Hori M. Plaque gruel of atheromatous coronary lesion may contribute to the no-reflow phenomenon in patients with acute coronary syndrome. Circulation. 2002;106:1672–1677. DOI: 10.1161/01.CIR.0000030189.27175.4E - 118.
Kawamoto T, Okura H, Koyama Y, Toda I, Taguchi H, Tamita K, Yamamuro A, Yoshimura Y, Neishi Y, Toyota E, Yoshida K. The relationship between coronary plaque characteristics and small embolic particles during coronary stent implantation. J Am Coll Cardiol. 2007;50:1635–1640. DOI: 10.1016/j.jacc.2007.05.050 - 119.
Goldstein JA, Grines C, Fischell T, Virmani R, Rizik D, Muller J, Dixon SR. Coronary embolization following balloon dilatation of lipid-core plaques. JACC Cardiovasc Imaging. 2009;2:1420–1424. DOI: 10.1016/j.jcmg.2009.10.003 - 120.
Papayannis AC, Abdel-Karim A-RR, Mahmood A, Rangan B V, Makke LB, Banerjee S, et al. Association of coronary lipid core plaque with intrastent thrombus formation: a near-infrared spectroscopy and optical coherence tomography study. Catheter Cardiovasc Interv. 2013; 81:488–493. DOI: 10.1002/ccd.23389 - 121.
Schultz CJ, Serruys PW, van der Ent M, Ligthart J, Mastik F, Garg S, et al. First-in-man clinical use of combined near-infrared spectroscopy and intravascular ultrasound: a potential key to predict distal embolization and no-reflow? J Am Coll Cardiol. 2010; 56:314. DOI: 10.1016/ j .jacc.2009.10.090 - 122.
Garcia BA, Wood F, Cipher D, Banerjee S, Brilakis ES. Reproductibility of near-infrared spectroscopy for the detection of lipid core coronary plaques and observed changes after coronary stent implantation. Catheter Cardiovasc Interv. 2010;76:359–365. DOI: 10.1002/ccd.22500 - 123.
Brilakis ES, Abdel-Karim A-RR, Papayannis AC, Michael TT, Rangan B V, Johnson JL, et al. Embolic protection device utilization during stenting of native coronary artery lesions with large lipid core plaques as detected by near-infrared spectroscopy. Catheter Cardiovasc Interv. 2012; 80:1157–1162. DOI: 10.1002/ccd.23507 - 124.
Maini A, Buyantseva L, Maini B. In vivo lipid core plaque modification with percutaneous coronary revascularization: a near-infrared spectroscopy study. J Invasive Cardiol. 2013;25:293–295. DOI: PMID: 23735355 - 125.
Stone GW, Maehara A, Muller JE, Rizik DG, Shunk KA, Ben-Yehuda O, Généreux P, Dressler O, Parvataneni R, Madden S, Shah P, Brilakis ES, Kini AS. Plaque characterization to inform the prediction and prevention of periprocedural myocardial infarction during percutaneous coronary intervention: the CANARY Trial (Coronary Assessment by Near-infrared of Atherosclerotic Rupture-prone Yellow). JACC Cardiovasc Interv. 2015;8:927–936. DOI: 10.1016/ j .jcin.2015.01.032 - 126.
Vlaar PJ, Svilaas T, van der Horst IC, Diercks GF, Fokkema ML, de Smet BJ, van den Heuvel AF, Anthonio RL, Jessurum GA, Tan ES, Suurmeijer AJ, Zijlstra F. Cardiac death and reinfarction after 1 year in the thrombus aspiration during percutaneous coronary intervention in acute myocardial infarction study (TAPAS): a 1-year follow-up study. Lancet. 2008;371:1915–1920. DOI: 10.1016/S0140-6736(08)60833-8 - 127.
Frobert O, Lagerqvist B, Olivercrona GK, Omerovic E, Gudnason T, Maeng M, Aasa M, Angeras O, Calais F, Danielewicz M, Erlinge D, Hellsten L, Jensen U, Johansson AC, Karegren A, Nilsson J, Robertson L, Sandhall L, Sjögren I, Ostlund O, Harnek J, James SK. Thrombus aspiration during ST-segment elevation myocardial infarction. N Engl J Med. 2013;369:1587–1597. DOI: 10.1056/NEJMoa1308789 - 128.
Jolly SS, Cairns JA, Yusuf S, Meeks B, Pogue J, Rokoss MJ, Kedev S, Thabane L, Stankovic G, Moreno R, Gershlick A, Chowdhary C, Lavi S, Niemelä K, Steg PG, Bernat I, Xu Y, Cantor WJ, Overgaard CB, Naber CK, Cheema AN, Welsh RC, Bertrand OF, Avezum A, Bhindi R, Pancholy S, Rao SV, Natarajan K, ten Berg JM, Shestakovska O, Gao P, Widimsky P, Dzavik V. Randomized trial of primary PCI with or without routine manual thrombectomy. N Engl J Med. 2015;372:1389–1398. DOI: 10.1056/NEJMoa1415098 - 129.
Erlinge D, Harnek J, Goncalves I, Gotberg M, Muller JE, Madder RD. Coronary liposuction during percutaneous coronary intervention: evidence by near-infrared spectroscopy that aspiration reduces culprit lesion lipid content prior to stent placement. Eur Heart J Cardiovasc Imaging. 2015;16:316–324. DOI: 10.1093/ehjci/jeu180 - 130.
Simsek C, van Geuns RJ, Magro M, Boersma E, Garcia-Garcia HM, Serruys PW. Change in near-infrared spectroscopy of a coronary artery after 1-year treatment with high dose rosuvastatin. Int J Cardiol. 2012;157:e54–e56. DOI: 10.1016/j.ijcard.2011.09.047 - 131.
Simsek C, Garcia-Garcia HM, van Geuns RJ, Magro M, Girasis C, van Mieghem N, Lenzen M, de Boer S, Regar E, van der Giessen W, Raichlen J, Duckers HJ, Zijlstra F, van der Steen T, Boersma E, Serruys PW. The ability of high dose rosuvastatin to improve plaque composition in non-intervened coronary arteries: rationale and design of the integrated biomarker and imaging study-3 (IBIS-3). EuroIntervention. 2012;8:234–241. DOI: 10.4244/EIJV912A37 - 132.
Jang IK.Near infrared spectroscopy.Another toy or indispensable diagnostic tool?Circ Cardiovasc Interv. 2012;5:10–11. DOI:10.1161/CIRCINTERVENTIONS.111.967935 - 133.
Kaul S, Narula J. In search of the vulnerable plaque: is there any light at the end of the catheter? J Am Coll Cardiol. 2014; 64:2519–24.10.1016/j.jacc.2014.10.017 - 134.
Jang J-S, Song Y-J, Kang W, Jin H-Y, Seo J-S, Yang T-H, et al. Intravascular ultrasound-guided implantation of drug-eluting stents to improve outcome: a meta-analysis. J Am Coll Cardiol Cardiovasc Interv. 2014; 7:233–243. DOI: 10.1016/j.jcin.2013.09.013