Huai Yu

Distinct Morphological Features of Ruptured Culprit Plaque for Acute Coronary Events Compared to Those With Silent Rupture and Thin-Cap Fibroatheroma : A Combined Optical Coherence Tomography and Intravascular Ultrasound Study

OBJECTIVES The study sought to identify specific morphological characteristics of ruptured culprit plaques (RCP) responsible for acute events, and compare them with ruptured nonculprit plaques (RNCP) and nonruptured thin-cap fibroatheroma (TCFA) in patients presenting with acute coronary syndromes (ACS). BACKGROUND Nonruptured TCFA and multiple ruptured plaques are detected in the same patients with ACS. It remains unknown whether certain morphological characteristics determine rupture of TCFA and subsequently result in ACS. METHODS We analyzed 126 plaques (RCP = 49, RNCP = 19, TCFA = 58) from 82 ACS patients using optical coherence tomography (OCT) and intravascular ultrasound (IVUS). Fibrous cap thickness was determined by OCT. Plaque burden and lumen area were measured with IVUS. RESULTS Fibrous cap was thinner in RCP (43 ± 11 μm) and RNCP (41 ± 10 μm) than in TCFA (56 ± 9 μm, p < 0.001 and p < 0.001, respectively). Plaque burden was greater in RCP (82 ± 7.2%), compared with RNCP (64 ± 7.2%, p < 0.001) and TCFA (62 ± 12.5%, p < 0.001). Lumen area was smaller in RCP (2.1 ± 0.9 mm(2)), compared with RNCP (4.6 ± 2.3 mm(2), p = 0.001) and TCFA (5.1 ± 2.7 mm(2), p < 0.001). The fibrous cap thickness <52 μm had good performance in discriminating ruptured plaque from TCFA (area under the curve [AUC] = 0.857, p < 0.001), and plaque burden >76% and lumen area <2.6 mm(2) had good performance in discriminating RCP from RNCP and TCFA (AUC = 0.923, p < 0.001 and AUC = 0.881, p < 0.001, respectively). CONCLUSIONS Fibrous cap thickness is a critical morphological discriminator between ruptured plaques and nonruptured TCFA, while plaque burden and lumen area appear to be important morphological features of RCP. These findings suggest that plaque rupture is determined by fibrous cap thickness, and a combination of large plaque burden and luminal narrowing result in ACS.

Vasa vasorum and plaque progression, and responses to atorvastatin in a rabbit model of atherosclerosis: contrast-enhanced ultrasound imaging and intravascular ultrasound study.

Objectives To serially investigate the relationship between vasa vasorum (VV) proliferation and plaque progression in vivo, and the effects of atorvastatin on VV and atherosclerosis as assessed by contrast-enhanced ultrasound (CEUS) and intravascular ultrasound (IVUS) imaging. Methods Carotid atherosclerosis was induced in rabbits with a high-cholesterol diet for 20 weeks and balloon injury. At week 16, following the imaging of the right common carotid arteries by CEUS and IVUS, 20 rabbits were randomised into a control or atorvastatin group (2 mg/kg/day). At week 20, CEUS and IVUS were repeated. Normalised maximal video-intensity enhancement (MVE) was calculated to quantify the density of VV. Plaque volume was determined by IVUS. Results When compared with the control group, lipid levels were not significantly lower following 4 weeks of atorvastatin administration. The increases in the normalised MVE over time were greater in the control group than in the atorvastatin group (p=0.001). The increase in plaque volume from 16 to 20 weeks was significantly greater in the control group than in the atorvastatin group (p=0.001). There was a positive relationship between changes in normalised MVE and plaque volume (r=0.72, p=0.002). Conclusions There was a positive correlation between VV density and plaque progression. Atorvastatin significantly inhibits the development of adventitial VV and progression of atherosclerosis independent of lowering the cholesterol level.

A Novel Model of Atherosclerosis in Rabbits Using Injury to Arterial Walls Induced by Ferric Chloride as Evaluated by Optical Coherence Tomography as well as Intravascular Ultrasound and Histology

This study aim was to develop a new model of atherosclerosis by FeCl3-induced injury to right common carotid arteries (CCAs) of rabbits. Right CCAs were induced in male New Zealand White rabbits (n = 15) by combination of a cholesterol-rich diet and FeCl3-induced injury to arterial walls. The right and left CCAs were evaluated by histology and in vivo intravascular ultrasound (IVUS) and optical coherence tomography (OCT) examinations of 24 hours (n = 3), 8 weeks (n = 6), and 12 weeks (n = 6) after injury. Each right CCA of the rabbits showed extensive white-yellow plaques. At eight and 12 weeks after injury, IVUS, OCT, and histological findings demonstrated that the right CCAs had evident eccentric plaques. Six plaques (50%) with evident positive remodeling were observed. Marked progression was clearly observed in the same plaque at 12 weeks after injury when it underwent repeat OCT and IVUS. We demonstrated, for the first time, a novel model of atherosclerosis induced by FeCl3. The model is simple, fast, inexpensive, and reproducible and has a high success rate. The eccentric plaques and remodeling of plaques were common in this model. We successfully carried out IVUS and OCT examinations twice in the same lesion within a relatively long period of time.

Association between cholesterol crystals and culprit lesion vulnerability in patients with acute coronary syndrome: An optical coherence tomography study.

BACKGROUND Cholesterol Crystals (ChCs) are recognized as a hallmark of advanced atherosclerotic lesions. Previous animal and histopathology studies have revealed that Cholesterol crystallization trigger a local inflammatory response and plaque rupture. We sought to investigate the in vivo relationship between ChCs and culprit lesion vulnerability in patients with acute coronary syndrome (ACS). METHODS 206 culprit lesions from 206 patients with ACS who underwent optical coherence tomography (OCT) imaging were divided into 2 groups based on the presence or absence of ChCs. Culprit lesions characteristics were compared between ChCs and Non-ChCs groups. RESULTS For overall ACS patients, culprit lesions with ChCs had higher incidence of macrophages accumulation (77.8% vs. 40.0%, p < 0.001), microchannel (67.9% vs. 24.8%, p < 0.001), plaque rupture (58.0% vs. 36.0%, p = 0.001), thrombosis (66.7% vs. 49.6%, p = 0.016) and spotty calcification (35.8% vs. 10.4%, p < 0.001). In addition, the mean lipid arc (274.2 ± 57.6° vs. 228.1 ± 66.3°, p < 0.001) was larger and the lipid index (3826.1 ± 2111.4 vs. 2855.0 ± 1753.0, p = 0.001) was greater. The frequency of ChCs was significantly higher in patients with STEMI, as compared with NSTEACS (50.8% vs. 34.7%, p = 0.032). Larger lipid arc, higher incidence of macrophages accumulation and that of microchannel were observed in culprit lesions with ChCs in both STEMI (p = 0.028, p < 0.001, and p = 0.002 respectively) and NSTEACS (p < 0.001, p < 0.001, and p < 0.001 respectively) subgroups. CONCLUSION ChCs were frequently associated with characteristics of vulnerable plaques in ACS culprit lesions as well as in STEMI and NSTEACS subgroups. ChCs and vulnerable plaque features were more often observed in culprit lesions of STEMI patients compared to NSTEACS patients.

In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study

Aims Plaque erosion is a significant substrate of acute coronary thrombosis. This study sought to determine in vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction (STEMI). Methods and results A prospective series of 822 STEMI patients underwent pre-intervention optical coherence tomography. Using established diagnostic criteria, 209 had plaque erosion (25.4%) and 564 had plaque rupture (68.6%). Plaque erosion was more frequent in women <50 years when compared with those ≥50 years of age (P = 0.009). There was a similar, but less striking, trend in men (P = 0.011). Patients with plaque erosion were more frequently current smokers but had fewer other coronary risk factors (dyslipidaemia, hypertension, chronic kidney disease, and diabetes mellitus) than those with plaque rupture. There was a preponderance of plaque erosion in the left anterior descending artery (LAD; 61.2%), whereas plaque rupture was more equally distributed in both the LAD (47.0%) and right coronary artery (43.3%). Despite the similar spatial distribution of erosions and ruptures over the lengths of the coronary arteries, plaque erosion occurred more frequently near a bifurcation (P < 0.001). In the multivariable analysis, age <50 years, current smoking, absence of other coronary risk factors, lack of multi-vessel disease, reduced lesion severity, larger vessel size, and nearby bifurcation were significantly associated with plaque erosion. Nearby bifurcation and current smoking were especially notable in men, while age <50 years was most predictive in women. Conclusions Plaque erosion was a predictable clinical entity distinct from plaque rupture in STEMI patients, and gender-specific role of risk factors in plaque erosion should be considered.

Patterns of coronary plaque progression: phasic versus gradual. A combined optical coherence tomography and intravascular ultrasound study.

ObjectiveSome plaques grow slowly in a linear manner, whereas others undergo a rapid phasic progression. However, the detailed in-vivo relationship between plaque characteristics and plaque progression pattern has not been reported. The current study aimed to investigate the plaque progression patterns with serial intravascular ultrasound (IVUS) examinations, and to correlate baseline plaque characteristics assessed by optical coherence tomography and IVUS with plaque progression patterns. MethodsA total of 248 coronary lesions from 157 patients were identified and imaged by both optical coherence tomography and IVUS at baseline. IVUS examination was repeated at 6 and 12 months. Plaque progression was defined as greater than or equal to 5% increase in percent atheroma volume by IVUS. The progression patterns were divided into three groups: no progression, rapid phasic progression, and gradual progression. ResultsAmong 248 lesions, 190 (77%) showed no progression. Among 58 lesions with progression, 20 (34%) showed gradual progression, whereas 38 (66%) showed rapid phasic progression. Multivariate analysis indicated that thin-cap fibroatheroma [odds ratio (OR)=5.24, 95% confidence interval (CI) 2.04–13.4; P=0.001], microvessel (OR=2.20, 95% CI 1.10–4.79; P=0.045), and positive remodeling (OR=2.64, 95% CI 1.19–5.81; P=0.016) were associated independently with rapid phasic progression. ConclusionThree-quarters of coronary plaques did not progress over time with contemporary medical treatment. Among the lesions with progression, one-third showed a gradual pattern and two-thirds showed a rapid phasic pattern. The presence of thin-cap fibroatheroma, microvessel, and positive remodeling were the independent predictors for rapid phasic pattern progression of coronary atherosclerotic plaques.

Optical Coherence Tomographic Observations of Polytetrafluoroethylene-Covered Sirolimus-Eluting Coronary Arterial Stent

The aim of this study was to evaluate neointimal coverage obtained using a new method of polytetrafluoroethylene-covered stent (PCS) implantation combined with underlying longer sirolimus-eluting stent (SES) implantation using optical coherence tomography. Nine patients were enrolled in this study, including patients with coronary artery perforations, original coronary aneurysms, and acquired coronary aneurysms after drug-eluting stent implantation. All patients were first treated with long SES implantation and then with focal PCS implantation. Postprocedural and follow-up angiographic and optical coherence tomographic examinations were performed in all patients, and intravascular ultrasound was performed in 5 patients. All patients were asymptomatic during follow-up, without recurrent angina. There was no stent-edge or stent-segment binary restenosis. Values of late loss for proximal SES segments, PCS segments, and distal SES segments were similar (0.09, 0.07, and 0.04 mm, respectively, p = 0.8113). The mean neointimal thickness of PCS was less than that of proximal and distal SES. However, no malapposed cross sections or uncovered cross sections were found in PCS segments compared with SES segments (p = 0.0011). In conclusion, the combination of PCS and underlying longer SES implantation can offer better angiographic follow-up results. High-resolution optical coherence tomography provided convincing proof of full neointimal coverage of PCS. This new method of combined PCS and SES implantation may be a better choice compared with direct PCS implantation in certain clinical settings.

Is lipoprotein-associated phospholipase A2 activity correlated with fibrous-cap thickness and plaque volume in patients with acute coronary syndrome?

BackgroundLipoprotein-associated phospholipase A2 (Lp-PLA2) is a specific biomarker specific for vascular inflammation. Inflammation has a significant association with plaque progression. The fibrous-cap thickness (FCT) is one of the major determinants of plaque vulnerability in atherosclerotic plaques. However, data on the relationship between Lp-PLA2 activity and FCT in lipid plaque are limited. This study aimed to evaluate the in-vivo association between changes in Lp-PLA2 activity and FCT and plaque volume in patients with acute coronary syndrome (ACS). Patients and methodsTwenty-four consecutive patients with ACS were enrolled between May 2010 and May 2012. The plaque volume and FCT of nonculprit lipid-rich plaques were assessed by intravascular ultrasound and optical coherence tomography, respectively, at baseline and after 12 months. Lp-PLA2 activity was determined using the colorimetric assay kit. ResultsDuring the 12 months of observation, FCT increased significantly from baseline to follow-up, with a mean percent change of 74.4±46.8%. A significant correlation was observed between changes in Lp-PLA2 activity and changes in FCT (r=−0.56, P=0.006). Changes in plaque volume were also correlated significantly with changes in Lp-PLA2 activity during the study period (r=0.52, P=0.01). ConclusionSignificant associations between serial changes in Lp-PLA2 activity and changes in FCT and plaque volume were observed in patients with ACS.