Angioscopy and ischemic heart disease

Angioscopy allows direct visualization of the coronary artery lumen and provides detailed information regarding the surface characteristics of the vessel wall and specific lesions causing acute coronary syndromes. Disruption of a plaque, ulceration, tears, fissures, lipid-rich or fibrous lesions, and luminal or mural thrombus can be readily detected in vivo. Characterization of culprit lesions in various coronary syndromes reveals the different mechanisms of ischemia. The predominant lesion in acute myocardial infarction is an ulcerated, yellow plaque with thrombus. In unstable angina, different substrates can be seen, from the lipid-rich lesion with thrombus to the fibrous smooth plaque, reflecting a varied physiopathology. Because of its ability to detect superficial lipid pools, angioscopy may be valuable for the detection of vulnerable plaques.     

Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study

OBJECTIVES: To test our hypothesis that the development of vulnerable plaques is not limited to the culprit lesions, but is a pan-coronary process, we directly observed all three major coronary arteries by angioscopy and evaluated the prevalence of yellow plaques in patients with myocardial infarction (MI). BACKGROUND: Although pathologic studies have suggested that the disruption of atheromatous plaque plays a major role in the development of acute MI, the prevalence of yellow plaques in the whole coronary arteries of patients with MI has not been clarified. METHODS: Thirty-two patients undergoing follow-up catheterization one month after the onset of MI were prospectively and consecutively enrolled in this study. The prevalence of yellow plaques and thrombus in the major coronary arteries was successfully evaluated in 20 patients (58 coronary arteries, 21 culprit lesions) by coronary angioscopy. The diameter stenosis (DS) of the culprit lesions and the maximal diameter stenosis (maxDS) of nonculprit segments were angiographically measured for each coronary artery. RESULTS: The DS of the culprit lesions and maxDS were 27 +/- 17% and 19 +/- 13%, respectively. Yellow plaques and thrombus were detected in 19 (90%) and 17 (81%) of 21 culprit lesions, respectively. Yellow plaques were equally prevalent in the infarct-related and non-infarct-related coronary arteries (3.7 +/- 1.6 vs. 3.4 +/- 1.8 plaques/artery). However, thrombus was only detected in the nonculprit segments of one (2%) coronary artery. CONCLUSIONS: In patients with MI, all three major coronary arteries are widely diseased and have multiple yellow though nondisrupted plaques. Acute MI may represent the pan-coronary process of vulnerable plaque development.     

High yellow color intensity by angioscopy with quantitative colorimetry to identify high-risk features in culprit lesions of patients with acute coronary syndromes

High yellow color intensity (HYCI) regions of atherosclerotic plaque, determined by angioscopy with quantitative colorimetry, are associated with lipid cores underneath thin fibrous caps in ex vivo tissue samples. To determine whether HYCI regions of coronary plaque are associated with disruption or thrombus in living patients, quantitative colorimetry was applied to angioscopy, and the color of culprit lesions was measured in patients with acute coronary syndromes. In 46 patients with acute coronary syndromes (acute myocardial infarction, n = 14; unstable angina pectoris [UAP] with culprit thrombus, n = 16; and UAP without culprit thrombus, n = 16), the recorded angioscopic images of culprit lesions were analyzed using a quantitative colorimetric method based on the L*a*b* color space applied to angioscopy (positive b* = yellow color intensity). HYCI was defined as b* value >23. Plaque disruption was significantly more prevalent in 19 of 24 HYCI regions (79%) than in 9 of 22 non-HYCI regions (41%) (p = 0.007). Culprit HYCI regions were prevalent in patients with myocardial infarction (11 of 14 [79%]), followed by those with UAP with thrombus (9 of 16 [56%]) and UAP without thrombus (4 of 16 [25%]) (p = 0.01 for trend), and were significantly more prevalent in 66% of patients with myocardial infarction and UAP with thrombus compared with 25% of those with UAP without thrombus (p = 0.007). In conclusion, HYCI regions of coronary plaque may be indicative of high-risk lesions vulnerable to thrombosis. Coronary angioscopy with quantitative colorimetry could be used to study the association between high-risk coronary lesions and future cardiovascular events.     

The healing process of infarct-related plaques: Insights from 18 months of serial angioscopic follow-up

OBJECTIVES: To clarify the healing process of disrupted culprit plaques of acute myocardial infarction (MI), we serially observed the culprit plaques for 18 months after the onset of acute MI by angioscopy. BACKGROUND: Although it has been reported that disruption of the yellow plaque and subsequent thrombosis cause acute MI and that the thrombogenicity of the plaque lasts for a month, the healing process of the plaque after disruption has not been clarified. METHODS: Eighty-five patients with acute MI were prospectively and consecutively enrolled. Angioscopic studies were performed immediately and at 1, 6 and 18 months after successful reperfusion. The prevalence of yellow plaques and thrombus was examined. The color grade of the plaque was determined as 0 (white), 1 (light yellow), 2 (yellow) or 3 (bright yellow). RESULTS: Although yellow plaque was present at the culprit lesion in most patients throughout follow-up, its color grade was reduced from one to six months (1.9 +/- 0.6 vs. 1.1 +/- 0.7, p = 0.0003) after reperfusion, especially in the patients without hyperlipidemia (HL). The incidence of thrombus was 92.5% immediately after reperfusion, which was reduced significantly to 63.8%, 4.8% and 11.8% at 1, 6 and 18 months, respectively. The incidence of thrombus (77.8% vs. 45.0%, p = 0.03) at one month was higher in the patients with diabetes mellitus (DM). CONCLUSIONS: The healing process of yellow plaques at the culprit lesions of MI was detected by angioscopy as reductions of color grade and thrombogenicity at six months and partially at one month after the onset of acute MI. This healing process appears to deteriorate by complicating cases of DM or HL.     

Plaque disruption and thrombus in Ambrose's angiographic coronary lesion types

Lesion eccentricity with irregularities on coronary angiography is associated with ruptured plaques and thrombus based on postmortem and clinical angiographic studies. However, the predictive value of such angiographic markers of plaque disruption and thrombus remains to be determined in vivo. The purpose of this study was to establish whether Ambrose's angiographic coronary lesion types and other angiographic criteria predict the presence of disrupted plaques and thrombus using intracoronary angioscopy. Angioscopy was performed before angioplasty in 60 patients with various coronary syndromes and culprit lesions that were not totally occlusive. Lesions were classified angiographically according to Ambrose's criteria as concentric, type I and II eccentric, and multiple irregularities, or as complex or noncomplex, and then compared with the corresponding angioscopic findings. Disruption and/or thrombus were seen in 17 of 19 type II eccentric lesions and 21 of 23 angiographically complex lesions and had the highest positive predictive value to detect complicated atherosclerotic plaques (type II eccentric lesions: positive predictive value 89%, 95% confidence intervals 67% to 99%; complex lesions: 91%, 95% confidence intervals 72% to 99%). We conclude that Ambrose's type II eccentric stenoses and angiographically complex lesions are strongly associated with disrupted plaques and/or thrombus as assessed by angioscopy in patients and represent unstable plaque substrates.     

Number of yellow plaques detected in a coronary artery is associated with future risk of acute coronary syndrome: detection of vulnerable patients by angioscopy.

OBJECTIVES: We sought to test whether the risk of acute coronary syndrome (ACS) can be estimated by angioscopy. BACKGROUND: Disruption of vulnerable plaque and subsequent thrombosis is regarded as a major mechanism of ACS. Although yellow plaques are supposedly vulnerable, the association between angioscopically determined extent of coronary atherosclerosis and risk of ACS events has not been reported. METHODS: Patients (n = 552) who received catheterization and angioscopic examination for the diagnosis of coronary artery diseases were prospectively included and followed up for new onset of ACS events. Yellow color intensities of all detected yellow plaques were graded as 1, 2, or 3 according to the standard colors. Number of yellow plaques (NYP) in a coronary artery and maximum color grade of detected yellow plaques (maxYP) were determined. Association between the incidence of ACS events and angioscopic findings were analyzed. RESULTS: Follow-up interval was 57.3 +/- 22.1 months. Acute coronary syndrome events were detected in 39 patients (7.1%). Although maxYP was not statistically different (2.0 +/- 0.7 vs. 1.8 +/- 0.9; p = 0.18), NYP was higher in the patients with an ACS event than those without the event (3.1 +/- 1.8 vs. 2.2 +/- 1.5; p = 0.008). Patients with NYP > or =2 and those with NYP > or =5 had 2.2- and 3.8-fold higher event rates, respectively, than those with NYP 0 or 1 (9.0% and 15.6%, respectively, vs. 4.1%; p = 0.02). Multivariate logistic regression analysis revealed NYP and multivessel disease as the independent risk factors of ACS events. CONCLUSIONS: Patients with multiple yellow plaques per vessel have a higher risk of suffering ACS events than those with NYP 0 or 1. Angioscopy would be useful to detect vulnerable patients.     

Frequency and healing of nonculprit coronary artery plaque disruptions in patients with acute myocardial infarction

The pathophysiology of plaque disruption and healing in nonculprit segments has not been clarified. Therefore, we investigated the frequency of plaque disruptions in nonculprit segments and whether those plaques are stabilized during follow-ups in patients with acute myocardial infarction (AMI) by serial angioscopic observations. Analyzed were 13 consecutive patients with AMI in whom infarct-related arteries were serially observed by angioscopy immediately after reperfusion and at 1- and 6-month follow-ups. Color of plaques was graded as 0 (white), 1 (slight yellow), 2 (yellow), or 3 (intensive yellow). Plaques with thrombus were defined as disrupted. Although number of nonculprit yellow plaques did not change from immediately after reperfusion to 6 months, the maximum color grade of those plaques and incidence of disrupted plaques in nonculprit segments (immediate vs 1 month vs 6 months 31% vs 8% vs 0%) decreased significantly by 6 months. Plaque stabilization as shown by disappearance of thrombus was significantly associated with plaque regression as shown by a decrease of maximum yellow color grade in nonculprit segments. In conclusion, patients with AMI frequently had disrupted and actively thrombogenic yellow plaques in nonculprit segments of the culprit vessel, and those plaques healed with decreases of yellow color grade and thrombogenicity during 6-months follow-up. Plaque disruption and healing occur not only at the culprit lesion but may be a pan-coronary process in patients with AMI.     

Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions

OBJECTIVES: Changes of ruptured plaques in nonculprit lesions were evaluated using coronary angioscopy. BACKGROUND: The concept of multiple coronary plaque ruptures has been established. However, no detailed follow-up studies of ruptured plaques in nonculprit lesions have yet been reported. METHODS: Forty-eight thrombi in 50 ruptured coronary plaques in nonculprit lesions in 30 patients were identified by angioscopy. The percent diameter stenosis (%DS) at the target plaques on quantitative coronary angiographic analysis and the serum C-reactive protein (CRP) level were measured. RESULTS: The mean angioscopic follow-up period was 13 +/- 9 months. Thirty-five superimposed thrombi still remained at follow-up, and the predominant thrombus color changed from red (56%) at baseline to pinkish-white (83%) at follow-up. The healing rate increased according to the angioscopic follow-up period (23% at 12 months, p = 0.044). The %DS at the healed plaque increased from baseline to follow-up (12.3 +/- 5.8% vs. 22.7 +/- 11.6%, respectively; p = 0.0004). The serum CRP level in patients with healed plaques (n = 10) was lower than that in those without healed plaques (n = 19; 0.07 +/- 0.03 mg/dl vs. 0.15 +/- 0.11 mg/dl, respectively; p = 0.007). CONCLUSIONS: The present study demonstrated that: 1) ruptured plaques in nonculprit lesions tend to heal slowly with a progression of angiographic stenosis; and 2) the serum CRP level might reflect the disease activity of the plaque ruptures.     

Update on coronary angioscopy: review of a 20-year experience and potential application for detection of vulnerable plaque

Predicting the occurrence of future acute coronary syndromes remains an important challenge of contemporary cardiology. It is thought that detecting the individual vulnerable plaques in patients can be an important step to preventing myocardial infarction and sudden cardiac death. Coronary angioscopy can provide detailed information of the luminal surface of plaque, such as color, thrombus, or disruption, and is one of a few possibly useful imaging modalities for identifying vulnerable plaques. During its 20-year history, coronary angioscopy has been used as a diagnostic tool or to guide coronary angioplasty, and has contributed to our understanding of the pathophysiology of coronary artery disease. Yellow plaques seen during angioscopy seem to have many characteristics of high risk or vulnerable plaques, most consistent with the thin-cap fibroatheroma. Moreover, differences in yellow color have been reported to reflect differences in the structure or composition of plaques. Development of quantitative methods to assess plaque color and histopathologic correlations in conjunction with prospective natural history studies may lead to advances in vulnerable plaque detection by coronary angioscopy. Although current angioscopic devices are limited by the need to displace the column of blood in order to see the vessel wall, and by the lack of quantitative colorimetric methods, advances in technology may lead to new device versions that could be practical for expanded clinical use.     

Morphologic changes in infarct-related plaque after coronary stent placement: a serial angioscopy study

OBJECTIVES: The aim of this study was to investigate the morphologic changes in infarct-related lesions after stenting in acute or recent myocardial infarction (MI) with coronary angioscopy. BACKGROUND: There is no information on the serial morphologic changes, which occur after stenting, and the time course of neointimal coverage of stents for disrupted unstable plaques. METHODS: Forty-three patients with MI within seven days of onset were examined. Angioscopy was serially performed for the infarct-related lesions at baseline (n = 43), after balloon angioplasty (n = 35), and after stenting following balloon angioplasty (n = 39) and at one (n = 36) and six months (n = 30) after stenting. RESULTS: At baseline, most of the lesions had complex morphology, yellow plaque color, and protruding thrombus (96%, 96%, and 74%, respectively). Although balloon angioplasty reduced the protruding thrombus, it remained in 37%, and an intimal flap was observed in 89% of the lesions. After stenting, the protruding thrombus and intimal flap disappeared, with an increased luminal size obtained in all lesions. At one-month follow-up, an irregular and yellow surface, along with a lining thrombus, was still observed, with partial neointimal stent coverage in most of the lesions. At six-month follow-up, the neointima was found to have sufficiently formed over the stent. The plaque shape and color were almost all classified as smooth (97%) and white (93%). CONCLUSIONS: These results suggest that a stent not only compressed and covered a disrupted plaque with a protruding thrombus and intimal flap, leading to a wide vessel lumen, but also helped to seal the unstable plaque through neointimal proliferation.     

Assessment of plaque vulnerability by angioscopic classification of plaque color

Background

The disruption of yellow plaque and subsequent thrombosis is regarded as the mechanism of acute coronary syndrome. However, there are limited reports on the assessment of plaque vulnerability. Therefore, we tested whether the angioscopically determined yellow color intensity of plaque is associated with the prevalence of thrombosis on the plaque.

Methods

The angioscopic images of 843 patients who underwent catheterization and angioscopic examination from November 1999 to July 2003 for the diagnosis of coronary artery diseases were analyzed. Suspected culprit vessel was observed by angioscopy, and the yellow color intensity (1, light yellow; 2, yellow; 3, intensive yellow) of all yellow plaques (n = 1253) detected in the nonstenotic (diameter stenosis <50%) coronary segments was determined, as well as whether there was thrombosis on the plaques.

Results

The number of detected yellow plaques was 345, 721, and 187 for color grade 1, 2, and 3, respectively. The prevalence of thrombosis detected by angioscopy (15%, 26%, and 52% on the plaque of color grade 1, 2, and 3, respectively, P < .0001) was significantly higher on the plaque of higher yellow color grade.

Conclusions

The yellow color intensity of plaque determined by angioscopy was strongly related with the prevalence of thrombosis on the plaque. The yellow color intensity may be a marker of plaque vulnerability.     

The clinical utility of angioscopy during intracoronary stent implantation

Angiographic evidence of thrombus may have important implications during coronary stent deployment procedures. The periprocedural presence of thrombus has been shown to increase the risk of subsequent stent thrombosis. Coronary angioscopy is a new technology that may prove more accurate for the detection of coronary thrombus. Angiographic filling defects suspicious for thrombus were observed in 15 (22%) of 64 patients undergoing coronary angioscopy during stent implantation procedures. Angioscopy confirmed the presence of thrombus in 9 (60%) of these 15 patients. Protruding thrombus was found in four cases and only mural thrombus in five. In six cases (40%) thrombus was not visualized and angioscopy provided an alternative explanation for the angiographic filling defect. Bulky atherosclerotic plaque was seen protruding into the lumen in two cases, disection with protruding fronds of tissue was found in three cases and a ruptured venus valve was found in one final case. Thrombolytic therapy was administered in all four cases containing protruding thrombus, in only two of the five cases containing mural thrombus, and in none of the cases where thrombus was not visualized. Angioscopy was more accurate than angiography for the diagnosis of thrombus and allowed more precise tailoring of the intervention to the underlying anatomical substraight. This resulted in an excellent clinical outcome, with no episodes of stent thrombosis and limitation of the risks associated with thrombolytic therapy to only those patients at increased risk of a thrombotic complication.     

Recent advances in coronary angioscopy

Angioscopy enables macroscopic pathological diagnosis of cardiovascular diseases from the inside. This imaging modality has been intensively directed to characterizing vulnerable coronary plaques. Scoring of plaque color was developed, and based on prospective studies; dark yellow or glistening yellow plaques were proposed as vulnerable ones. Colorimetry apparatus was developed to assess the yellow color of the plaques quantitatively. The effects of lipid-lowering therapies on coronary plaques were confirmed by angioscopy. However, since observation is limited to surface color and morphology, pitfalls of this imaging technology became evident. Dye-staining angioscopy and near-infrared fluorescence angioscopy were developed for molecular imaging, and the latter method was successfully applied to patients. Color fluorescence angioscopy was also established for molecular and chemical basis characterization of vulnerable coronary plaques in both in vitro and in vivo. Drug-eluting stents (DES) reduce coronary restenosis significantly, however, late stent thrombosis (LST) occurs, which requires long-term antiplatelet therapy. Angioscopic grading of neointimal coverage of coronary stent struts was established, and it was revealed that neointimal formation is incomplete and prevalence of LST is higher in DES when compared to bare-metal stent. Many new stents were devised and they are now under experimental or clinical investigations to overcome the shortcomings of the stents that have been employed clinically. Endothelial cells are highly anti-thrombotic. Neoendothelial cell damage is considered to be caused by friction between the cells and stent struts due to the thin neointima between them that might act as a cushion. Therefore, development of a DES that causes an appropriate thickness (around 100 μm) of the neointima is a potential option with which to prevent neoendothelial cell damage and consequent LST while preventing restenosis.     

不稳定性心绞痛患者冠状动脉内粥样斑块的稳定性与血栓形成关系的探讨

目的　应用冠状动脉血管内视镜技术对不稳定性心绞痛(unstableanginapectoris, UA)患者的罪犯血管内粥样斑块的稳定性与血栓形成之间的关系进行探讨,为研究急性冠状动脉综合征(acutecoronarysyndromes, ACS)的发生提供临床病理基础。方法　选择UA患者68例,男性48例,女性20例,年龄40~73(62.4±8 .6)岁,除外心肌梗死后心绞痛和变异性心绞痛患者。上述患者在进行冠状动脉介入性检查和治疗的同时,对其“罪犯”血管进行血管内视镜检查。结果　(1) 68例患者(68支“罪犯”血管)中均观察到粥样斑块(100% ),其中有血栓者63例(92 .7% ),有内膜损伤者46例(67. 7% )。(2)68例冠状动脉粥样斑块者中,黄色斑块者48例( 70 .5% ),淡黄色斑块者18例(26. 5% ),白色斑块者2例(2. 9% )。(3)63例血栓均为附壁性非闭塞性血栓,其中红色或混合性血栓11例(17. 5% ),白色或粉红色血栓52例(82. 5% )。(4)46例内膜损伤者中均可见到血栓形成,其中红色或混合性血栓11例(23.9% ),白色或粉红色血栓35例(76. 1% )。结论　在UP患者中观察到黄色不稳定性斑块破裂及其伴随的血栓形成,是引起UA的病理基础。因此,在黄色斑块破裂之前采取何种治疗措施使其稳定化,是预防ACS的关键。     

Relation between plasma adiponectin, high-sensitivity C-reactive protein, and coronary plaque components in patients with acute coronary syndrome

The present study investigated the relation between plasma high-sensitivity C-reactive protein (hs-CRP) and adiponectin and coronary plaque components in patients with acute coronary syndrome (ACS). Previous studies showed a pivotal role of inflammation in the progression of atherosclerosis and the prognostic value of several biomarkers. However, relations among inflammatory biomarkers and plaque characteristics were unknown. Ninety-three culprit plaques (ACS n = 50, non-ACS n = 43) and 56 nonculprit plaques (ACS n = 28, non-ACS n = 28) were analyzed using Virtual Histology intravascular ultrasound to examine relations among plasma hs-CRP, adiponectin, and ratios of each coronary plaque component. Plasma adiponectin was significantly lower and plasma hs-CRP was significantly higher in patients with than without ACS. Culprit plaques in patients with ACS had greater amounts of necrotic core plaque than those in patients without ACS. There was an inverse relation between serum hs-CRP and adiponectin with regard to necrotic core ratio in both culprit and nonculprit lesions in patients with ACS, but not those without ACS. In conclusion, increased plasma hs-CRP and hypoadiponectinemia might be related to the progression of ACS.     

Comparison of virtual histology to intravascular ultrasound of culprit coronary lesions in acute coronary syndrome and target coronary lesions in stable angina pectoris

Coronary plaque composition cannot be assessed accurately using gray-scale intravascular ultrasound (IVUS). Using virtual histology IVUS (VH-IVUS), a comparison of coronary plaque composition between acute coronary syndromes (ACS) and stable angina pectoris (SAP) was performed. Preintervention IVUS of de novo culprit and target lesions was performed in 318 patients (123 with ACS and 195 with SAP). Using VH-IVUS, plaque was characterized as fibrotic, fibrofatty, dense calcium, and necrotic core. VH-IVUS-derived thin-cap fibroatheroma (VH-TCFA) was defined as necrotic core>or=10% of plaque area without overlying fibrous tissue in a plaque burden>or=40%. Lesions were classified into 3 groups: ruptured, VH-TCFA, and non-VH-TCFA plaque. Unstable lesions were defined as either VH-TCFA or ruptured plaque. Compared with patients with SAP, those with ACS had significantly more unstable lesions (89% vs 62%, p<0.001). Planar VH-IVUS analysis at the minimum luminal site and at the largest necrotic core site and volumetric analysis over a 10-mm-long segment centered at the minimum luminal site showed that the percentage of necrotic core was significantly greater and that the percentage of fibrofatty plaque was significantly smaller in patients with ACS. The percentages of fibrotic and fibrofatty plaque areas and volumes were smaller, and the percentages of necrotic core areas and volumes were larger in VH-TCFAs compared with non-TCFAs. Ruptured plaques in VH-IVUS analyses showed intermediate findings between VH-TCFAs and non-VH-TCFAs. In conclusion, culprit lesions in patients with ACS were more unstable and had greater amounts of necrotic core and smaller amounts of fibrofatty plaque compared with target lesions in patients with SAP.     

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.     

多层螺旋CT评价急性冠状动脉综合征及稳定性心绞痛患者斑块特征的作用

目的利用多层螺旋CT评价急性冠状动脉综合征(ACS)及稳定性心绞痛(SAP)患者冠状动脉病变的差异。方法连续性入选诊断为ACS及SAP、并于介入治疗前72h内行多层螺旋CT检查的患者45例,将诊断为ACS的31例作为ACS组,诊断为SAP的14例作为SAP组,将ACS组的病变分为罪犯病变和非罪犯病变,SAP组的病变定义为稳定病变;比较冠状动脉病变性质。结果 2组共有60处病变,ACS组40处,SAP组20处;ACS组罪犯病变非钙化斑块和脂质斑块比例明显高于同组非罪犯病变及SAP组的稳定病变(96.8%vs 55.6%vs 20.0%,83.3%vs 40.0%vs 25.0%,P<0.01);ACS组罪犯病变的血管截面积、斑块面积、重构指数、斑块的偏心指数明显高于同组的非罪犯病变及SAP组的稳定病变(P<0.05)。结论多层螺旋CT作为无创的影像学工具,可识别ACS与SAP患者冠状动脉斑块病变的差异。     

Multiple ruptures of atherosclerotic plaques in acute coronary syndrome. Endocoronary ultrasonography study of three arteries

The aim of this study was to assess the three coronary arteries systematically by endocoronary ultrasonography in patients with unstable angina to check the hypothesis of global destabilisation of atherosclerotic plaques in acute coronary syndromes (ACS). Sixty two coronary arteries were examined (2.6 per patient). Fifty plaque ruptures were diagnosed (2.08 per patient). Rupture of a plaque of the culprit lesion of the ACS was clearly detected in 9 patients (37.5%). At least one ruptured plaque on a site other than the culprit lesion was observed in 19 patients (79%), on another artery in 70.8% of cases and on two other arteries in 12.5% of cases. A complete endocoronary ultrasonic examination of the three coronary arteries in patients with a first ACS demonstrated that: multiple atherosclerotic plaque rupture may be detected by endocoronary ultrasonography; these multiple plaque ruptures occur simultaneously with the culprit lesion; they are frequent and can be situated on the three main coronary vessels and multiple plaque rupture other than the culprit lesion are less severe, non stenotic and less calcified. Thus, although a single lesion is clinically symptomatic, ACS seems to be associated with global coronary instability.