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   

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.     

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.     

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.     

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.     

Pathological characterization of yellow and white plaques under angioscopy

Recently it has been reported that the lipid core area and the fibrous cap thickness cannot be deduced from the stenotic ratio. However, there is no comparative study between yellow and white plaques. This study assessed the precise characterization of yellow and white plaques using angioscopy. We observed 198 segments of coronary from autopsy artery using angioscopy, then 46 yellow plaque lesions and 61 white plaque lesions of atheroma were excised and prepared for pathological examination. The stenotic ratio, the plaque area (PA), the lipid core size as a percentage of total vessel area (%C), and the minimum fibrous cap thickness (FCt) were measured and compared between yellow and white plaque groups. In this study, the stenotic ratio and the PA were significantly larger in the white plaque group (p<.001). The FCt was significantly thinner in the yellow plaque group (58±18 µm vs. 648±356 µm p<.0001). There was no correlation between the stenotic ratio and the %C in the whole cases (r=.22). Although it was the same in the white plaque group (r=.13), significant correlation between them was shown in the yellow plaque group (r=.64). No significant correlation was observed between the stenotic ratio and the FCt in each plaque group. We concluded that a yellow plaque with moderate stenosis could be diagnosed as a vulnerable plaque by the combination of coronary angiography and angioscopy.     

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.     

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。     

Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study in vivo

OBJECTIVES: This study was designed to identify potential differences between the intravascular ultrasound (IVUS) characteristics of spontaneously ruptured and nonruptured coronary plaques. BACKGROUND: The identification of vulnerable plaques in vivo may allow targeted prevention of acute coronary events and more effective evaluation of novel therapeutic approaches. METHODS: Intravascular ultrasound was used to identify 29 ruptured plaques in arteries containing another nonruptured plaque in an adjacent segment. Intravascular ultrasound characteristics of these plaques were compared with plaques of computer-matched controls without evidence of plaque rupture. Plaque distribution was assessed by measuring the eccentricity of lumen location (inside the total vessel). Lumen cross-sectional area narrowing was calculated as [1 - (target/reference lumen area)] x 100%. A remodeling index was calculated as lesion/reference arterial area (>1.05 = compensatory enlargement, <0.95 = shrinkage). RESULTS: Among the three groups of plaques, there was no significant difference in quantitative angiographic parameters, IVUS reference dimensions and IVUS lumen cross-sectional area narrowing. There was a difference in plaque distribution; lumen location by IVUS was significantly more eccentric in ruptured than in nonruptured (p = 0.002) and control plaques (p < 0.0001). The arc of disease-free vessel wall was larger in ruptured than in control plaques (p < 0.0001). The remodeling pattern of ruptured and nonruptured plaques differed significantly from that of the control plaques (p = 0.0001 and 0.003); compensatory enlargement was found in 66%, 48%, and 17%, whereas shrinkage was found in 7%, 10% and 48%, respectively. CONCLUSIONS: Intravascular ultrasound assessment of plaque distribution and vascular remodeling may help to classify plaques with the highest probability of spontaneous rupture.     

Morphology of vulnerable coronary plaque: insights from follow-up of patients examined by intravascular ultrasound before an acute coronary syndrome

OBJECTIVES: To determine the morphologic features of coronary plaques associated with acute coronary syndrome, we prospectively followed patients with atherosclerotic disease identified by intravascular ultrasound (IVUS). BACKGROUND: Although clinical evaluation of the vulnerable atherosclerotic plaque is important, few data exist regarding the morphology of the vulnerable plaque in clinical settings. METHODS: We examined 114 coronary sites without significant stenosis by angiography (<50% diameter stenosis) in 106 patients. All the sites exhibited atherosclerotic lesions by IVUS. These lesions consisted of 22 concentric and 92 eccentric plaques with a percent plaque area averaging 59 +/- 12%. RESULTS: During the follow-up period of 21.8 +/- 6.4 months (range 1 to 24), 12 patients had an acute coronary event at a previously examined coronary site at an average of 4.0 +/- 3.4 months after the initial IVUS study. All the preexisting plaques related to the acute events exhibited an eccentric pattern and the mean percent plaque area was 67 +/- 9%, which was greater than plaque area in the other 90 patients without acute events (57 +/- 12%, p < 0.05). There was no statistically significant difference in lumen area between two patient groups (6.7 +/- 3.0 vs. 7.5 +/- 3.7 mm2). Among 12 coronary sites with an acute occlusion, 10 sites contained the echolucent zones, eight of these shallow and two deep, likely representing a lipid-rich core. In 90 sites without acute events, an echolucent zone in the shallow portion was seen at only four sites (p < 0.05). CONCLUSIONS: Large eccentric plaque containing an echolucent zone by IVUS can be at increased risk for instability even though the lumen area is preserved at the time of initial study. Compensatory enlargement of vessel wall due to remodeling may contribute to the relatively small degree of stenosis by angiography.     

Assessment of vulnerable plaques causing acute coronary syndrome using integrated backscatter intravascular ultrasound.

OBJECTIVES: This study aims to define tissue characteristics of vulnerable plaques before acute coronary syndrome (ACS) by use of integrated backscatter intravascular ultrasound (IB-IVUS). BACKGROUND: Tissue characterization of coronary plaques is possible with the use of IB-IVUS. METHODS: The subjects were 140 patients with angina pectoris, and we selected 160 coronary lesions without significant stenosis for evaluation. Ultrasound signals were obtained by an IVUS system using a 40-MHz catheter. RESULTS: At the follow-up (30 +/- 7 months), 12 plaques caused ACS after the initial IVUS examination. Ten of the 12 plaques had IVUS parameters recorded at baseline. These 10 plaques were classified as vulnerable plaques (VP), and the other plaques were classified as stable plaques (SP; n = 143). There was no significant difference of vessel area, lumen area, and plaque area between VP and SP. However, plaque burden (60 +/- 9% vs. 52 +/- 9%; p = 0.014), eccentricity (0.70 +/- 0.10 vs. 0.55 +/- 0.17; p = 0.013), remodeling index (1.30 +/- 0.08 vs. 1.16 +/- 0.16; p = 0.006) and percentage lipid area (72 +/- 10% vs. 50 +/- 16%; p < 0.0001) were greater in VP than in SP. Percentage fibrous area (23 +/- 6% vs. 47 +/- 14%; p < 0.0001) was smaller in VP than in SP. The sensitivities, specificities, and positive predictive values of percentage fibrous area (90%, 96%, and 69%, respectively) and percentage lipid area (80%, 90%, and 42%, respectively) for classifying VP were evaluated. CONCLUSIONS: Tissue characteristics of VP before ACS were different from those of SP. This suggests that VP and SP as classified by IB-IVUS are useful in predicting ACS.     

Plaque Characterization and Atherosclerosis Evaluation by Coronary Angioscopy

When observed by angioscopy, the culprit lesions of acute coronary syndrome (ACS) have a common appearance of a yellow plaque with irregular surface covered by a thrombus. Angioscopy is a powerful device to detect not only the ruptured plaques at ACS lesions but also the yellow plaques in their early stages. The culprit lesions of ACS are sometimes detected by angioscopy even in the angiographically normal segments of coronary arteries. Angioscopy can further classify the culprit lesions of ACS as (1) vasospasm, (2) plaque rupture, or (3) plaque erosion according to the angioscopic definitions. These classifications may be beneficial to determine the treatment strategy. Anti-vasospastic medications rather than stenting may be more suitable for the treatment of vasospasm-induced ACS. Percutaneous coronary intervention (PCI) of ruptured plaque rather than of erosive plaque tends to cause more distal embolization with thrombus and plaque contents. Therefore, distal protection device may be more beneficial for those cases. Although angioscopy may be able to identify vulnerable plaques as the plaques of intensive yellow color, it may be more practical to identify the patients at high risk of suffering ACS by evaluating the extent of coronary atherosclerosis. The process and the time course of plaque formation, maturation, and disruption are left to be clarified, however, the number of yellow plaques or the yellow color intensity of those plaques may be a marker of coronary atherosclerosis. Angioscopy should be useful not only as a diagnostic tool but also as an investigational tool. The effect of medications that regress coronary atherosclerosis may be evaluated by the angioscopically determined markers of coronary atherosclerosis.     

Relation between baseline plaque burden and subsequent remodelling of atherosclerotic left main coronary arteries: a serial intravascular ultrasound study with long-term (> or =12 months) follow-up.

AIMS: Glagov's histopathological observation and non-serial intravascular ultrasound studies (IVUS) concluded that compensatory coronary remodelling diminishes as 40% atherosclerotic plaque burden is reached. We tested this hypothesis with serial IVUS. METHODS AND RESULTS: Serial IVUS examinations of 46 atherosclerotic non-stenotic left main stems (18+/-8 months apart) were analysed to assess the relation between baseline plaque burden (=plaque+media area/vessel area) vs. serial remodelling (=vessel area at baseline - at follow-up). There were 25 plaques with baseline plaque burden <40% (30.1+/-6.6%, group A) and 21 plaques with baseline plaque burden > or =40% (46.1+/-5.8%, group B). There was no relation between baseline plaque burden vs. subsequent changes in vessel area overall (r=0.07, P=0.7), for group A (r=0.03, P=0.6), and group B (r=0.01, P=0.8). The frequency of positive serial remodelling (vessel area increase) vs. negative or intermediate serial remodelling (no change or decrease) were similar in group A [17 (68%) vs. 8 (32%)] and group B lesions [18 (86%) vs. 3 (14%)] (P=0.2). CONCLUSION: IVUS demonstrates that serial coronary remodelling is not related to baseline plaque burden. Lesions with baseline plaque burden <40% may subsequently show a lack of compensation or frank arterial shrinkage, whereas lesions with baseline plaque burden >40% may continue to develop compensatory enlargement.     

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.     

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.     

Changes in coronary plaque color and morphology by lipid-lowering therapy with atorvastatin: serial evaluation by coronary angioscopy

OBJECTIVES: Changes in coronary plaque color and morphology by statin therapy were evaluated using coronary angioscopy. BACKGROUND: Coronary plaque stabilization by statin therapy has not been clarified in humans. METHODS: Thirty-one patients with coronary artery disease were divided into either the comparison group (n = 16) or the atorvastatin group (n = 15). Before treatment and 12 months after, the color and complexity of 145 coronary plaques were determined according to angioscopic findings. The yellow score of the plaque was defined as 0 (white), 1 (light yellow), 2 (yellow), or 3 (dark yellow), and its disrupted score was defined as 0 (smooth surface) or 1 (irregular surface) and as 0 (without thrombus) or 1 (with thrombus). In each patient, the mean yellow score and mean disrupted score were calculated. RESULTS: Mean low-density lipoprotein cholesterol (LDL-C) decreased by 45% in the atorvastatin group, whereas an increase of 9% was seen in the comparison group. The mean yellow score decreased from 2.03 to 1.13 in the atorvastatin group, whereas it increased from 1.67 to 1.99 in the comparison group. There was a good correlation between the change in the mean yellow score and the change in LDL-C levels (r = 0.81, p < 0.0001). The change in the mean yellow score and mean disrupted score differed significantly between the two groups (p = 0.002 and p = 0.03, respectively). CONCLUSIONS: This is the first report clarifying detailed changes in coronary plaque by statin in humans. This study indicated that lipid-lowering therapy changes plaque color and morphology and should then lead to coronary plaque stabilization.     

Intravascular ultrasonic analysis of plaque characteristics associated with coronary artery remodeling.

We sought to determine the patient and plaque characteristics associated with the different forms of arterial remodeling as seen by intravascular ultrasound (IVUS) before coronary intervention. Remodeling in response to plaque accumulation may occur in the form of compensatory enlargement and/or focal vessel contraction. Previous studies report variation in the frequency and form of arterial remodeling. We performed preintervention IVUS imaging on 169 patients. Vessels were categorized as exhibiting compensatory enlargement or focal contraction if the arterial area at the lesion was larger or smaller, respectively, than both proximal and distal reference arterial areas; otherwise the artery was considered not to have undergone significant remodeling. Calcification was assessed and noncalcified plaque density was measured by videodensitometry. Sixty-one of 169 patients (66 narrowings) (46 men and 15 women, age 56+/-11 years) had adequate reference segments. Remodeling occurred in 43 of 66 patients (65%): compensatory enlargement in 27 of 66 (41%) and focal contraction in 16 of 66 (24%). Lesions with focal contraction had significantly smaller arterial area (13.3+/-3.3 vs. 18.1+/-7.0 mm2, p = 0.02) and plaque area (9.5+/-2.8 vs 13.7+/-5.5 mm2, p<0.01). Cross-sectional stenosis was similar (71+/-9% vs. 75+/-10%, p = NS), as was plaque density (p = 0.20), eccentricity, and calcium. Patient age, gender, and lesion location were not related to the form of remodeling. Similarly, history of diabetes, hypercholesterolemia, or hypertension was not predictive. Smoking was the only risk factor associated with focal contraction (p<0.01). Thus, whereas compensatory enlargement appears to be the most common form of coronary artery remodeling, focal contraction occurs more often in smokers.     

Carotid atherosclerotic plaque instability in patients with acute myocardial infarction

The instability of atherosclerotic plaque is partly determined by local factors, but systemic factors such as infection, inflammation, autoimmunity or genes might also be important. We aimed to analyze whether patients with acute myocardial infarction (AMI) might have a higher proportion of unstable plaques in the carotid arteries compared with patients who had had no acute coronary events. METHODS: Sixty-nine consecutive patients with AMI (Group 1) and 95 patients without acute coronary events (Group 2) had carotid artery duplex ultrasounds. Carotid atherosclerosis was quantified by number of plaques in the two carotid arteries, intimal media thickening and degree of maximal stenosis. According to their morphology, plaques were divided into stable (fibrocalcific) and unstable (soft and/or not homogeneous). RESULTS: The two groups did not differ as regards age (66+/-8 vs. 68+/-19; p=0.3), female sex (13% vs. 21%; p=0.3), mean number of carotid plaques (2.8+/-1 vs. 2.5+/-2; p=0.2), degree of stenosis (59+/-2% vs. 36+/-1%; p=0.2) or intimal media thickening (1.04+/-0.2 vs. 1.06+/-0.2; p=0.8). However, Group 1 pts more frequently had unstable carotid plaques compared with Group 2 (43% vs. 15%; p=0.004), and had a greater number of unstable carotid plaques (0.51+/-0.6 vs. 0.16+/-0.4: p<0.0001) and a higher ratio of unstable to stable plaque (19% vs. 8%; p=0.005). In the overall population, logistic regression analysis showed that after adjustment for degree of maximal stenosis, the presence of coronary artery event (AMI pts) predicted the presence of unstable carotid plaque (OR: 4.3 95% CI: 2.0-9.2; p=0.0002). CONCLUSION: Patients with unstable coronary artery disease expressed clinically as AMI, frequently had unstable atherosclerotic plaques in other arterial sites such as carotid arteries. This finding supports the hypothesis that plaque instability might reflect a systemic process.     

Angioscopic predictors of restenosis following coronary angioplasty--the impact of yellow smooth plaques

Despite angioscopy being used for more than 10 years, data regarding the prognostic significance are still limited. This study evaluated the prognostic relevance of the angioscopic lesion morphology and plaque colour on restenosis rate following coronary angioplasty. Out of 66 patients with coronary angioscopy prior to an angioplasty procedure, 46 patients with successful balloon dilation and 16 patients with stenting were included into the study. Angioscopic plaque morphology and plaque colour were correlated with the anginal status, the angiographic lesion morphology, the procedural result, and the restenosis rate during six months follow-up. Clinical follow-up was obtained from all patients, re-angiography was performed in 61%. Angioscopically complicated lesions were more frequent in patients with unstable versus stable angina (63% versus 28%, p < 0.005) and ACC/AHA type B2/C versus A/B1 stenoses (86% versus 7%, p < 0.03). In addition yellow plaques were more often seen in unstable versus stable angina (80% versus 50%, p < 0.02) and in type B2/C versus A/B1 lesions (81% versus 47%, p < 0.005). There were no deaths or myocardial infarctions during follow-up. Restenosis (n = 11) occurred significantly more frequent in patients with smooth, yellow lesions (37%) compared to all other lesion morphologies (9%, p < 0.02). Logistic regression analysis revealed angioscopically smooth, yellow plaques (p < 0.05) and angiographically type B2/C lesions (p < 0.03) as independent predictors for restenosis. We conclude that angioscopically smooth, yellow plaques covered by an intact inner vessel surface are associated with a higher incidence of restenosis following coronary angioplasty, potentially indicating a higher proliferative response after a mechanical trauma of such lesions.     

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.