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Abstract-Vulnerable plaque generally contains a thin fibrous cap, lipid pools, and reduced internal plaque collagen.Arterial fluorescence analysis can differentiate atherosclerotic lesions from normal arteries; however, the contribution of the lipid core to atherosclerotic arterial fluorescence remains controversial. This study aimed to identify lipid core fluorophores and to differentiate the lipid core from normal artery and atheroma. The helium-cadmium laser-induced fluorescence spectra of cadaveric arteries and known chemical constituents were recorded. Lipid core fluorescence spectra exhibited marked red shifts and broadening compared with the fluorescence spectra of normal tissue and atheroma. Similar fluorescence spectra were obtained for lipid core and oxidized low density lipoprotein, for atheroma and collagen, and for normal artery and elastin. A classification based on collagen, elastin, and oxidized low density lipoprotein spectral decomposition could discriminate the lipid core (nϭ29), normal artery (nϭ74), atheroma (nϭ73), and preatheroma (nϭ10) A theromatous plaque consists of a lipid-rich core covered with a collagen-rich fibrous cap, varying widely in thickness. Plaque disruption is associated with varying degrees of internal hemorrhage and luminal thrombosis because the lipid core and exposed collagen are thrombogenic. 1 Acute coronary syndrome usually occurs as a consequence of such disruption or ulceration of vulnerable plaque. Vulnerable plaque is characterized by lipid pools, a thin fibrous cap, and reduced internal plaque collagen. 2-8 The ability to characterize plaque and detect vulnerable plaque would contribute to the treatment of plaque and prevention of acute coronary syndrome.Laser-induced fluorescence spectroscopy of the cardiovascular system has been used not only to identify atheroma but also to measure intimal thickness. Many classification indexes for differentiating plaque types and measuring intimal thickness have been derived from empirical studies of fluorescence spectra. 9 -14 Therefore, understanding the nature of arterial fluorophores 15-18 is important for accurate classification of arterial tissues. A classification algorithm 15 based on fluorescence spectral decomposition of elastin and collagen can be used to discriminate between normal and atherosclerotic arterial tissues. Knowing the major fluorophores of the lipid core is essential for identifying vulnerable plaque. Fluorescence intensities of 500 and 600 nm characterize fatty plaque 11 ; whether the lipid core (lipids) contributes to atherosclerotic and normal arterial fluorescence is controversial.The present study was undertaken to (1) observe laserinduced fluorescence spectra from normal artery, atheromatous plaque, and ulcerated plaque (lipid core); (2) clarify the fluorophores of the lipid core and derive a classification algorithm to distinguish these 3 tissue types on the basis of arterial fluorophores; and (3) characterize changes in fluorescence spectra during fibrous cap removal and estimate fibrous ca...

High levels of osteopontin (OPN) mRNA and proteins were reported in atherosclerotic plaques. 1,2 Recently, we reported plasma OPN levels to be high in patients with coronary artery disease (CAD) and to correlate with the severity of CAD. 3 However, no association between plasma OPN levels and restenosis after percutaneous coronary intervention (PCI) has yet been demonstrated.We measured plasma OPN levels in 90 patients with CAD undergoing elective coronary angiography for suspected restenosis. They had undergone PCI 0.6Ϯ0.4 years ago, of whom 52 (58%) had been treated with bare metal stents. OPN levels were also measured in 60 age-and gender-matched CAD patients with no history of PCI. Patients with acute coronary syndrome were excluded. Our study was approved by institutional ethics committee. After informed consent was obtained, fasting blood samples were taken. Plasma OPN levels were measured by ELISA (Human OPN assay kit; IBL), which measures total concentration of phosphorylated and nonphosphorylated forms of OPN. CAD was defined as at least one coronary artery having Ͼ50% luminar diameter stenosis. Restenosis was defined as Ͼ50% luminar diameter stenosis in the segment treated by PCI. Differences between 2 groups were evaluated by unpaired t test for parametric variables, by Mann-Whitney U test for nonparametric variables, and by 2 test for categorical variables. A probability value Ͻ0.05 was considered significant.Of the 90 CAD patients with a history of PCI, 42 had restenosis. Compared with 48 CAD patients without restenosis, 42 with restenosis tended to have a higher rate of diabetes and a lower rate of smoking (Table). Among 3 groups, there was no difference in age, gender, or risk factors, except for total cholesterol levels. Plasma OPN levels were higher in CAD patients with restenosis than in those without restenosis and those with no history of PCI (PϽ0.01; Figure). CAD patients with restenosis more often had OPN level Ͼ600 ng/mL than those without restenosis and those with no history of PCI (38% versus 15% and 18%, PϽ0.05). OPN levels did not correlate with hsCRP, HbA1c, or fasting glucose levels. Clinical variables (age, gender, hypertension, hyperlipidemia, diabetes, smoking, stent, and hsCRP and OPN levels) were entered into multivariate logistic regression model. In addition to diabetes and smoking, OPN levels were independently associated with restenosis. Odds ratio for the presence of restenosis was 1.7 (95%CIϭ1.2 to 2.5; PϽ0.01) for a 100 ng/mL increase in OPN levels.Restenosis after angioplasty is caused by negative arterial remodeling and neointimal proliferation, whereas in-stent restenosis is caused mainly by neointimal proliferation. 4 In vitro, OPN promotes the migration and proliferation of smooth muscle cells. 2 Increased OPN mRNA was shown in neointimal smooth muscle cells after

Aim:Resistin is an adipocytokine that may link inflammation and atherosclerosis.We studied the associations of resistin levels with cardiovascular events and restenosis. Methods: We measured pre-procedural serum resistin levels in 140 patients with coronary artery disease undergoing elective percutaneous coronary intervention (PCI), of whom 97 had a stent. Restenosis was defined as 50% stenosis at follow-up angiography. Patients were followed for 3 years for major adverse cardiovascular events (MACE). Resistin correlated with CRP levels (r 0.31). To clarify the association between MACE and resistin, patients were divided into 2 groups by resistin levels. Kaplan-Meier analysis showed a lower event-free survival rate in patients with resistin 4.0 ng/mL than without it (p 0.001). On multivariate analysis, resistin, but not CRP, was an independent predictor of MACE. The hazard ratio for MACE was 3.6 (95%CI 1.4-9.2) for resistin 4.0 ng/mL. Conclusion: Serum resistin levels were found to be associated with further cardiovascular events in patients undergoing PCI.

Objective-Coronary plaque instability causes myocardial infarction (MI). Angiographic lesions with such instability are complex lesions. Complex carotid plaques were reported to be prevalent in unstable angina. We investigated associations between coronary plaque instability, such as MI and angiographic complex coronary lesions, and aortic plaques. Methods and Results-Aortic MRI was performed in 146 patients undergoing coronary angiography, of whom 108 had coronary artery disease (CAD) and 44 also had MI. Prevalence of plaques in thoracic and abdominal aortas was higher in patients with than without CAD (73% and 94% versus 32% and 79%), but it was similar in CAD patients with and without MI. Notably, complex plaques in abdominal aorta were more prevalent in CAD patients with than without MI (36% versus 14%; PϽ0.025). In multivariate analysis, abdominal complex plaques were associated with MI (odds ratio [OR], 4.5; 95% CI, 1.5 to 13.8). Among patients without MI, thoracic and abdominal complex plaques were more prevalent in patients with than without complex coronary lesions (22% and 33% versus 2% and 7%; PϽ0.05).Abdominal complex plaques were also associated with complex coronary lesions (OR, 9.8; 95% CI, 1.1 to 85.9). Key Words: aorta Ⅲ coronary artery disease Ⅲ myocardial infarction Ⅲ MRI P laque instability is a main cause of acute coronary syndrome, such as myocardial infarction (MI). 1 Angiographic features of coronary lesions associated with plaque instability are sharp overhanging edge, irregular border, and intraluminal lucency, so-called complex lesions. 2,3 Although angiographic complex coronary lesions are seen in 10% to 20% of patients with stable angina, 2 such lesions are known to be common in acute coronary syndrome and to be predictive of coronary events. 2,4,5 Recently, complex plaques in carotid arteries were reported to be more prevalent in patients with unstable angina than in those with stable angina, suggesting a link between coronary and carotid plaque instability. 6 Plaque instability in patients with coronary artery disease (CAD) may not be confined to coronary arteries, but it may also involve other arteries. Complex plaques in thoracic aorta, detected by transesophageal echocardiography (TEE), were reported to be associated with systemic embolic events. 7,8 However, the association between coronary plaque instability and complex aortic plaques has not yet been elucidated. Conclusion-ComplexRecently, MRI became a useful tool for noninvasively detecting plaques in both thoracic and abdominal aortas. 9,10 We 11,12 and others 13 showed the good correlations for plaque morphology and characterization in the aortas between in vivo and ex vivo MRI findings and histopathology in animal models. In humans, we reported that MRI evaluations of thoracic aorta closely correlated with TEE findings. 9 Using MRI, we previously reported the association between the severity of coronary stenosis and the extents of aortic plaques in 102 patients undergoing coronary angiography. 10 In the present study, we ...