Biomedical subjects

Mehmet Cilingiroglu

Publications and source records attributed to Mehmet Cilingiroglu.

7 recordsLinked to original sources

PubMed2006

Detection of vulnerable plaque in a murine model of atherosclerosis with optical coherence tomography.

OBJECTIVES: The aim of this study was to evaluate the feasibility of optical coherence tomography (OCT) to identify the components of vulnerable plaques in a well-established murine model of human atherosclerosis. BACKGROUND: Although the pathologic features that predict plaque rupture at autopsy are well known, the development of a technology to identify these high risk features in vivo is lacking. OCT uses reflected light to provide histology-like images of plaque with higher resolution than competing imaging modalities. Whether OCT can reliably identify the features of an atherosclerotic plaque that define it as vulnerable-thin fibrous cap, large lipid core, and high percent of lipid in the artery-requires further study. METHODS: OCT images of the atherosclerotic innominate artery segments from the apolipoprotein E knockout (apoE(-/-)) mice were recorded and correlated with histology in both in vivo (n = 7) and well as in ex vivo experiments (n = 12). RESULTS: Excellent correlation between the OCT and histology measurements for fibrous cap thickness, lipid core size, and percentage lipid content was found. The fibrous cap thicknesses examined span those of human fibrous caps known to rupture (< 65 microm). Regions of greatest light reflection in OCT images were observed when calcium hydroxy-apatite was scattered in lipid, less in fibrous tissue, and least in lipid. CONCLUSIONS: These findings suggest that OCT holds promise for the identification of features defining vulnerable plaque including fibrous cap thickness, lipid core size, and the percentage of lipid content.

Animals↗

PubMed2006

Long-term effects of novel biolimus eluting DEVAX AXXESS plus nitinol self-expanding stent in a porcine coronary model.

OBJECTIVE: The purpose of this study was to evaluate the long-term effects of the DEVAX AXXESS biolimus eluting stent (BES) in a porcine coronary model, compared with those of bare metal stent (BMS) and polymer only stent (POS) controls. BACKGROUND: Excessive neointimal growth has been identified as a major cause of late failure of percutaneous coronary interventions. The effect of drug eluting from self-expanding stents for prevention of neointimal hyperplasia has not been studied before. The DEVAX AXXESS is a self-expanding nickel titanium stent, coated with antiproliferative compound-biolimus. METHODS: Twenty juvenile farm swine, 25-35 kg in weight, 3-6 months in age were used. Each animal received a stent to the left anterior descending artery, left circumflex or right coronary arteries as permitted per anatomy. The chronic vascular response after BES implantation was compared with that after BMS and POS implantation at 28, 90, and 180 days follow-up. RESULTS: The 28-day outcome by quantitative coronary angiography (QCA) showed significant increase in minimal luminal diameter (MLD) in the BES (MLD: 2.90 +/- 0.97, 2.39 +/- 0.90, 1.59 +/- 0.91; P = 0.009) compared with BMS and POS, respectively. By histomorphometric analysis, there was also a corresponding significant reduction in neointimal tissue proliferation in the BES (average neointimal area: 2.78 +/- 0.07, 5.46 +/- 0.66, 8.42 +/- 0.85; P = 0.002) compared with that in BMS and POS controls, respectively at 28-days follow-up. At 90 and 180 days, the mean neointimal area was not significantly different between the BES and the controls. CONCLUSIONS: BES favorably modulates the neointimal tissue formation for 28 days, in the porcine coronary model. Long-term inhibition of neointimal hyperplasia is not sustained most likely because of the delayed cellular proliferation and inflammation in the vessel wall.

Alloys↗

PubMed2006

Optical coherence tomography and its use in detection of vulnerable plaque.

Acute coronary syndromes and their associated complications related to coronary ischemia continue to be the leading cause of morbidity and mortality in the world. The most commonly encountered pathophysiologic cascade of events resulting in this picture is initiated by formation of a vulnerable plaque. Despite the widespread use of a variety of imaging technologies, high-resolution detection of the vulnerable plaque and designing a method to correlate the results of the imaging modality with disease severity and prognosis have proven to be an arduous task. The recent introduction of optical coherence tomography has proven to be an innovative contribution to the diagnostic armamentarium for the cardiologist. This article presents an overview of vulnerable plaque and methods for its imaging. It focuses on how optical coherence tomography comes into play and how it compares with other modalities in regard to plaque characterization.

Animals↗

PubMed2005

The lectin-like oxidized low-density lipoprotein receptor and its role in atherosclerosis.

The lectin-like oxidized low-density lipoprotein receptor (LOX-1), a recently identified receptor that plays a role in the uptake of oxidized low-density lipoproteins into endothelial cells, has a pivotal role in the pathogenesis of atherosclerosis. The ways this receptor takes part in atherosclerosis is through uptake of oxidized low-density lipoproteins into endothelial cells, smooth muscle cells, and macrophages; decreasing nitric oxide production; increasing inflammatory cell recruitment; and increasing smooth muscle cell proliferation. LOX-1 is inducible and regulated by multiple factors known to underlie atherogenesis. Further understanding of this receptor may lead to potential molecular targets for prevention and treatment of atherosclerosis.

Animals↗

PubMed2005

Vulnerable plaque: definition, detection, treatment, and future implications.

Atherosclerosis continues to account for significant morbidity and mortality in most of the world. The major proportion of atherosclerosis mortality is related to atherosclerotic coronary artery disease, yet there still is not an optimal method for making the diagnosis of vulnerable plaque in vivo. The search for such an undefined method, along with studies on amelioration of currently available technology, gains special significance when the association between the qualitative definition of lesions in an individual and cardiovascular risks are considered. We, therefore, start by defining the critical lesion of coronary atherosclerosis and review the advantages and potential for clinical use of various methods to detect the vulnerable plaque and comment on possible future implications in this field.

Adrenergic beta-Antagonists↗

PubMed2004

Endothelial lipase and cholesterol metabolism.

Endothelial lipase (EL), a new member of the lipase gene family, was recently cloned and has a significant role in plasma high-density lipoprotein levels (HDL). EL has a highly similar molecular homology to lipoprotein lipase and hepatic lipase. It is synthesized by endothelial cells and functions at the cell surface. EL primarily has phospholipase A1 activity. Animals that overexpress EL showed decreased HDL cholesterol levels and those that lack EL show elevated levels of HDL cholesterol. The expression is highly regulated by cytokines and physical forces. These data suggest that EL may play a significant role in atherosclerosis.

Animals↗

PubMed2003

Endothelial lipase is a major genetic determinant for high-density lipoprotein concentration, structure, and metabolism.

High-density lipoprotein (HDL) protects against atherosclerosis. Endothelial lipase (EL) has been postulated to be involved in lipoprotein, and possibly HDL, metabolism, yet the evidence has been scarce and conflicting. We have inactivated EL in mice by gene targeting. EL(-/-) mice have elevated plasma and HDL cholesterol, and increased apolipoproteins A-I and E. NMR analysis reveals an abundance of large HDL particles. There is down-regulation of the transcripts for phospholipid transfer protein, but up-regulation of those for hepatic lipase and lipoprotein lipase. Plasma lecithin:cholesterol acyltransferase is unchanged despite an increase in hepatic mRNA; lecithin:cholesterol acyltransferase activity toward endogenous EL(-/-) substrate is, however, reduced by 50%. HDL clearance is decreased in EL(-/-) mice; both the structure of HDL and the presence of EL are factors that determine the rate of clearance. To determine EL's role in humans, we find a significant association between a single-nucleotide polymorphism 584C/T in the EL (LIPG) gene and HDL cholesterol in a well characterized population of 372 individuals. We conclude that EL is a major determinant of HDL concentration, structure, and metabolism in mice, and a major determinant of HDL concentration in humans.

Animals↗