Coronary Artery Disease

1999

DOI: 10.1097/00019501-199910000-00009

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Intravascular ultrasound classification of atherosclerotic lesions according to American Heart Association recommendation

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In Vivo Studies Using Intravascular Ultrasound2

Lesions In Chimeras Lacking Cd44 In Both Non-bone Marrow-der1

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Cited by 37 publications

(30 citation statements)

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“…Lesions were characterized based on morphology according to previously published criteria. 19 We did not observe any differences in the types of early lesions between the various groups. However, based on ␣-SMA expression as detected by immunohistochemical staining and total collagen content as determined by trichrome staining, we found that among more advanced lesions, mice deficient in CD44 in both compartments (DKO f DKO) had significantly more fibroatheromas compared to the chimeras that expressed CD44 in both compartments (apoE Ϫ/Ϫ f apoE Ϫ/Ϫ ; Figure 5).…”

Section: Lesions In Chimeras Lacking Cd44 In Both Non-bone Marrow-dermentioning

confidence: 51%

CD44 Expressed on Both Bone Marrow–Derived and Non–Bone Marrow–Derived Cells Promotes Atherogenesis in ApoE-Deficient Mice

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Objective-The purpose of this study was to distinguish the contributions of CD44 expressed on bone marrow-derived and non-bone marrow-derived cells to atherosclerosis. Methods and Results-Using bone marrow chimeras, we compared the contributions of CD44 expressed on bone marrow-derived cells versus non-bone marrow-derived cells to the vascular inflammation underlying atherosclerosis. We show that CD44 in both bone marrow-derived and non-bone marrow-derived compartments promotes atherosclerosis in apoE Ϫ/Ϫ mice and mediates macrophage and T cell recruitment to lesions in vivo. We also demonstrate that CD44 on endothelial cells (ECs) as well as on macrophages and T cells enhances leukocyte-endothelial cell adhesion and transendothelial migration in vitro. Furthermore, CD44 on vascular smooth muscle cells (VSMCs) regulates their hyaluronan (HA)-dependent migration. Interestingly, in mice lacking CD44 in both compartments, where we observed the least inflammation, we also observed enhanced fibrous cap formation. Conclusions-CD44 expressed on bone marrow-derived and non-bone marrow-derived cells both promote atherosclerosis in apoE-deficient mice. Furthermore, CD44 plays a pivotal role in determining the balance between inflammation and fibrosis in atherosclerotic lesions which can impact clinical outcome in humans. (Arterioscler Thromb Vasc Biol. 2008;28:1283-1289)Key Words: CD44 Ⅲ atherosclerosis Ⅲ apoE Ⅲ bone marrow chimera Ⅲ fibrous cap B oth vascular and inflammatory cells are critical to atherogenesis, but the distinct mechanisms by which these lineages contribute to disease are incompletely understood. Atherosclerosis is initiated by proinflammatory changes in the endothelium caused by insults such as the accumulation of oxidized or other modified lipoproteins and flow-induced mechano-signal transduction. 1,2 The resulting upregulation of endothelial cell (EC) adhesion molecules and production of proinflammatory cytokines and chemokines promotes recruitment of inflammatory cells including monocytes and T cells. 3,4 Vascular injury also promotes vascular remodeling by inducing proliferation and migration of vascular smooth muscle cells (VSMCs). Interestingly, evidence suggests that the balance between the fibrotic response, which promotes the formation of fibrous caps, and the inflammatory response, which inhibits formation of fibrous caps, governs the structure of the atheroma. The overall structure of atheroma in turn determines the susceptibility of plaques to rupture. 5 CD44 is known to be upregulated in human and mouse atherosclerotic lesions and is expressed on all cell types known to play a role in atherogenesis. 6,7 Moreover, ligands for CD44, such as the extra-/pericellular matrix glycosaminoglycan hyaluronan (HA) and osteopontin, accumulate in atherosclerotic lesions. 8,9 We previously demonstrated that CD44-null apoE Ϫ/Ϫ mice develop less extensive atherosclerosis attributable to impaired recruitment of macrophages to atherosclerotic lesions and regulation of vascular smooth muscle cell (VSMC) pro...

“…Lesions were characterized based on morphology according to previously published criteria. 19 We did not observe any differences in the types of early lesions between the various groups. However, based on ␣-SMA expression as detected by immunohistochemical staining and total collagen content as determined by trichrome staining, we found that among more advanced lesions, mice deficient in CD44 in both compartments (DKO f DKO) had significantly more fibroatheromas compared to the chimeras that expressed CD44 in both compartments (apoE Ϫ/Ϫ f apoE Ϫ/Ϫ ; Figure 5).…”

Section: Lesions In Chimeras Lacking Cd44 In Both Non-bone Marrow-dermentioning

confidence: 51%

CD44 Expressed on Both Bone Marrow–Derived and Non–Bone Marrow–Derived Cells Promotes Atherogenesis in ApoE-Deficient Mice

¹

,

²

,

³

et al. 2008

View full text Add to dashboard Cite

Objective-The purpose of this study was to distinguish the contributions of CD44 expressed on bone marrow-derived and non-bone marrow-derived cells to atherosclerosis. Methods and Results-Using bone marrow chimeras, we compared the contributions of CD44 expressed on bone marrow-derived cells versus non-bone marrow-derived cells to the vascular inflammation underlying atherosclerosis. We show that CD44 in both bone marrow-derived and non-bone marrow-derived compartments promotes atherosclerosis in apoE Ϫ/Ϫ mice and mediates macrophage and T cell recruitment to lesions in vivo. We also demonstrate that CD44 on endothelial cells (ECs) as well as on macrophages and T cells enhances leukocyte-endothelial cell adhesion and transendothelial migration in vitro. Furthermore, CD44 on vascular smooth muscle cells (VSMCs) regulates their hyaluronan (HA)-dependent migration. Interestingly, in mice lacking CD44 in both compartments, where we observed the least inflammation, we also observed enhanced fibrous cap formation. Conclusions-CD44 expressed on bone marrow-derived and non-bone marrow-derived cells both promote atherosclerosis in apoE-deficient mice. Furthermore, CD44 plays a pivotal role in determining the balance between inflammation and fibrosis in atherosclerotic lesions which can impact clinical outcome in humans. (Arterioscler Thromb Vasc Biol. 2008;28:1283-1289)Key Words: CD44 Ⅲ atherosclerosis Ⅲ apoE Ⅲ bone marrow chimera Ⅲ fibrous cap B oth vascular and inflammatory cells are critical to atherogenesis, but the distinct mechanisms by which these lineages contribute to disease are incompletely understood. Atherosclerosis is initiated by proinflammatory changes in the endothelium caused by insults such as the accumulation of oxidized or other modified lipoproteins and flow-induced mechano-signal transduction. 1,2 The resulting upregulation of endothelial cell (EC) adhesion molecules and production of proinflammatory cytokines and chemokines promotes recruitment of inflammatory cells including monocytes and T cells. 3,4 Vascular injury also promotes vascular remodeling by inducing proliferation and migration of vascular smooth muscle cells (VSMCs). Interestingly, evidence suggests that the balance between the fibrotic response, which promotes the formation of fibrous caps, and the inflammatory response, which inhibits formation of fibrous caps, governs the structure of the atheroma. The overall structure of atheroma in turn determines the susceptibility of plaques to rupture. 5 CD44 is known to be upregulated in human and mouse atherosclerotic lesions and is expressed on all cell types known to play a role in atherogenesis. 6,7 Moreover, ligands for CD44, such as the extra-/pericellular matrix glycosaminoglycan hyaluronan (HA) and osteopontin, accumulate in atherosclerotic lesions. 8,9 We previously demonstrated that CD44-null apoE Ϫ/Ϫ mice develop less extensive atherosclerosis attributable to impaired recruitment of macrophages to atherosclerotic lesions and regulation of vascular smooth muscle cell (VSMC) pro...

“…The abovementioned classification of coronary lesions suggested by the AHA can be reproduced using IVUS ( Figure 3). 19 Indeed, clinical symptoms-stable or unstable angina-are related to plaque morphology described by IVUS in analogy to the AHA classification rather than to angiographic stenosis severity. 19 In particular, IVUS enables the detection of plaque rupture.…”

Section: In Vivo Studies Using Intravascular Ultrasoundmentioning

confidence: 99%

“…19 Indeed, clinical symptoms-stable or unstable angina-are related to plaque morphology described by IVUS in analogy to the AHA classification rather than to angiographic stenosis severity. 19 In particular, IVUS enables the detection of plaque rupture. 19 -21 The changes in plaque morphology can be examined over time.…”

Section: In Vivo Studies Using Intravascular Ultrasoundmentioning

confidence: 99%

Unstable Coronary Plaque and Its Relation to Coronary Calcium

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2001

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Abstract-Coronary calcium is intimately associated with coronary atherosclerotic plaque development. The use of electron-beam computed tomography (EBCT) for accurate quantitative measurements has led to an increased interest in understanding the clinical importance of coronary calcium, particularly in terms of the ability to identify unstable coronary plaques that underlie the clinical acute coronary syndromes. Histopathologic studies have demonstrated that calcium is a frequent feature of ruptured plaques, but the presence or absence of calcium does not allow for reliable distinction between unstable versus stable plaques. This issue is complicated by the lack of a prospective definition for "unstable." Plaque rupture is sometimes found in apparently healthy subjects and in patients with clinically stable disease. Coronary atherosclerosis is a coronary systemic disease process. Imaging of coronary calcium, although unable to identify a localized unstable plaque, potentially can identify the more clinically pertinent "unstable patient." Almost all patients with a recent acute coronary syndrome have measurable coronary calcium because moderate-to-advanced coronary plaque disease is already present, although obstructive disease frequently is not. Prospective studies have demonstrated that extensive coronary calcium detected by EBCT is associated with a significantly increased incidence of subsequent myocardial infarction, need for revascularization, and coronary death. The incremental prognostic value of coronary calcium compared with that of risk factor assessment remains to be fully defined. The occurrence of an acute coronary syndrome is determined by many factors apart from the extent of atherosclerotic plaque disease. Large prospective trials in the general population are needed to define the subgroups that will benefit most from quantitative assessment of coronary calcium.

“…Coronary angiography has been considered to be the gold standard for evaluating coronary artery disease but is not sensitive enough to evaluate the early stages of the disease (12). Intravascular ultrasound (IVUS) examination of the coronary arteries can reveal pathological findings in angiographically normal arteries (13). The present study aimed to evaluate the prevalence of silent coronary atheromatosis and its relation to long-term HbA 1c in patients with type 1 diabetes of long duration and no symptoms of coronary heart disease.…”

mentioning

confidence: 96%

Silent Coronary Atheromatosis in Type 1 Diabetic Patients and Its Relation to Long-Term Glycemic Control

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Type 1 diabetic patients have a pronounced risk of premature coronary artery disease and death. We sought to evaluate the prevalence of silent coronary atheromatosis and to evaluate the relation between coronary atheromatosis and glycemic control. Coronary atheromatosis was evaluated in type 1 diabetic patients with no symptoms of coronary artery disease by exercise electrocardiogram (ECG) in 39 patients and quantitative coronary angiography and by intravascular ultrasound (IVUS) examinations in 29 patients. The findings from the IVUS examinations were related to mean HbA 1c collected prospectively over 18 years. Abnormal exercise ECGs were found in 15% of patients, and angiographic diameter stenosis of >50% in one or more of the main coronary arteries was found in 34% of patients. All patients examined with intracoronary ultrasound had developed atherosclerotic plaques with an increased intimal thickness (>0.5 mm) in one or more of the coronary arteries. Coronary artery plaque formation, as judged by ultrasound, was significantly related to mean HbA 1c during 18 years (P < 0.05) after adjustment for total cholesterol and age. This study demonstrates a high prevalence of silent coronary atheromatosis in type 1 diabetic patients with no symptoms of coronary heart disease. Long-term glycemic control was shown to be associated with coronary atheromatosis.

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