Assessment of culprit and remote coronary narrowings using optical coherence tomography with long-term outcomes

Much currently known information about vulnerable plaque stems from postmortem studies that identified several characteristics making them prone to rupture, including the presence of a thin fibrous cap and a large lipid core. This study used optical coherence tomography (OCT) to assess culprit and remote coronary narrowings and investigate whether intracoronary OCT in living patients was able to visualize morphologic features associated with vulnerable plaque in postmortem studies. Twenty-three patients successfully underwent OCT before percutaneous coronary intervention. The culprit lesion and mild to moderate coronary narrowings remote from the target stenosis were investigated. Using OCT, the culprit lesion was found to be fibrous in 39.1%, fibrocalcific in 34.4%, and lipid rich in 26.1% of cases. Two patients met criteria for thin-cap fibroatheroma (TCFA; defined as the presence of a signal-rich fibrous cap covering a signal-poor lipid/necrotic core with cap thickness <0.2 mm). Most plaques at remote segments were proximal to the culprit lesion (73.9%) and predominantly fibrous and lipid rich. OCT identified 7 TCFA lesions in 6 patients with a mean cap thickness of 0.19 +/- 0.05 mm, extending for 103 degrees +/- 49 degrees of the total vessel circumference. At 24 months of clinical follow-up, the only event occurred in a patient with in-stent restenosis who underwent repeated percutaneous revascularization. There were no clinically apparent plaque rupture-related events in the 6 patients found to have remote TCFA. This study showed that OCT can be safely applied to image beyond the culprit lesion and can detect in vivo morphologic features associated with plaque vulnerability using retrospective pathologic examination. In conclusion, detection of TCFA, particularly in stable patients, is desirable and may principally allow for early intervention and prevention of adverse events.     

In vivo comparison of optical coherence tomography and angioscopy for the evaluation of coronary plaque characteristics

Atherosclerotic yellow plaques identified by coronary angioscopy are considered as vulnerable plaques. However, characteristics of yellow plaques are not well understood. Optical coherence tomography (OCT) provides accurate tissue characterization in vivo and has the capability to measure fibrous cap thickness covering a lipid plaque. Characteristics of yellow plaques identified by angioscopy were evaluated by OCT. We examined 205 plaques of 41 coronary arteries in 26 patients. In OCT analysis, plaques were classified as fibrous or lipid. Minimal lumen area of the plaque, arch of the lipid, and fibrous cap thickness on the lipid plaque were measured. Yellow grade of the plaque was defined as 0 (white), 1 (light yellow), 2 (medium yellow), or 3 (dark yellow) based on the angioscopy. A total of 149 plaques were diagnosed as lipid plaques. Neither the minimal lumen area nor the arch of the lipid was related to the yellow grade. There was an inverse relationship between color grade and the fibrous cap thickness (grade 0 [n = 45] 218 +/- 89 microm, grade 1 [n = 40] 101 +/- 8 microm, grade 2 [n = 46] 72 +/- 10 microm, and grade 3 [n = 18] 40 +/- 14 microm; p <0.05). Sensitivity and specificity of the angioscopy-identified yellow plaque for having a thin fibrous cap (thickness 相似文献   

稳定斑块——治疗急性冠状动脉综合征的新策略

急性冠状动脉综合征主要由于不稳定的冠状动脉粥样硬化斑块受侵蚀或破裂继发血栓引起。不稳定斑块的特征包括巨大的脂核、炎症细胞和炎症介质的增多以及较薄的纤维帽。对此进行干预可望达到稳定斑块的目的,从而给急性冠状动脉综合征的防治带来新的前景。     

Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging.

OBJECTIVES: This study theoretically examined the longitudinal structural determinants of plaque vulnerability using a color-coded stress mapping technique for several hypothetical vessel models as well as three-dimensional intravascular ultrasound (IVUS) images with use of a finite element analysis. BACKGROUND: It has been shown that an excessive concentration of stress is related to atherosclerotic plaque rupture. However, the local determinants of in-plaque longitudinal stress distribution along the coronary arterial wall remain unclear. METHODS: Using a finite element analysis, we performed a color mapping of equivalent stress distribution within plaques for three-dimensional vessel models as well as longitudinal IVUS plaque images (n = 15). Then, the effects of plaque size, shape, expansive remodeling, calcification, and lipid core on the equivalent stress distribution were examined. RESULTS: The color mapping of vessel models revealed a concentration of equivalent stress at the top of the hills and the shoulders of homogeneous fibrous plaques. Expansive remodeling and the lipid core augmented the surface equivalent stress, whereas luminal stenosis and superficial calcification attenuated the equivalent stress. The location of excessive stress concentration was modified by the distribution of the lipid core and calcification. The thickness of the fibrous cap was inversely related to the equivalent stress within the fibrous cap. However, the color mapping of IVUS plaque images showed that the equivalent stress value at the fibrous cap varied with changes in plaque shape and superficial calcification, even when the thickness of the fibrous cap remained constant. CONCLUSIONS: A distribution analysis of longitudinal stress revealed specific effects of plaque shape, size, and remodeling, as well as effects of the interior distribution of tissue components, on the concentration of stress at the plaque surface. Moreover, fibrous caps of the same thickness did not consistently represent the same vulnerability to rupture.     

Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels.

It is likely that factors other than stenosis severity predispose some atherosclerotic plaques to rupture. Because focal increases in circumferential stress may be an important mechanism of plaque rupture, we examined peak circumferential stress of atherosclerotic lesions by using finite element analysis based on idealized two-dimensional cross sections of diseased vessels similar to intravascular ultrasound images. The study was designed to test the hypothesis that subintimal plaque structural features such as thickness of the fibrous cap are more important factors in the distribution of stress in the plaque than stenosis severity. The analysis incorporated equilibrium biomechanical parameters from normal and diseased vessels and determined the stress distribution within the plaque at a mean luminal internal pressure of 110 mm Hg. With a constant luminal area reduction of 70%, maximum circumferential stress (sigma max) normalized to luminal pressure (sigma max/P) increased from 6.0 to 24.8 as the thickness of the lipid pool was increased from 38% to 54% of the plaque thickness because of the thinner fibrous cap over the lipid pool. When the lipid pool thickness was constant, increasing the stenosis severity from 70% to 91% by increasing the fibrous cap thickness decreased sigma max/P from 24.8 to 4.7. When no lipid pool was present and the stenosis severity was increased from 70% to 99%, sigma max/P decreased from 5.3 to 4.7. Thus, reducing the fibrous cap thickness dramatically increases peak circumferential stress in the plaque, whereas increasing the stenosis severity actually decreases peak stress in the plaque.(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of carotid plaque vulnerability using structural and geometrical determinants

BACKGROUND: Because many acute cerebral ischemic events are caused by rupture of vulnerable carotid atheroma and subsequent thrombosis, the present study used both idealized and patient-specific carotid atheromatous plaque models to evaluate the effect of structural determinants on stress distributions within plaque. METHODS AND RESULTS: Using a finite element method, structural analysis was performed using models derived from in vivo high-resolution magnetic resonance imaging (MRI) of carotid atheroma in 40 non-consecutive patients (20 symptomatic, 20 asymptomatic). Plaque components were modeled as hyper-elastic materials. The effects of varying fibrous cap thickness, lipid core size and lumen curvature on plaque stress distributions were examined. Lumen curvature and fibrous cap thickness were found to be major determinants of plaque stress. The size of the lipid core did not alter plaque stress significantly when the fibrous cap was relatively thick. The correlation between plaque stress and lumen curvature was significant for both symptomatic (p=0.01; correlation coefficient: 0.689) and asymptomatic patients (p=0.01; correlation coefficient: 0.862). Lumen curvature in plaques of symptomatic patients was significantly larger than those of asymptomatic patients (1.50+/-1.0 mm(-1) vs 1.25+/-0.75 mm(-1); p=0.01). CONCLUSION: Specific plaque morphology (large lumen curvature and thin fibrous cap) is closely related to plaque vulnerability. Structural analysis using high-resolution MRI of carotid atheroma may help in detecting vulnerable atheromatous plaque and aid the risk stratification of patients with carotid disease.     

Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy.

OBJECTIVES: The aim of the present study was to evaluate the ability of optical coherence tomography (OCT) for assessment of the culprit lesion morphology in acute myocardial infarction (AMI) in comparison with intravascular ultrasound (IVUS) and coronary angioscopy (CAS). BACKGROUND: Optical coherence tomography is a new intravascular imaging method with a high resolution of approximately 10 microm. This may allow us to assess the vulnerable plaques in detail in vivo. METHODS: We enrolled 30 patients with AMI, and analyzed the culprit lesion by OCT, CAS, and IVUS. RESULTS: The average duration from the onset of symptom to OCT imaging was 3.8 +/- 1.0 h. The incidence of plaque rupture observed by OCT was 73%, and it was significantly higher than that by CAS (47%, p = 0.035) and IVUS (40%, p = 0.009). Furthermore, OCT (23%) was superior to CAS (3%, p = 0.022) and IVUS (0%, p = 0.005) in the detection of fibrous cap erosion. The intracoronary thrombus was observed in all cases by OCT and CAS, but it was identified in 33% by IVUS (vs. OCT, p < 0.001). Only OCT could estimate the fibrous cap thickness, and it was 49 +/- 21 microm. The incidence of thin cap fibroatheroma (TCFA) was 83% in this population by OCT. CONCLUSIONS: Optical coherence tomography is a feasible imaging modality in patients with AMI and allows us to identify not only plaque rupture, but also fibrous cap erosion, intracoronary thrombus, and TCFA in vivo more frequently compared with conventional imaging techniques.     

Fluorescence analysis of biochemical constituents identifies atherosclerotic plaque with a thin fibrous cap

Vulnerable plaque generally contains a thin fibrous cap, lipid pools, and reduced internal plaque collagen. Arterial fluorescence analysis can differentiate atherosclerotic lesions from normal arteries; however, the contribution of the lipid core to atherosclerotic arterial fluorescence remains controversial. This study aimed to identify lipid core fluorophores and to differentiate the lipid core from normal artery and atheroma. The helium-cadmium laser-induced fluorescence spectra of cadaveric arteries and known chemical constituents were recorded. Lipid core fluorescence spectra exhibited marked red shifts and broadening compared with the fluorescence spectra of normal tissue and atheroma. Similar fluorescence spectra were obtained for lipid core and oxidized low density lipoprotein, for atheroma and collagen, and for normal artery and elastin. A classification based on collagen, elastin, and oxidized low density lipoprotein spectral decomposition could discriminate the lipid core (n=29), normal artery (n=74), atheroma (n=73), and preatheroma (n=10) with 86% accuracy. Fibrous cap thickness was correlated with the spectral collagen content index (r=0.65, P<0.0001), especially at a thickness of <200 microm. We conclude that a classification algorithm based on chemical spectral decomposition can accurately classify the fluorescence spectra of normal artery, atheroma, and lipid core and may be useful in identifying vulnerable atheroma in vivo.     

基质金属蛋白酶与冠状动脉斑块稳定性相关研究

目的 :探讨基质金属蛋白酶 1(MMP 1)、基质金属蛋白酶抑制剂 1(TIMP 1)、TIMP 1/MMP 1与冠状动脉 (冠脉 )粥样硬化斑块稳定性的相关性。方法 :以冠脉血管内超声检出冠脉粥样硬化斑块的软硬特性 ,将急性冠脉综合征患者分为不稳定斑块组 (n =2 2 )和稳定斑块组 (n =12 )。测定两组间血浆MMP 1、TIMP 1浓度 ,并与冠脉血管内超声测定的斑块大小、斑块纤维帽厚度、脂核或无回声带大小、脂核或无回声带与斑块比及面积狭窄率进行相关性分析。结果 :在冠状静脉窦血和外周血中 ,不稳定斑块组MMP 1浓度明显大于稳定斑块组 (P <0 0 1) ,TIMP 1/MMP 1明显小于稳定斑块组 (P <0 0 0 1) ,有非常显著性差异。血浆MMP 1浓度与纤维帽厚度呈负相关 ,与脂核或无回声带面积、脂核与斑块比和面积狭窄率呈正相关 ,与斑块大小无关。TIMP 1/MMP 1与纤维帽厚度、面积狭窄率呈正相关 ,与脂核或无回声带面积、脂核与斑块比呈负相关。结论 :MMP 1和TIMP 1/MMP 1与冠脉斑块不稳定性呈密切相关 ,可望作为冠脉斑块不稳定性的参考指标。     

Atheromatous plaque cap thickness can be determined by quantitative color analysis during angioscopy: implications for identifying the vulnerable plaque

BACKGROUND: Coronary angioscopy in acute myocardial infarction has frequently revealed disrupted yellow lesions. Furthermore, postmortem studies have demonstrated that these lesions have thin collagenous caps with underlying lipid-rich cores. HYPOTHESIS: We hypothesized that the yellow color is due to visualization of reflected light from the lipid-rich yellow core through a thin fibrous cap. Thus, quantification of yellow color saturation may estimate plaque cap thickness and identify vulnerable plaques. METHODS: To test this hypothesis, the feasibility of detecting cap thickness was tested using both a model of lipid-rich plaque and human atherosclerotic plaque. The model was constructed by injecting a yellow beta-carotene-lipid emulsion subendothelially into normal bovine aorta. Human plaque was obtained from cadaver aorta. Digitized images were obtained by angioscopy, and percent yellow saturation was analyzed using a custom computer program. Plaque cap thickness was measured by planimetry of digitized images on stained tissue sections. Percent yellow saturation was then correlated with plaque cap thickness. RESULTS: In the bovine model, plaque cap thickness and percent yellow saturation correlated inversely (r2 = 0.91; p = 0.0001). In human plaques, yellow saturation was significantly greater in atheromatous than in white plaques (p < 0.0004). Also, there was a high correlation between plaque cap thickness and yellow saturation at various angles of view between 40 degrees and 90 degrees, the greatest between 50 degrees and 80 degrees (r2 = 0.75 to 0.88). CONCLUSION: Plaque cap thickness is a determinant of plaque color, and this can be assessed by quantitative colorimetry. Thus, plaque color by angioscopy may be useful for detecting vulnerable plaques.     

Morphological and biomechanical aspects of vulnerable coronary plaque

Vulnerable plaque morphology has been described by gross pathology and intravascular ultrasound, but morphological criteria cannot fully explain vulnerability, which involves four distinct factors: 1) inflammatory and biological processes; 2) geometry; 3) composition; and 4) hemodynamic stress. These last three aspects underlie the biomechanical study of vulnerable plaque. By virtue of the nature of their evolution, atherosclerotic plaques tend to be excentric, and this is a crucial morphological feature, causing circumferential stress to peak in very specific juxta-luminal locations, where it can exceed the rupture threshold of collagen, the basic constituent of arterial architecture. The lipido-necrotic core covered by a fibrous cap, formed in young plaques, is another morphological feature, which, can also increase and concentrate circumference stress in the juxta-luminal fibrous cap. The larger the lipid core, the thinner the fibrous cap and the greater is the stress. There are also inflammatory processes in such areas, which tend to reduce cap thickness. Ruptures occur when this thickness falls below 65 microns. Heart rate, blood pressure and pulse pressure are all biomechanical factors affecting vulnerable arterial walls, increasing circumferential stress and material fatigue. Vulnerable plaques are almost always associated with positive arterial remodeling. Numerical simulation has shown such so-called compensatory remodeling to be exclusively due to the healthy arc stretching in vulnerable plaques. Positive remodeling is optimal when the healthy arc is around 170 degrees, which keeps the lumen area relatively stable as long as the plaque does not exceed 40% to 50%. This mechanism does not apply to concentric plaques. In conclusion, the mechanism of vulnerable plaque rupture is highly complex and multifactorial. This complexity more or less precludes prediction in individual cases: we are in the realms of chaos theory and acute sensitivity to initial conditions. The greatest caution is therefore required in any attempt to predict rupture from diagnostic imagery, which provides only morphological data on plaque's nature.     

Association of statin therapy with reduced coronary plaque rupture: an optical coherence tomography study

OBJECTIVE: Statin therapy induces plaque regression and may stabilize atheromatous plaques. Optical coherence tomography (OCT) is a high-resolution in-vivo imaging modality that allows characterization of atherosclerotic plaques. We aimed to demonstrate the potential utility of OCT in evaluating coronary plaques in patients with or without statin therapy. METHODS: Patients undergoing cardiac catheterization were enrolled. We identified culprit lesions and performed intracoronary OCT imaging. Plaque lipid pool, fibrous cap thickness, and frequency of thin-cap fibroatheroma were evaluated using previously validated criteria. Macrophage density was determined from optical signals within fibrous caps. Presence of calcification, thrombosis, and rupture was assessed. RESULTS: Forty-eight patients were included (26 on statins, 22 without statins). Baseline characteristics were similar apart from lipid profile. Patients on statin therapy had lower total and low-density lipoprotein cholesterol concentrations (4.45+/-1.35 vs. 5.26+/-0.83 mmol/l, P=0.02; 2.23+/-0.78 vs. 3.26+/-0.62 mmol/l, P<0.001, respectively). Frequencies of lipid-rich plaque (69 vs. 82%), thin-cap fibroatheroma (31 vs. 50%), plaque calcification (15 vs. 5%) and thrombosis (15 vs. 32%), and fibrous cap macrophage density were comparable between statin and nonstatin groups (5.9 vs. 6.3%; all P=NS). Ruptured plaques were, however, significantly less frequent in patients on established statin therapy (8 vs. 36%; P=0.03) with a trend toward increased minimum fibrous cap thickness (78 vs. 49 microm; P=0.07). CONCLUSION: We demonstrated the use of OCT in plaque characterization and found that patients on prior statin therapy have reduced incidence of ruptured plaques and a trend toward thicker fibrous caps. This suggests that statins may stabilize coronary plaques.     

Targeting the inflammatory component in atherosclerotic lesions vulnerable to rupture

Thrombosis of the coronary artery following plaque rupture is the commonest substrate of acute coronary events. The detection of atherosclerotic plaques prone to rupture would allow identifying patients at risk for acute coronary events and aggressive intervention. It has been assumed that the plaque morphology happens to be the major determinant for clinical outcome. The risk of plaque rupture depends upon the prevalence of plaques that have a large lipid core, a thin fibrous cap, and a dense inflammation of the fibrous cap. Evaluating monocytes and the lipid core and their proportions in the atherosclerotic lesion by novel radionuclide imaging strategies may predict a likelihood of an acute coronary event.     

Intravascular Palpography for High-Risk Vulnerable Plaque Assessment

BACKGROUND: The composition of an atherosclerotic plaque is considered more important than the degree of stenosis. An unstable lesion may rupture and cause an acute thrombotic reaction. Most of these lesions contain a large lipid pool covered by an inflamed thin fibrous cap. The stress in the cap increases with decreasing cap thickness and increasing macrophage infiltration. Intravascular ultrasound (IVUS) palpography might be an ideal technique to assess the mechanical properties of high-risk plaques. TECHNIQUE: Palpography assesses the local mechanical properties of tissue using its deformation caused by the intraluminal pressure. IN VITRO VALIDATION: The technique was validated in vitro using diseased human coronary and femoral arteries. Especially between fibrous and fatty tissue, a highly significant difference in strain (p = 0.0012) was found. Additionally, the predictive value to identify the vulnerable plaque was investigated. A high-strain region at the lumen-vessel wall boundary has an 88% sensitivity and 89% specificity for identifying such plaques. IN VIVO VALIDATION: In vivo, the technique was validated in an atherosclerotic Yucatan minipig animal model. This study also revealed higher strain values in fatty than fibrous plaques (p < 0.001). The presence of a high-strain region at the lumenplaque interface has a high predictive value to identify macrophages. PATIENT STUDIES: Patient studies revealed high-strain values (1-2%) in thin-cap fibrous atheroma. Calcified material showed low strain values (0-0.2%). With the development of three-dimensional (3-D) palpography, identification of highstrain spots over the full length of a coronary artery becomes available. CONCLUSION: Intravascular palpography is a unique tool to assess lesion composition and vulnerability. The development of 3-D palpography provides a technique that may develop into a clinical tool to identify the high-risk plaque.     

光学相干断层扫描比较不稳定性和稳定性心绞痛患者粥样硬化斑块特征

目的 应用光学相干断层成像(OCT)技术比较不稳定性心绞痛(UAP)和稳定性心绞痛(SAP)患者冠状动脉粥样硬化斑块特征.方法 对临床诊断的23例UAP和24例SAP患者,在完成冠状动脉造影并确诊冠心病后进行OCT检查.根据OCT结果 回顾性比较分析UAP和SAP患者冠状动脉粥样硬化斑块特征,包括富含脂质斑块(≥2个象限的脂质斑块)、斑块纤维帽厚度、薄纤维帽粥样斑块(TCFA)、斑块破裂、钙化和血栓等.结果 47例患者中有44例成功进行OCT检查,包括22例UAP和22例SAP患者.UAP患者冠状动脉富含脂质斑块为91%(20/22),多于SAP患者的73%(16/22),但差异无统计学意义(P=0.741).UAP患者冠状动脉脂质斑块表面纤维帽厚度明显小于SAP患者[(69.5±34.7)μm比(141.1±68.5)μm,P=0.000],纤维帽侵蚀比例为59%(13/22),明显多于SAP患者的9%(2/22,P=0.000);TCFA[73%(16/22)比14%(3/22),P=0.000]和斑块破裂[50%(11/22)比9%(2/22),P=0.003]多于SAP患者.UAP患者冠状动脉斑块表而可见血栓形成多于SAP患者,但差异无统计学意义[27%(6/22)比9%(2/22),P=0.761].在斑块钙化方面,UAP与SAP患者之间差异无统计学意义.结论 OCT技术可清晰显示冠状动脉粥样斑块特征.与SAP患者比较,UAP患者冠状动脉粥样硬化斑块表现为纤维帽更薄、更多的纤维帽侵蚀、更多的破裂斑块和TCFA.     

What Have We Learned About Plaque Rupture in Acute Coronary Syndromes?

The most common cause of acute coronary syndrome (ACS) is rupture of an atherosclerotic lesion containing a large necrotic core and a thin fibrous cap followed by acute luminal thrombosis because the rupture of the thin fibrous cap allows contact of the platelets with the highly thrombogenic necrotic core. Pathologic studies have suggested that the precursor of the ruptured plaque is the so-called thin cap fibroatheroma (TCFA). Unfortunately, true natural history studies of TCFAs and their transition to ruptured plaques are rare. Most of the data and concepts have been inferred from studies performed at a single point in time. Intravascular ultrasound (IVUS) studies have shown ruptured plaques in approximately two thirds of ACS culprit lesions and occur in predictable locations. The features that differentiate secondary, nonculprit plaque ruptures from those that cause ACS events appear to be superimposed thrombosis and lumen compromise, either from the thrombus or from the underlying lesion. Secondary plaque ruptures appear to heal with optimal medical therapy. In vivo definitions of TCFAs have been derived from pathology study to include positive remodeling, a fibrous cap less than 100 μm (and perhaps <65 μm) at its minimum thickness, macrophage infiltration especially in the thin fibrous cap, a large lipid/necrotic core often containing hemorrhage and/or speckled or diffuse calcification (not enough to increase plaque stability although the absence of any calcium is also rare in rupture-prone plaques), and abundant intraplaque vasa vasorum and/or hemorrhage. Early data from in vivo imaging have substantiated the pathologic observations, but have also suggested that spontaneous stabilization of TCFAs with medical therapy alone is possible.     

Role of intravascular ultrasound imaging in identifying vulnerable plaques

A plaque that has a large lipid core and a thin fibrous cap may undergo rupture. Once it ruptures, it may lead to thrombus formation and subsequent vessel occlusion. To identify unstable plaques before they rupture is essential for clinical management and patient's prognosis. Intravascular ultrasound (IVUS) opens a new window for the assessment of plaque morphology to identify vulnerable plaques and plaque rupture. We examined 144 patients with angina and ischemic ECG changes using IVUS. Ruptured plaques, characterized by a plaque cavity and a tear on the thin fibrous cap, were identified in 31 patients (group A) of which 23/31 (74%) clinically presented as unstable angina. Plaque rupture was confirmed by injecting contrast medium filling the plaque cavity during IVUS examination. Of the patients without plaque rupture (group B, n = 108), only 19 (18%) had unstable angina. No significant differences between the 2 groups were found concerning the vessel and plaque areas (p > 0.05). The percent stenosis in group A (56.2 +/- 16.5%) was significantly lower than in group B (67.9 +/- 13.4%) (p < 0.001). Area of the plaque cavity in group A (4.1 +/- 3.2 mm2) was significantly larger than the echolucent zone in group B (1.32 +/- 0.79 mm2) (p < 0.001). The plaque cavity/plaque ratio in group A (38.5 +/- 17.1%) was larger than the echolucent area/plaque ratio in group B (11.2 +/- 8.9%) (p < 0.001). The thickness of the fibrous cap in group A (0.47 +/- 0.20 mm) was significantly thinner than that (0.96 +/- 0.94 mm) in group B (p < 0.001). CONCLUSIONS: Plaques seem to be prone to rupture when the echolucent area is larger than 1 mm2, the echolucent area/plaque ratio greater than 20% and the fibrous cap thinner than 0.7 mm. IVUS has the capacity of identifying plaque rupture and vulnerable plaques. This may have potential influence on patients management and therapy.     

急性冠状动脉综合征患者易损斑块的临床病理分析

目的 观察易损斑块在急性冠状动脉综合征患者( ACS)中的病理组织学特点。方法 本研究回顾了北京医院1992-2006年尸检患者127例,分为ACS组67例;与其年龄、性别相匹配的临床表现无ACS的病例60例,从斑块的形态如有无血栓、粥池最大横切面占斑块面积、纤维帽最小厚度、炎细胞浸润密度等10个方面进行形态学观察,观...     

Visualization of coronary atherosclerotic plaques in patients using optical coherence tomography: comparison with intravascular ultrasound

OBJECTIVES: The aim of this study was to evaluate the feasibility and the ability of intravascular optical coherence tomography (OCT) to visualize the components of coronary plaques in living patients. BACKGROUND: Disruption of a vulnerable coronary plaque with subsequent thrombosis is currently recognized as the primary mechanism for acute myocardial infarction. Although such plaques are considered to have a thin fibrous cap overlying a lipid pool, imaging modalities in current clinical practice do not have sufficient resolution to identify thin (< 65 microm) fibrous caps. Optical coherence tomography is a new imaging modality capable of obtaining cross-sectional images of coronary vessels at a resolution of approximately 10 microm. METHODS: The OCT images and corresponding histology of 42 coronary plaques were compared to establish OCT criteria for different types of plaques. Atherosclerotic lesions with mild to moderate stenosis were identified on angiograms in 10 patients undergoing cardiac catheterization. Optical coherence tomography and intravascular ultrasound (IVUS) images of these sites were obtained in all patients without complication. RESULTS: Comparison between OCT and histology demonstrated that lipid-rich plaques and fibrous plaques have distinct OCT characteristics. A total of 17 IVUS and OCT image pairs obtained from patients were compared. Axial resolution measured 13 +/- 3 microm with OCT and 98 +/- 19 microm with IVUS. All fibrous plaques, macrocalcifications and echolucent regions identified by IVUS were visualized in corresponding OCT images. Intimal hyperplasia and echolucent regions, which may correspond to lipid pools, were identified more frequently by OCT than by IVUS. CONCLUSIONS: Intracoronary OCT appears to be feasible and safe. Optical coherence tomography identified most architectural features detected by IVUS and may provide additional detailed structural information.     

Vasa vasorum imaging: A new window to the clinical detection of vulnerable atherosclerotic plaques

Complications of vulnerable atherosclerotic plaques (rupture, luminal and mural thrombosis, intraplaque hemorrhage, rapid progression to stenosis, spasm, and so forth) lead to heart attacks and strokes. It remains difficult to identify what plaques are vulnerable to these complications. Despite recent developments such as thermography, spectroscopy, and magnetic resonance imaging, none of them is approved for clinical use. Intravascular ultrasound (IVUS), a relatively old yet widely available clinical tool for guiding intracoronary procedures, is increasingly used for characterization of atherosclerotic plaques. However, inability of IVUS in measuring plaque activity limits its value in detection of vulnerable plaques. In this review, we present new information suggesting that microbubble contrast-enhanced IVUS can measure activity and inflammation within atherosclerotic plaques by imaging vasa vasorum density. An increasing body of evidence indicates that vasa vasorum density may be a strong marker for plaque vulnerability. We suggest that a combination of structural assessment (cap thickness, lipid core, calcification, etc) and vasa vasorum density imaging by IVUS can serve as the most powerful clinically available tool for characterization of vulnerable plaques. Due to space limitations, all IVUS images and movies are posted on the website of the Ultimate IVUS Collaborative Project: http://www.ultimateivus.com