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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of lipoprotein (a) (Lp[a]) as an atherogenic condition related to hypercholesterolemia, we studied the serum concentration of Lp(a) as measured by immunonephelometry in relation to the presence of asymptomatic echographic plaques in the peripheral arteries of 103 untreated hypercholesterolemic, normotensive, middle-aged men. Plaque was found at carotid, aortic, and femoral sites in 36%, 51%, and 53% of subjects, respectively. The Lp(a) level was higher in the group with carotid plaques than in the group without (0.29 +/- 0.20 versus 0.17 +/- 0.14 g/l, p < 0.01), not significantly higher in the group with aortics plaque than in the group without (0.24 +/- 0.19 versus 0.19 +/- 0.16 g/l), and not different between groups with and without femoral plaques (0.21 +/- 0.18 versus 0.22 +/- 0.17 g/l). A logistic regression analysis confirmed that Lp(a) was associated with carotid plaques (p = 0.004), independent of other risk factors. However, in patients with low density lipoprotein cholesterol values above the group median value (4.7 mmol/l), Lp(a) was associated not only with carotid plaques (p < 0.01) but also with aortic plaques (p < 0.05), as well as with the number of diseased sites (p = 0.02). In contrast, in patients with low density lipoprotein cholesterol levels below or equal to 4.7 mmol/l, Lp(a) only remained associated with carotid plaques (p < 0.05). Thus, in symptom-free, hypercholesterolemic men, early atherosclerosis was influenced by serum Lp(a), particularly in the carotid arteries, as well as by the presence of a higher level of low density lipoprotein cholesterol.
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PMID:Serum Lp(a) as a discriminant marker of early atherosclerotic plaque at three extracoronary sites in hypercholesterolemic men. The PCVMETRA Group. 142 94

The initiation of atherosclerosis may result from blood flow oscillatory shear stress in certain vascular sites (bending points, bifurcations, etc.) producing chronic minimal injury resulting in functional alteration of the arterial endothelium type I injury; experimentally, this is potentiated by atherogenic risk factors such as hypercholesterolemia, hypertension, immunocomplexes, viral infections, and tobacco smoke. Such minimal injury leads to accumulation of lipid and monocytes (macrophages), and subsequently, toxic products released by the macrophages produce damage of the intimal surface with denuding endothelium type II injury or damage, which attracts platelets; all of these cells release growth factors, prompting migration and proliferation of smooth muscle cells and producing a "fibro-intimal lesion" or the outside of the capsule of a predominant "lipid lesion." The lipid lesions surrounded by a thin capsule tend to be small and rupture easily, causing type III injury or damage; that is, they are soft and weak, contain large numbers of macrophages, which may release collagenase and elastase to form abscesses, and by their location, are under the effect of flow shear forces. After plaque disruption there is thrombus formation; when thrombi are small, they can become organized and contribute to the growth of the atherosclerotic plaque; when thrombi are large and occlusive, they lead to the acute coronary syndromes. New data suggest that, at the time of plaque disruption, certain "thrombogenic" risk factors modulate the degree of thrombogenicity and, thereby, the growth of the plaque versus the various acute coronary syndromes. Aside from the need for better understanding of the basic biology of atherogenesis, emphasis on identifying and modifying the primary atherogenic and thrombogenic risk factors should continue for primary prevention. Also, new approaches should focus on the identification, stabilization, and regression of the small "lipid plaques" prone to rupture (these are not necessarily angiographically apparent), as well as on the use of better and safer antithrombotic agents for prevention of progression.
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PMID:Clinical-pathological correlations of coronary disease progression and regression. 142 42

New experimental evidence has shed light on a number of fundamental processes that contribute to atherosclerotic plaque formation. Recent data suggest that oxidized low-density lipoprotein (LDL) may be more avidly bound and taken up by macrophages, and thus more atherogenic, than unmodified LDL. A subclass of LDL, lipoprotein(a), is also of interest with respect to atherogenic potential, particularly since it has a plasminogen-like moiety as part of its structure. It may promote platelet aggregation and thrombus formation and thereby contribute to atherosclerotic plaque growth. Hypercholesterolemia, hypertension, and possibly other factors may induce changes in endothelial structure and function, which appear to be relatively early events associated with arterial injury. Smooth muscle cell proliferation and accumulation are hallmarks of arterial lesions induced by both hypertension and hypercholesterolemia, and several growth factors have been potentially implicated in these responses. Hypertension by itself causes arterial damage, but it does not appear to induce atherosclerosis when plasma lipid concentrations are low. In combination with hypercholesterolemia, however, it is a potent promoter of atherogenesis, and the mechanisms for this more-than-addictive effect are now the focus of considerable investigative attention.
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PMID:Pathophysiology of atherosclerosis. 144 96

The study is to evaluate the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease using noninvasive B-mode ultrasonography and X-ray computed tomography. The sensitivity of bruits for diagnosing severe carotid stenosis was also evaluated. A total of 229 consecutive Japanese patients were recruited for this study, of which 97 had chronic-stage ischemic cerebrovascular disease and remaining 132 patients had at least one risk factor for atherosclerosis. Carotid atherosclerosis was evaluated by B-mode ultrasonography. Ischemic cerebrovascular disease was assessed by history taking, neurological findings and X-ray CT examination. The severity of carotid atherosclerosis was assessed by using two indices; plaque score and maximum percentage diameter stenosis. We also evaluated whether it was ulcerated plaque or not. Plaque score was computed by summing up all carotid plaque thicknesses (mm) on both sides. According to the CT findings, cerebral infarction was divided into two types; deep subcortical infarction and cortical infarction. The incidence of cerebral infarction increased in relation to plaque score and maximum percentage stenosis. Although the incidence of cerebral infarction in patients without carotid atherosclerosis was only 33% (38/116), it in patients with moderate carotid atherosclerosis (plaque score > 5) was 59% (26/44) (p < 0.05, chi-square test). The incidence of ipsilateral infarction was revealed to be higher in patients with severe (50% or more) carotid stenosis (61%) than in cases of mild stenosis (28%) (p < 0.05). Thirteen patients had ulcerated plaques and they suffered more frequently cerebral infarction than patients without ulcerated lesions. Cortical infarction was more frequent in patients with severe carotid stenosis than in patients without carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An ultrasonic study of the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease in Japanese]. 146 Jul 77

An autopsy case of spontaneous rupture of aortic arch through an atheromatous plaque which resulted in pseudoaneurysm is reported. The aorta was involved by severe atherosclerosis with scattered calcifications over the entire surface, and there was a fusiform aneurysm protruding from a transmural tear in the aortic arch. Histopathologically, no evidence of dissection or inflammatory change was noted in the aorta, and no histologic component of the aortic media was observed in the aneurysmal wall. However, degenerative change of cystic and laminar medial necrosis were recognized near the ruptured site. Such localized degenerative change was considered to be caused by circulatory disturbance which originated from disruption of the vasa vasorum due to aortic rupture.
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PMID:Spontaneous rupture of aortic arch through an atheromatous plaque resulting in pseudoaneurysm. 146 45

Atherosclerosis is the most frequent disease in the majority of cardiovascular arteries. It is a complex disease with peculiar characteristics, including its principal localisation in the inner stratum of the artery (the intima). The paper examines 36 atherosclerotic lesions in elderly patients in which the presence of stenosing atherosclerotic plaque had been diagnosed. The presence of replicating DNA was demonstrated using flow cytometry together with a proliferative phenomenon within the fibrous-atherosclerotic plaque due to an hypothesised migration of smooth muscle cells inside the intima, leading to the final result, a gradual restriction of the arterial gauge and consequent alteration to blood flow. The plaques examined were localised at the bifurcation of the carotid artery, an area in which it is easier to find the physical and biochemical factors facilitating platelet adhesion, which together with other cells produce mitogenic activity since they release growth factors and create the conditions for the proliferation of fibrous tissue.
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PMID:[The atheromatous-fibrous plaque studied by cytofluorimetry]. 147 Mar 89

Decreased fibrinolytic capacity has been suggested to accelerate the process of arterial atherogenesis by facilitating thrombosis and fibrin deposition within developing atherosclerotic lesions. Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tissue-type plasminogen activator and has been found to be increased in a number of clinical conditions generally defined as prothrombotic. To investigate the potential role of this inhibitor in atherosclerosis, we examined the expression of PAI-1 mRNA in segments of 11 severely diseased and 5 relatively normal human arteries obtained from 16 different patients undergoing reconstructive surgery for aortic occlusive or aneurysmal disease. Densitometric scanning of RNA (Northern) blot autoradiograms revealed significantly increased levels of PAI-1 mRNA in severely atherosclerotic vessels (mean densitometric value, 1.7 +/- 0.28 SEM) compared with normal or mildly affected arteries (mean densitometric value, 0.63 +/- 0.09 SEM; P less than 0.05). In most instances, the level of PAI-1 mRNA was correlated with the degree of atherosclerosis. Analysis of adjacent tissue sections from the same patients by in situ hybridization demonstrated an abundance of PAI-1 mRNA-positive cells within the thickened intima of atherosclerotic arteries, mainly around the base of the plaque. PAI-1 mRNA could also be detected in cells scattered within the necrotic material and in endothelial cells of adventitial vessels. In contrast to these results, PAI-1 mRNA was visualized primarily within luminal endothelial cells of normal-appearing aortic tissue. Our data provide initial evidence for the increased expression of PAI-1 mRNA in severely atherosclerotic human arteries and suggest a role for PAI-1 in the progression of human atherosclerotic disease.
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PMID:Increased type 1 plasminogen activator inhibitor gene expression in atherosclerotic human arteries. 149 92

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.
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PMID:Smoking and cardiovascular disease. 149 5

It has been proposed that diffuse coronary atherosclerosis influences the myocardial perfusion. We performed a study of 94 young men with previous myocardial infarction in order to find out whether the presence and extent of diffuse coronary atherosclerosis affected the relation between maximal stenosis and myocardial perfusion in areas remote from the infarction. The patients were examined by planar-imaging thallium-201 scintigraphy, following exercise, and coronary angiography within 6 months after myocardial infarction. The maximal distinct stenosis and diffuse coronary atherosclerosis, comprising both plaque size and extent, were semiquantitatively assessed. The correlation coefficients between maximal stenosis within the LAD, RCA, and LCX vascular territories and the corresponding initial uptake of thallium were 0.52 (P = 0.0001), 0.30 (P = 0.04), and 0.46 (P = 0.02), respectively. No change of the correlations was found, except for a slight increase of the r-value from 0.30 to 0.37 in regions corresponding to RCA, after controlling for the diffuse atherosclerosis score in a multiple stepwise regression analysis. These findings indicate no impact of diffuse coronary atherosclerosis on regional myocardial perfusion in areas remote from the infarction.
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PMID:Does diffuse coronary atherosclerosis affect the relation between coronary stenoses and uptake of thallium-201 after exercise? 150 69

The immediate cause of arterial, predominantly coronary thrombosis is almost always cracking or fissuring of the cap of an atheromatous plaque. This exposes collagen and lipids to the flowing blood and thereby initiates thrombotic platelet aggregation, almost immediately followed by coagulation. The thrombi tend to extend into the arterial lumen, causing obstruction to blood flow and clinical symptoms and signs. Evidence for this sequence of events comes, inter alia, from angiograms of patients with unstable angina and developing myocardial infarction. Direct angioscopy in life is also visualising mural thrombi over fissured plaques in atheromatous coronary arteries. We are investigating the initial development of atheromatous plaques liable to fissuring. The cap over such plaques covers a "lipid pool". We have discovered that one factor promoting the uptake of lipid, in the form of plasma low-density lipoprotein, is the concentration of circulating catecholamines (Cardona-Sanclemente LE, Gorog P, Born GVR (1992) J Physiol London, in press). We are also investigating the immediate cause(s) of plaque fissure. We have evidence for a complex interaction of different determinants, including the concentration of macrophages, presumably as foam cells, in the plaque caps (Lendon CL, Davies MJ, Born BVR, Richardson PD (1991) Atherosclerosis 87: 87).
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PMID:Plaque fissure: the link between atherosclerosis and thrombosis. 152 97


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