Two distinct phenotypes of plaque erosion assessed by multimodality intracoronary imaging: a case series.
ABSTRACT: AbstractBackground?Pathological studies have reported that patients with acute coronary syndrome (ACS) may have different plaque morphologies at culprit lesions, and one of the underlying mechanisms for ACS is plaque erosion. However, the morphological features of plaque erosion obtained by multiple intracoronary imaging modalities have not been fully elucidated.Case summary?We experienced two cases with ACS of culprit lesions exhibiting optical coherence tomography (OCT)-defined plaque erosion. Additional examinations using near-infrared spectroscopy (NIRS)–intravascular ultrasound and coronary angioscopy suggested the presence of two distinct phenotypes of plaque erosion. These two types of erosion differ in the extent of NIRS-derived lipid core burden and coronary angioscopy-derived luminal surface colour.Discussion?OCT-defined plaque erosion may not be the unique entity but have at least two distinct plaque morphologies, and NIRS and/or coronary angioscopy may provide incremental ability of discriminating these plaque phenotypes classified as plaque erosion by OCT.
Project description:The aim of this study was to characterize the morphological features of plaque erosion and calcified nodule in patients with acute coronary syndrome (ACS) by optical coherence tomography (OCT).Plaque erosion and calcified nodule have not been systematically investigated in vivo.A total of 126 patients with ACS who had undergone pre-intervention OCT imaging were included. The culprit lesions were classified as plaque rupture (PR), erosion (OCT-erosion), calcified nodule (OCT-CN), or with a new set of diagnostic criteria for OCT.The incidences of PR, OCT-erosion, and OCT-CN were 43.7%, 31.0%, and 7.9%, respectively. Patients with OCT-erosion were the youngest, compared with those with PR and OCT-CN (53.8 ± 13.1 years vs. 60.6 ± 11.5 years, 65.1 ± 5.0 years, p = 0.005). Compared with patients with PR, presentation with non-ST-segment elevation ACS was more common in patients with OCT-erosion (61.5% vs. 29.1%, p = 0.008) and OCT-CN (100% vs. 29.1%, p < 0.001). The OCT-erosion had a lower frequency of lipid plaque (43.6% vs. 100%, p < 0.001), thicker fibrous cap (169.3 ± 99.1 ?m vs. 60.4 ± 16.6 ?m, p < 0.001), and smaller lipid arc (202.8 ± 73.6° vs. 275.8 ± 60.4°, p < 0.001) than PR. The diameter stenosis was least severe in OCT-erosion, followed by OCT-CN and PR (55.4 ± 14.7% vs. 66.1 ± 13.5% vs. 68.8 ± 12.9%, p < 0.001).Optical coherence tomography is a promising modality for identifying OCT-erosion and OCT-CN in vivo. The OCT-erosion is a frequent finding in patients with ACS, especially in those with non-ST-segment elevation ACS and younger patients. The OCT-CN is the least common etiology for ACS and is more common in older patients. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).
Project description:A combination optical coherence tomography and near-infrared spectroscopy (OCT-NIRS) coronary imaging system is being developed to improve the care of coronary patients. While stenting has improved, complications continue to occur at the stented site and new events are caused by unrecognized vulnerable plaques. An OCT-NIRS device has potential to improve secondary prevention by optimizing stenting and by identifying vulnerable patients and vulnerable plaques. OCT is already in widespread use world-wide to optimize coronary artery stenting. It provides automated lumen detection and can identify features of coronary plaques not accurately identified by angiography or intravascular ultrasound. The ILUMIEN IV study, to be completed in 2022, will determine if OCT-guided stenting will yield better clinical outcomes than angiographic guidance alone. While the superb spatial resolution of OCT enables the identification of many plaque structural features, the detection by OCT of lipids, an important component of vulnerable plaques, is limited by suboptimal specificity and interobserver agreement. In contrast, NIRS has been extensively validated for lipid-rich plaque detection against the gold-standard of histology and is the only FDA-approved method to identify coronary lipids. Studies in patients have demonstrated that NIRS detects lipid in culprit lesions causing coronary events. In 2019, the positive results of the prospective Lipid-Rich Plaque Study led to FDA approval of NIRS for detection of high-risk plaques and patients. The complementarity of OCT for plaque structure and NIRS for plaque composition led to the sequential performance of NIRS and OCT imaging in patients. NIRS identified lipid while OCT determined the thickness of the cap over the lipid pool. The positive results obtained with OCT and NIRS imaging led to development of a prototype combined OCT-NIRS catheter that can provide co-registered OCT and NIRS data in a single pullback. The data will provide structural and chemical information likely to improve stenting and deliver more accurate identification of vulnerable plaques and vulnerable patients. More precise diagnosis will then lead to OCT-NIRS guided treatment trials to improve secondary prevention. Success in secondary prevention will then facilitate development of improved primary prevention with invasive imaging and effective treatment of patients identified by non-invasive methods.
Project description:Lipoprotein Lp(a) represents an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden and lipid rich plaques prone to rupture in patients with acute coronary syndrome (ACS) still remains unknown. These data aim to investigate the association among serum Lipoprotein(a) (Lpa) levels, coronary atherosclerotic burden and features of culprit plaque in patients with ACS and obstructive CAD. For his reason, a total of 500 ACS patients were enrolled for the angiographic cohort and 51 ACS patients were enrolled for the optical coherence tomography (OCT) cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index, whereas OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment. In the angiographic cohort, Lp(a) was a weak independent predictor of Sullivan score (p<0.0001), stenosis score (p<0.0001) and extent index (p<0.0001). In the OCT cohort, patients with higher Lp(a) levels (>30 md/dl) compared to patients with lower Lp(a) levels (<30 md/dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (P=0.02), a wider lipid arc (p=0.003) and a higher prevalence of thin-cap fibroatheroma (p=0.004).
Project description:Plaque rupture and erosion are the 2 most common mechanisms for acute coronary syndromes. However, the outcome of these 2 distinct pathologies in patients with acute coronary syndromes has never been studied.We retrospectively studied 141 patients with acute coronary syndromes who underwent optical coherence tomography (OCT) imaging of the culprit lesion prior to stenting from the Massachusetts General Hospital OCT Registry. Management (stent versus no stent), poststent OCT findings, and outcomes were compared. Among the 141 culprit lesions, rupture was found in 79 (56%) patients and erosion in 62 (44%). Stent implantation was performed in 77 (97.5%) patients with rupture versus 49 (79.0%) in those with erosion (P<0.001). Immediately after percutaneous coronary intervention, OCT showed a higher incidence of malapposition (37.5% versus 7.3%, P<0.001), thrombus (59.4% versus 14.6%, P<0.001), and protrusion (93.8% versus 73.2%, P=0.008) in the rupture group compared with the erosion group. Plaque rupture was associated with a higher incidence of no reflow or slow flow and distal embolization. Although cardiac event rates were comparable between the two groups at the 1-year follow-up, none of the erosion patients who were treated conservatively without stenting had adverse cardiac events.Unfavorable poststent OCT findings were more frequent in rupture patients compared with erosion patients. A subset of erosion patients who were treated conservatively without stenting remained free of adverse cardiac events for up to 1 year.
Project description:Acute coronary syndromes (ACS) secondary to coronary vessel plaques represent a major cause of cardiovascular morbidity and mortality worldwide. Advancements in imaging technology over the last 3 decades have continuously enabled the study of coronary plaques via invasive imaging methods like intravascular ultrasound (IVUS) and optical coherence tomography (OCT). The introduction of near-infrared spectroscopy (NIRS) as a modality that could detect the lipid (cholesterol) content of atherosclerotic plaques in the early nineties, opened the potential of studying "vulnerable" or rupture-prone, lipid-rich coronary plaques in ACS patients. Most recently, the ability of NIRS-IVUS to identify patients at risk of future adverse events was shown in a prospective multicenter trial, the Lipid-Rich-plaque Study. Intracoronary NIRS-IVUS imaging offers a unique method of coronary lipid-plaque characterization and could become a valuable clinical diagnostic and treatment monitoring tool.
Project description:The relation of serial changes in plaque morphology of obstructive nonculprit lesions to HDL efflux, inflammation and transcriptome perturbations in response to high-dose statin therapy (YELLOW II study). YELLOW II is a prospective single center study. Stable patients who were scheduled for elective coronary angiography and/or coronary artery stenting were screened for this study. The final target population were patients with multivessel disease requiring staged intervention, culprit vessel initially and non-culprit vessel later, with maxLCBI4mm greater than 150 by NIRS. Patients underwent PCI for a culprit lesion followed by OCT and NIRS/IVUS of an obstructive non-culprit lesion (NCL). All subjects received rosuvastatin, 40 mg every day for 8-12 weeks. The NCL was reimaged and underwent intervention as a part of staged intervention. Blood samples were obtained for cholesterol efflux capacity (CEC) quantification and peripheral PBMC isolation. Despite the extensive evidence for the beneficial effects of statins on clinical outcomes, the mechanisms underlying these effects in remain elusive. In a prospective study, 85 patients with stable multivessel coronary artery disease underwent percutaneous coronary intervention for a culprit lesion followed by intracoronary multi-modality imaging including optical coherence tomography (OCT) of an obstructive NCL. All subjects received 40 mg of rosuvastatin every day for 8-12 weeks, when the NCL was reimaged and intervention was performed. Blood samples were drawn at both times to assess cholesterol efflux capacity (CEC) and transcriptomic profile in peripheral blood mononuclear cells (PBMC). Overall design: Paired, sibship enabled study with baseline and followup expression data analyses.
Project description:Importance:Patients with culprit plaque rupture are known to have pancoronary plaque vulnerability. However, the characteristics of nonculprit plaques in patients with acute coronary syndromes caused by plaque erosion are unknown. Objective:To investigate the nonculprit plaque phenotype in patients with acute coronary syndrome according to culprit plaque pathology (erosion vs rupture) by 3-vessel optical coherence tomography imaging. Design, Setting, and Participants:In this observational cohort study, between August 2010 and May 2014, 82 patients with acute coronary syndrome who underwent preintervention optical coherence tomography imaging of all 3 major epicardial coronary arteries were enrolled at the Massachusetts General Hospital Optical Coherence Tomography Registry database. Analysis of the data was conducted between November 2016 and July 2017. Patients were classified into 2 groups based on the culprit lesion pathology: 17 patients with culprit plaque erosion and 34 patients with culprit plaque rupture. Thirty-one patients with the absence of culprit rupture or erosion were excluded from further analysis. Exposures:Preintervention 3-vessel optical coherence tomography imaging. Main Outcomes and Measures:Plaque characteristics at the culprit and nonculprit lesions evaluated by optical coherence tomography. Results:In 51 patients (37 men; mean age, 58.7 years), the characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed. In patients with culprit erosion, the mean (SD) number of nonculprit plaques per patient was smaller (3.4 [1.9] in erosion vs 4.7 [2.1] in rupture, P?=?.05). Patient-based analysis showed that none of 17 patients with culprit plaque erosion had nonculprit plaque rupture, whereas 26% of the patients (9 of 34) with culprit plaque rupture had nonculprit plaque rupture (P?=?.02). Plaque-based analysis showed that, compared with the culprit rupture group (n?=?158), the culprit erosion group (n?=?58) had lower prevalence of plaque rupture (0% vs 8%; P?<?.001), macrophage accumulation (29% vs 53%; P?=?.01), microvessels (21% vs 42%; P?=?.003), and spotty calcium (5% vs 22%; P?=?.006) in the nonculprit lesions. The prevalence of lipid-rich plaque, thin-cap fibroatheroma, and thrombus did not differ between the groups. Conclusions and Relevance:Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.
Project description:Background:Thinning of the fibrous cap of atherosclerotic plaque is a major component of plaque vulnerability. The high resolution of optical coherence tomography (OCT) provides an accurate measurement of fibrous-cap thickness. Endothelial dysfunction is associated with inflammation and enhanced local expression of matrix metalloproteinases. We investigated the association between endothelial dysfunction and OCT-derived thin-cap fibroatheroma (TCFA) in patients with acute coronary syndromes (ACS). Methods:Seventy-four patients with ACS, who underwent both OCT examinations of the culprit lesion before percutaneous coronary intervention and peripheral endothelial function assessment as assessed by logarithmic value of reactive hyperemia index (Ln_RHI), were enrolled. Age-, sex-, hypertension-, and diabetes-matched non-coronary artery disease (non-CAD) patients were also enrolled (n=15). Results:Ln_RHI levels were significantly lower in ACS patients compared with non-CAD patients (0.56±0.26 vs 0.74±0.22, P=0.01). Furthermore, the Ln_RHIs of ACS patients with TCFA (n=44) were significantly lower than those of ACS patients without TCFA (n=30) (0.50±0.24 vs 0.65±0.26, P=0.01). There was a weak but significant positive correlation between Ln_RHI and fibrous-cap thickness (Spearman's ρ=0.25, P=0.03). Multivariate logistic regression analysis identified lower Ln_RHI as an independent factor associated with TCFA in ACS patients (OR per 0.1 increase in Ln_RHI: 0.78 [95% CI: 0.62-0.98], P=0.03). Conclusion:Advanced endothelial dysfunction significantly correlates with a thin fibrous cap of coronary plaques in patients with ACS.
Project description:Objectives:The objectives of this study were to investigate if findings by intracoronary near-infrared spectroscopy (NIRS) and intravascular ultrasound (IVUS) are associated with future cardiovascular events and if NIRS can differentiate culprit from non-culprit segments in patients with coronary artery disease. Methods:The study included 144 patients with coronary artery disease undergoing percutaneous coronary intervention and combined NIRS-IVUS imaging at two Swedish hospitals. The NIRS-derived lipid core burden index (LCBI), the 4 mm segment with maximum LCBI (MaxLCBI4mm) and the IVUS-derived maximum plaque burden (MaxPB) were analysed within the culprit segment and continuous 10?mm non-culprit segments of the index culprit vessels. The association with future major adverse cardiovascular and cerebrovascular events (MACCE), defined as all-cause mortality, acute coronary syndrome requiring revascularisation and cerebrovascular events during follow-up was evaluated using multivariable Cox regressions. A receiver operating characteristic (ROC) analysis was performed to test the ability of NIRS to discriminate culprit against non-culprit segments. Results:A non-culprit maxLCBI4mm ?400 (HR: 3.67, 95%?CI 1.46 to 9.23, p=0.006) and a non-culprit LCBI ? median (HR: 3.08, 95%?CI 1.11 to 8.56, p=0.031) were both significantly associated with MACCE, whereas a non-culprit MaxPB ?70% (HR: 0.61, 95%?CI 0.08 to 4.59, p=0.63) was not. The culprit segments had larger lipid cores compared with non-culprit segments (MaxLCBI4mm 425 vs 74, p<0.001), and the ROC analysis showed that NIRS can differentiate culprit against non-culprit segments (c-statistics: 0.85, 95%?CI 0.81 to 0.89). Conclusion:A maxLCBI4mm ?400 and LCBI ? median, assessed by NIRS in non-culprit segments of a culprit artery, were significantly associated with patient-level MACCE. NIRS furthermore adequately discriminated culprit against non-culprit segments in patients with coronary disease.
Project description:BACKGROUND AND AIMS:Total coronary artery calcium (CAC) burden is associated with an increased cardiovascular risk, while local CAC may represent stable plaques. We determined differences in relationship of total CAC with acute coronary syndrome (ACS) and local CAC with culprit lesions in patients with suspected ACS. METHODS:We performed computed tomography (CT) for CAC and CT angiography to assess the presence of significant stenosis and high-risk plaque (positive remodeling, low CT attenuation, napkin-ring sign, spotty calcium) in 37 patients with ACS and 223 controls. Total and segmental Agatston scores were measured. Culprit lesions were assessed in subjects with ACS. RESULTS:Patients (n?=?260) with vs. without ACS had higher total CAC score (median 229, 25th-75th percentile 75-517 vs. 27, 25th-75th percentile 0-99, p<0.001), higher prevalence of significant stenosis (78% vs. 7%, p<0.001) and high-risk plaque (95% vs. 59%, p<0.001). In those with ACS, culprit (n?=?41) vs. non-culprit (n?=?200) lesions, had similar segmental CAC score (median 22, 25th-75th percentile 4-71 vs. 14, 25th-75th percentile 0-51; p=0.37), but higher prevalence of significant stenosis (81% vs. 11%, p<0.001) and high-risk plaque (76% vs. 51%, p=0.005). Significant stenosis (odds ratio 40.2, 95%CI 15.6-103.9, p<0.001) and high-risk plaque (odds ratio 3.4, 95%CI 1.3-9.1, p=0.02), but not segmental CAC score (odds ratio 1.0, 95%CI 1.0-1.0, p=0.47), were associated with culprit lesions of ACS. CONCLUSIONS:Total CAC burden was associated with ACS but segmental CAC was not associated with culprit lesions. Our findings suggest that total but not local CAC is a marker of ACS risk and support the hypothesis that extensive local CAC is a marker of plaque stability.