Intact Fibrous Cap Research Articles

In vivo vulnerability grading system of plaques causing acute coronary syndromes: An intravascular imaging study

BackgroundAutopsy studies shed light on the interplay between fatal acute coronary syndromes (ACS) and features of plaque vulnerability. This is a prospective pilot study designed for generating a new in vivo imaging grading system of plaque vulnerability. MethodsWe studied 87 coronary vessels in 63 consecutive patients: 48 with Acute Coronary Syndrome (ACS) and 15 with stable coronary artery disease using IntraVascular-Ultrasound Near-Infrared-Spectroscopy (IVUS-NIRS) and Optical Coherence Tomography (OCT). We identified 99 lesions: 21 were the ACS culprit lesions (18 ulcerations and 3 with intact fibrous cap), 78 were non-culprit lesions including plaques located in the same ACS culprit vessel (N12), plaques located in a non-culprit vessel in patients with ACS (28) and target lesions of stable patients (N 38). A second analysis focused on lipid plaques, comparing the 18 ACS culprit ulcerated lesions and the 55 non-culprit lesions. ResultsThe co-presence of the following three features of vulnerability [Minimal Luminal Area (MLA) <4 mm2, Fibrous Cap Thickness (FCT) < 75 μm and superficial macrophages] was by far more frequent in ACS culprit lesions than in controls (OR 40.6 for all lesions and OR 45.7 for ulcerated culprit lesions only). The triple-feature OCT grading identified vulnerable plaques with a much higher accuracy than that obtained applying each single feature of vulnerability. ConclusionsThe co-presence of the 3 OCT features of vulnerability (MLA < 4 mm2, FCT < 75 μm and superficial macrophages) identifies culprit ACS lesions with a very high odd ratio. This finding could set the basis for a new OCT vulnerability grading system including superficial macrophages.

CLINICAL SIGNIFICANCE OF LIPID-RICH PLAQUE WITH INTACT FIBROUS CAP DEFINED BY OPTICAL COHERENCE TOMOGRAPHY IN ACUTE MYOCARDIAL INFARCTION

Lipid-rich plaque (LRP) is thought to be a precursor to cardiac events. Intact fibrous cap (IFC) has different underlying pathology in comparison with plaque rupture. Nevertheless, clinical significance of LRP with IFC in acute myocardial infarction (AMI) culprit lesions has not fully elucidated in

Optical Coherence Tomography Guidance in Management of Acute Coronary Syndrome Caused by Plaque Erosion.

For several decades, most physicians have believed that acute coronary syndrome (ACS) is caused by coronary thrombosis resulting from rupture of vulnerable plaque characterized by a thin fibrous cap overlying a large necrotic core and massive inflammatory cell infiltration. However, nearly one-third of ACS cases are caused by plaque erosion characterized by intact fibrous cap, less or absent necrotic core, less inflammation, and large lumen. Because of the limitations of current imaging modalities, including angiography and intravascular ultrasound, the importance of plaque erosion as a cause of acute coronary events is less well known. Optical coherence tomography (OCT) as an emerging modality with extremely high resolution is the only intravascular imaging modality available for identification of plaque erosion in vivo, which provides new insight into the mechanism of ACS. More importantly, the introduction of OCT to clinical practice enables us to differentiate the patients with ACS caused by plaque erosion from those caused by plaque rupture, thereby providing precise and personalized therapy based on the different underlying mechanisms. We systematically review the morphological characteristics of plaque erosion identified by OCT and its implications for the management of ACS.

P1779Differential cytokine expression between the coronary and peripheral circulation in patients with ruptured and intact fibrous caps presenting with ST segment myocardial infarction

P1779Differential cytokine expression between the coronary and peripheral circulation in patients with ruptured and intact fibrous caps presenting with ST segment myocardial infarction

Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST-Segment Elevation Myocardial Infarction.

BackgroundPlaque erosion causes 30% of ST‐segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo.Methods and ResultsForty ST‐segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct‐related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real‐time polymerase chain reaction. Twenty‐three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I‐TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted P<0.001; ELISA IFC 10.2 versus RFC 10.8 log2 pg/mL; P=0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted P<0.001; ELISA IFC 7.42 versus RFC 6.63 log2 pg/mL, P=0.036) and thrombospondin 1 (significance analysis of microarrays adjusted P=0.03; ELISA IFC 10.4 versus RFC 8.65 log2 ng/mL, P=0.0041). Thrombectomy mRNA showed elevated I‐TAC in RFC (P=0.0007) epidermal growth factor expression in IFC (P=0.0264) but no differences in expression of thrombospondin 1.ConclusionsThese results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion.

Presencia de trombo y erosión de placa en pacientes con angina vasospástica mediante tomografía de coherencia óptica

Introduction and objectivesVasospastic angina (VSA) can result in endothelial damage and thrombus formation. The aim of this study was to evaluate the incidence of thrombus and plaque characteristics at coronary spasm segments compared with nonspasm segments by using optical coherence tomography (OCT) in patients with suspected VSA. MethodsOne hundred and eighty-three patients with suspected VSA were enrolled in this study. The ergonovine provocation test was performed in all patients for the diagnosis of VSA except in patients with spontaneous spasm. All target lesions were analyzed by OCT. Plaque erosion was defined as the presence of attached thrombus overlying an intact fibrous cap and visualized plaque on multiple adjacent OCT frames. ResultsOne hundred and nine spasm segments (93 patients) were compared with 55 nonspasm segments (39 patients). Thrombus was more frequently seen at spasm segments than at nonspasm segments (28.4% vs 7.3%; P = .026) and thrombus size was larger at spasm segments than at nonspasm segments (0.26 ± 0.50mm2 vs 0.04 ± 0.01mm2; P = .023). Thin-cap fibroatheroma was more frequently seen at nonspasm segments than at spasm segments (16.4% vs 1.8%; P = .006). Plaque erosion was more prevalent at spasm segments than at nonspasm segments (25.7% vs 5.4%; P = .001). ConclusionsThrombus and plaque erosion were more common at spasm segments than at nonspasm segments assessed by OCT in patients with suspected VSA. These findings suggest the potential benefit and treatment role of antiplatelet therapy in vasospastic angina.Full English text available from:www.revespcardiol.org/en

Thrombus and Plaque Erosion Characterized by Optical Coherence Tomography in Patients With Vasospastic Angina

Introduction and objectivesVasospastic angina (VSA) can result in endothelial damage and thrombus formation. The aim of this study was to evaluate the incidence of thrombus and plaque characteristics at coronary spasm segments compared with nonspasm segments by using optical coherence tomography (OCT) in patients with suspected VSA. MethodsOne hundred and eighty-three patients with suspected VSA were enrolled in this study. The ergonovine provocation test was performed in all patients for the diagnosis of VSA except in patients with spontaneous spasm. All target lesions were analyzed by OCT. Plaque erosion was defined as the presence of attached thrombus overlying an intact fibrous cap and visualized plaque on multiple adjacent OCT frames. ResultsOne hundred and nine spasm segments (93 patients) were compared with 55 nonspasm segments (39 patients). Thrombus was more frequently seen at spasm segments than at nonspasm segments (28.4% vs 7.3%; P = .026) and thrombus size was larger at spasm segments than at nonspasm segments (0.26 ± 0.50 mm2 vs 0.04 ± 0.01 mm2; P = .023). Thin-cap fibroatheroma was more frequently seen at nonspasm segments than at spasm segments (16.4% vs 1.8%; P = .006). Plaque erosion was more prevalent at spasm segments than at nonspasm segments (25.7% vs 5.4%; P = .001). ConclusionsThrombus and plaque erosion were more common at spasm segments than at nonspasm segments assessed by OCT in patients with suspected VSA. These findings suggest the potential benefit and treatment role of antiplatelet therapy in vasospastic angina.

Culprit plaque morphology in STEMI - an optical coherence tomography study: insights from the TOTAL-OCT substudy.

Our aim was to compare stenosis severity and plaque content between STEMI culprit lesions with intact fibrous cap (IFC) and those with plaque rupture (PR) in a prospective study. We evaluated 93 patients undergoing OCT and thrombectomy as part of a prospective substudy of the TOTAL (ThrOmbecTomy versus PCI ALone) trial. Culprit lesion morphology was assessable by OCT in 70/93 (75.3%). IFC was found in 31 (44.3%), PR in 34 (48.6%) and calcified nodule in five (7.1%) patients. Following thrombectomy, OCT demonstrated similar lumen area stenosis in IFC (79.3%) and PR (79.6%) (p=0.88). Lumen area stenosis <50% was observed in none of the patients with PR and in one patient with IFC. IFC had fewer quadrants with lipid plaque as compared to PR (28.16±15.02 vs. 39.12±14.23, p=0.004). However, in both lesion types, lipid was the predominant plaque type (83.9 vs. 63.7% of diseased quadrants). In a prospective study of STEMI patients treated with thrombectomy, mild residual stenoses were uncommon in IFC lesions. Although lipid content was lower than in PR lesions, lipid composed the majority of the diseased segments in IFC.

Acute coronary syndromes without coronary plaque rupture.

The latest advances in plaque imaging have provided clinicians with opportunities to treat acute coronary syndrome (ACS) and provide individualized treatment recommendations based not only on clinical manifestations, angiographic characteristics, and biomarker data, but also on the findings of plaque morphology. Although a substantial proportion of ACS events originate from plaques with an intact fibrous cap (IFC), clinicians predominantly equate ACS with plaque rupture arising from thin-cap fibroatheromas. In this Review, we discuss the recent advances in our understanding of plaque morphology in ACS with IFC, reviewing contemporary data from intravascular imaging. We also explore whether use of such imaging might provide a roadmap for more effective management of patients with ACS.

Abstract 12442: Hypercholesterolemia and Angiotensin II Induces Spontaneous Atherothrombotic Occlusion of balloon-injured Rabbit Iliac Arteries; Effects of Lipid-Lowering Therapies

Background: Atherothrombotic occlusion of a coronary artery with an intact fibrous cap is a major cause of acute coronary syndrome that is attributed to plaque erosion. We developed an animal model of spontaneous atherothrombotic occlusion of fibrous cap-intact arteries in rabbits. Methods and Results: We performed balloon injury in bilateral iliofemoral arteries in male Japanese white rabbits fed with high (2 %) cholesterol diet and infused with angiotensin II (50 ng/kg/min). Animals were divided into 3 groups; 1. no treatment, 2. Ezetimibe 0.6 mg/kg/day, and 3. Rosuvastatin 1.0 mg/kg/day. We examined the occurrence of atherothrombosis by high-resolution ultrasonograpy (Vevo2100) 3 times/week. (Fig. A) After the occurrence of acute thrombotic occlusion, the presence of thrombosis was confirmed by angiographic and histopathologic examination. Histochemical analysis in the atherothrombotic sites revealed; 1) no severe stenosis (% stenosis: 49±7), 2) no plaque rupture or lipid core, and 3) no PECAM1-positive endothelial layer. Interestingly, there were smooth muscle-like cells (αSMA+/SM1, SM2, SMemb and calponin-) with tissue factor expression at the neointima-thrombus interface. Oral treatment with Ezetimibe but not Rosuvastatin significantly reduced the incidence of atherothrombotic occlusion (Fig. B). Serum from the model rabbits induced TF in cultured rat smooth muscle cells. TF induction by serum from Ezetimibe-treated rabbits was significantly less compared with those from animals without treatment or with Rosuvastatin treatment (Fig. C). Conclusions: We established for the first time an appropriate animal model of spontaneous atherothromobotic occlusion in rabbits, which mimicked the pathological features of plaque erosion observed in human coronary arteries. This model may provide a clue to a mechanistic understanding and potential therapeutic approaches for plaque erosion.

Plaque morphologies and the clinical prognosis of acute coronary syndrome caused by lesions with intact fibrous cap diagnosed by optical coherence tomography

BackgroundPathological studies have suggested that acute coronary syndrome (ACS) may be caused by culprit lesions with intact fibrous cap (IFC), including plaque erosions. This study sought to evaluate the morphological features and clinical outcomes of patients with ACS caused by lesions with IFC. MethodsA total of 318 patients with ACS who underwent optical coherence tomography (OCT) of a culprit lesion were investigated. The culprit lesions were categorized as follows: those with plaque rupture (PR group), those with an IFC (IFC group), and those with a massive thrombus precluding plaque visualization (MT group). Intravascular ultrasound (IVUS) was performed in 297 patients. Clinical follow-up data were collected regarding adverse cardiac events, including death, myocardial infarction, revascularization, and congestive heart failure requiring hospitalization. ResultsCulprit lesions were categorized into 141 RPs, 131 IFCs, and 46 MTs. IFC group exhibited a smaller remodeling index and less frequently attenuated plaques on IVUS. Three hundred and seven patients (96.5%) were followed for a median follow-up duration of 576days. Adverse cardiac events were observed in 93 patients (30.3%). Kaplan–Meier analysis demonstrated a significantly lower event rate in IFC group compared with the RP and MT groups. Cox proportional hazard analysis demonstrated that an IFC and multivessel disease were independent predictors of adverse events [hazard ratio 0.57, 95% confidence interval (CI) 0.33–0.98, p=0.043 and hazard ratio 1.72, 95% CI 1.09-2.73, p=0.021]. ConclusionsCulprit lesions with IFC showed smaller remodeling indices by IVUS, and were associated with better long-term prognosis compared with those with plaque rupture.

TCT-316 Characteristics Of Culprit Lesions Vs. Non-Culprit Lesions In Patients With ST-Elevation Myocardial Infarction – An Optical Coherence Tomography Study. On Behalf Of The TOTAL-OCT Investigators

Autopsy and imaging studies have demonstrated that most ST-elevation myocardial infarctions (STEMI) are caused by plaque rupture of thin cap fibroatheroma. However, lesions with intact fibrous cap are also common as culprit lesions (CL) in myocardial infarction, suggesting that a thin fibrous cap

40. Optical coherence tomography correlates of complex lesions evaluated by coronary angiography in patients with acute coronary syndromes

Background Plaque rupture (PR) and superimposed thrombosis have been shown as the most frequent underlying substrate in acute coronary syndromes (ACS). Coronary angiography is a luminogram that is not able to define in-vivo features of the culprit plaques. The aim of the study was to use optical coherence tomography (OCT) to investigate the pathology underlying complex (CL) and non-complex angiographic lesions (NCL). Methods We retrospectively enrolled 107 ACS patients admitted to our institution; 83 with Non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction (STEMI). Coronary angiography was performed and culprit lesions were classified according to Ambrose criteria into NCL (n = 47) and CL (n = 60). In STEMI patients, angiographic and OCT analysis were performed after mechanical thrombus aspiration. OCT analysis of these culprit lesion was performed to identify plaque morphology; either PR or intact fibrous cap (IFC), as well as the presence of superimposed thrombosis, lipid rich plaque, thin cap fibroatheroma (TCFA), and minimal lumen area (MLA). Results OCT analysis showed that 58 lesions (54.2%) were classified as PR and 48 lesions (44.9%) were associated with thrombi. Lipid rich plaques were identified in 62 culprit plaques (57.9%). PR, intracoronary thrombi, lipid rich plaques and thin cap fibroatheroma (TCFA) were more frequent in CL compared with NCL (71.7% vs 31.9%, 63.3% vs 21.3%, 71.7% vs 40.4% and 46.7% vs 21.3% respectively). PR (31.9%) with superimposed thrombus (21.3%) may be also detected in NCL. In STEMI patients, there was no significant difference regarding OCT plaque features between NCL and CL. Conclusion In conclusion, OCT demonstrates PR and thrombosis in the majority of ACS patients presenting with CL. Of note, one third of NCL has PR and thrombosis by OCT. In STEMI, coronary angiography is of limited utility in identifying PR by means of CL and should be implemented with OCT to tailor future therapies.

OCT–Defined Morphological Characteristics of Coronary Artery Spasm Sites in Vasospastic Angina

ObjectivesThe aim of this study was to define the morphological features of coronary artery spasm sites using optical coherence tomography (OCT) in patients with vasospastic angina (VSA). BackgroundPlaque characteristics at coronary artery spasm sites have not been investigated systematically. MethodsSixty-nine consecutive patients (80 spasm sites) presenting with VSA who underwent OCT imaging were included in this study. Fibrous cap disruption was identified by the discontinuation of fibrous cap with or without intraplaque cavity formation. OCT-defined erosion was established by the presence of thrombus with or without lumen irregularity overlying an intact fibrous cap on multiple adjacent OCT frames. Other morphological features such as the absence of thrombus with or without lumen irregularity and those not in the previously mentioned criteria were also documented. ResultsPlaque was seen on OCT in 79 of the 80 spasm sites. Fibrous cap disruption was detected at 3 sites (4%). OCT-defined erosion was observed at 21 spasm sites (26%). Thrombus with lumen irregularity was observed in 20 sites, whereas 1 site had thrombus without lumen irregularity. Lumen irregularity without thrombus was observed at 49 spasm sites (61%). Spontaneous spasm was seen more frequently in patients with acute myocardial infarction and out-of-hospital cardiac arrest than in patients without these conditions (50.0% vs. 19.3%, p = 0.025). ConclusionsOur results show that OCT-defined erosion at spasm sites occurred in more than one-fourth of patients in this study. Luminal irregularity was observed in nearly two-thirds of the patients without overlying thrombus. These findings suggest the potential role of antiplatelet therapy in VSA.

Serial optical coherence tomography imaging of ACS-causing culprit plaques.

The aim of this study was to understand better the mechanisms of repair of plaque complications causing acute coronary syndrome. We used OCT in the acute phase and at follow-up (one to seven months) to investigate the plaque healing in 10 culprit plaques: five ruptured fibrous cap (RFC) and five intact fibrous cap (IFC) which were not treated with stent deployment and caused ST-segment elevation myocardial infarction (n=8) and non-STEMI (n=2). At follow-up OCT, the margins of the evacuated cavity in RFC plaques showed a smooth surface and a morphology similar to that of baseline images, while IFC plaques showed a smoothened intimal border and a double layering indicating organising thrombus incorporated in the superficial layers of the plaque. In the months following a successfully dissolved acute thrombosis, OCT revealed that the cavity of RFC plaques persists and is bordered by a smooth "neointima", while IFC plaques showed features suggesting partial incorporation of the deepest layers of thrombus in the plaque.

Eroded Versus Ruptured Plaques at the Culprit Site of STEMI: In Vivo Pathophysiological Features and Response to Primary PCI

ObjectivesThe aim of this study was to evaluate the pathophysiological features and response to primary percutaneous coronary intervention (PCI) of nonruptured/eroded plaque versus ruptured plaque as a cause of ST-segment elevation myocardial infarction (STEMI). BackgroundAutopsy series identified nonruptured/eroded plaque and ruptured plaque as the principal pathological substrates underlying coronary thrombosis in STEMI. The real incidence of different plaque morphologies, associated biological factors, superimposed thrombus, and their interaction with primary PCI remain largely unknown. MethodsIn a prospective study, 140 patients with STEMI underwent optical coherence tomography of the infarct-related artery (IRA) before PCI, after everolimus-eluting stent implantation and at 9-month follow-up. Histopathology and immunohistochemistry of thrombus aspirates and serum biomarkers were assessed at baseline. ResultsCulprit plaque morphology was adjudicated in 97 patients: 32 plaques (33.0%) with an intact fibrous cap (IFC), 63 (64.9%) plaques with a ruptured fibrous cap (RFC), and 2 (2.1%) spontaneous dissections. Patients with an IFC and RFC had similar clinical characteristics, and serum inflammatory and platelets biomarkers. An IFC presented more frequently with a patent IRA (56.2% vs. 34.9%; p = 0.047), and had fewer lipid areas (lipid-rich areas: 75.0% vs. 100.0%; p < 0.001) and less residual thrombus before stenting (white thrombus: 0.41 mm3 vs. 1.52 mm3; p = 0.001; red thrombus: 0 mm3 vs. 0.29 mm3; p = 0.001) with a lower peak of creatine kinase-myocardial band (66.6 IU/l vs. 149.8 IU/l; p = 0.025). At the 9-month optical coherence tomography, IFC and RFC had similar high rates of stent strut coverage (92.5% vs. 91.2%; p = 0.15) and similar percentage of volume obstruction (12.6% vs. 10.2%; p = 0.27). No significant differences in clinical outcomes were observed up to 2 years. ConclusionsIn the present study, an IFC was observed at the culprit lesion site of one-third of STEMIs. IFC, compared with RFC, was associated with higher rates of patent IRA at first angiography, fewer lipid areas, and residual endoluminal thrombus. However, no difference in vascular response to everolimus-eluting stent was observed. (Optical Coherence Tomography Assessment of Gender Diversity in Primary Angioplasty [OCTAVIA]; NCT01377207)

Plaque rupture and intact fibrous cap assessed by optical coherence tomography portend different outcomes in patients with acute coronary syndrome.

Patients presenting with acute coronary syndrome (ACS) may have different plaque morphologies at the culprit lesion. In particular, plaque rupture (PR) has been shown as the more frequent culprit plaque morphology in ACS. However, its prognostic value is still unknown. In this study, we evaluated the prognostic value of PR, compared with intact fibrous cap (IFC), in patients with ACS. We enrolled consecutive patients admitted to our Coronary Care Unit for ACS and undergoing coronary angiography followed by interpretable optical coherence tomography (OCT) imaging. Culprit lesion was classified as PR and IFC by OCT criteria. Prognosis was assessed according to such culprit lesion classification. Major adverse cardiac events (MACEs) were defined as the composite of cardiac death, non-fatal myocardial infarction, unstable angina, and target lesion revascularization (follow-up mean time 31.58 ± 4.69 months). The study comprised 139 consecutive ACS patients (mean age 64.3 ± 12.0 years, male 73.4%, 92 patients with non-ST elevation ACS and 47 with ST-elevation ACS). Plaque rupture was detected in 82/139 (59%) patients. There were no differences in clinical, angiographic, or procedural data between patients with PR when compared with those having IFC. Major adverse cardiac events occurred more frequently in patients with PR when compared with those having IFC (39.0 vs. 14.0%, P = 0.001). Plaque rupture was an independent predictor of outcome at multivariable analysis (odds ratio 3.735, confidence interval 1.358-9.735). Patients with ACS presenting with PR as culprit lesion by OCT have a worse prognosis compared with that of patients with IFC. This finding should be taken into account in risk stratification and management of patients with ACS.

Abstract 348: Serial MRI Differentiates the Natural History of Stable and Vulnerable Plaques in a Rabbit Aorta

Non-invasive monitoring of human atherosclerotic plaque progression would be extremely valuable for determining the characteristics of vulnerable plaques before they rupture and for evaluating therapeutic interventions. We have shown that MRI is a reliable method for differentiating stable and vulnerable aortic atherosclerotic plaques in a rabbit model of atherothrombosis. In this study, we imaged rabbits at 4 time points (baseline, 1, 2 and 3 months) to monitor the progression of plaques and investigate when stable and vulnerable plaques can be differentiated. MR images and histology of two plaques in the same rabbit aorta are compared below. The top row of black blood (BB) T1 images (with fat suppression) show no significant changes in the lumen or the vessel wall area, and no thrombus in the stable plaque after triggering to induce plaque rupture. The histology showed an intact fibrous cap, overlying diffuse lipids. In comparison, there is a marked increase in vessel wall area in the vulnerable plaque (from 4.1 to 15 mm2 over 3 months). The second row (T1BB FS with Gd) shows some uptake of Gd into the stable plaque and surrounding tissue, but the vulnerable plaque showed rapidly increased Gd uptake between months 2 and 3. The vulnerable plaque also showed a large luminal thrombus in the MR images of the live rabbit and in the corresponding histology slice. In addition, the vulnerable plaque showed excessive outward remodeling at 2 months (data not shown). Our study shows a progression of vulnerable features, clearly evident at 2 months, in the plaque that disrupted. We are currently investigating whether therapies initiated at 2 months will reduce the progression of plaque vulnerability.

Coronary CT angiographic characteristics of culprit lesions in acute coronary syndromes not related to plaque rupture as defined by optical coherence tomography and angioscopy

Pathological and clinical optical coherence tomography (OCT) studies have indicated that acute coronary syndrome (ACS) lesions have either ruptured fibrous caps (RFC-ACS) or intact fibrous caps (IFC-ACS). Although computed tomographic (CT) angiographic characteristics of RFC-ACS include low-attenuation plaques and positive plaque remodelling, features associated with IFC-ACS have not been previously described. The aim of this study was to assess the CT characteristics of IFC-ACS lesions. Seventy-four patients with ACS/stable angina consented to multimodality imaging, of which 66 underwent CT angiography. Of these, 57 culprit lesions in 57 patients were evaluated with sufficient image quality from all four of OCT, angioscopy, intravascular ultrasound, and CT angiography. Intraluminal thrombus was assessed by OCT/angioscopy, and culprit lesions further classified by OCT-based demonstration of fibrous cap integrity. Of 35 culprit lesions with ACS, OCT revealed IFC with thrombus in 10 (29%) and RFC in the remaining 25 (71%); all 22 lesions with stable angina had intact fibrous caps. Fibrous caps were significantly thinner in RFC-ACS than IFC-ACS and stable angina (45 ± 12, 131 ± 57, and 321 ± 146 μm, respectively; P = 0.001). CT angiography revealed that low-attenuation plaques were more frequently observed in RFC-ACS than IFC-ACS and stable angina (88, 40, and 18%; P = 0.001) lesions. Similarly, positive remodelling was more predominantly seen in RFC-ACS than IFC-ACS and stable angina (96, 20, and 14%; P = 0.001). However, none of the specific CT angiography features clearly distinguished IFC-ACS from stable lesions. In contrast to the situation with RFC-ACS, distinct culprit lesion characteristics associated with non-rupture-related mechanisms are not identified by CT angiography. It will therefore not be possible to differentiate plaques likely to develop IFC-ACS from stable plaques.

Multimodality Imaging of Carotid Artery Plaques

This study's objective was to compare (18)F-fluoro-2-deoxyglucose positron emission tomography ((18)F-FDG PET), CT, and MRI of carotid plaque assessment. Fifty patients with symptomatic carotid atherosclerosis underwent (18)F-FDG PET/CT and MRI. Correlations and agreement between imaging findings were assessed by Spearman and Pearson rank correlation tests, t tests, and Bland-Altman plots. Spearman rho between plaque (18)F-FDG standard uptake values and CT/MRI findings varied from -0.088 to 0.385. Maximum standard uptake value was significantly larger in plaques with intraplaque hemorrhage (1.56 vs 1.47; P=0.032). Standard uptake values did not significantly differ between plaques with an intact and thick fibrous cap and plaques with a thin or ruptured fibrous cap on MRI. (1.21 vs 1.23; P=0.323; and 1.45 vs 1.54; P=0.727). Pearson rho between CT and MRI measurements varied from 0.554 to 0.794 (P<0.001). For lipid-rich necrotic core volume, the CT-MRI correlation was stronger in mildly (<or=10%) than in severely (>10%) calcified plaques (Pearson rho 0.730 vs 0.475). Mean difference in measurement +/-95% limits of agreement between CT and MRI for minimum lumen area, volumes of vessel wall, lipid-rich necrotic core, calcifications, and fibrous tissue were 0.4+/-18.1 mm(2) (P=0.744), -41.9 +/-761.7 mm(3) (P=0.450), 78.4+/-305.0 mm(3) (P<0.001), 180.5+/-625.7 mm(3) (P=0.001), and -296.0+/-415.8 mm(3) (P<0.001), respectively. Overall, correlations between (18)F-FDG PET and CT/MRI findings are weak. Correlations between CT and MRI measurements are moderate to strong, but there is considerable variation in absolute differences.