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PubMed1992

Calcium overload--an important cellular mechanism in hypertension and arteriosclerosis.

Arterial hypertension and arteriosclerosis are dramatic consequences of vascular calcium overload. Acute intracellular calcium overload of vascular smooth muscle cells produces hypercontractility. Hypertension develops if a general increase in systemic arteriolar tone leads to a rise in peripheral flow resistance. Moreover, progressive elevation of calcium destroys the structural integrity of the arterial and arteriolar walls. Thus, in various animals models, calcium overload initiates lesions of an arteriosclerotic character. Interestingly, conventional human coronary plaques also represent a calcium-dominated type of arteriosclerosis. With the advent of specific calcium antagonists, the pathogenic effects of calcium overload and its deleterious consequences have become, for the first time, accessible to therapeutic intervention. Accordingly, adequate treatment with calcium antagonists prevents calcium overload and can thereby protect arteries and arterioles from functional disturbances and structural damage. In spontaneously hypertensive rats, specific calcium antagonists of the verapamil, nifedipine and diltiazem type normalise blood pressure (BP) by reducing transmembrane calcium influx into vascular smooth muscle cells. However, in addition to controlling BP, these drugs also act as tissue protective agents. The long term effects of calcium antagonists such as verapamil in experimental hypertension include the prevention of severe arteriosclerosis, myocardial hypertrophy, and malignant nephrosclerosis. In humans, the antihypertensive efficacy of verapamil is well documented. Further clinical studies have yet to evaluate the antiarteriosclerotic and tissue protective potential of verapamil in humans.

Animals↗

PubMed2000

Relationship between the blood coagulation-fibrinolysis system and the subclinical indicators of arteriosclerosis in a healthy male population.

A cross-sectional observation was performed to assess the relationship between the coagulation-fibrinolysis system and the subclinical indicators of arteriosclerosis in a healthy male population. Subjects were 445 workers (18.9-49.4, Av. 36.2 yrs) in viscose rayon manufacturing factories in Japan. Coagulation-fibrinolysis parameters determined were D-dimer(DD), thrombin antithrombin III complex (TAT), tissue plasminogen activator (TPA), and plasminogen activator inhibitor 1 (PAI1). The following indicators of arteriosclerosis were examined; systolic and diastolic blood pressure (SBP, DBP), stiffness parameter of the carotid artery using ultrasound (beta), pulse wave velocity of the aorta (PWV), and a number of lacunar infarctions from brain MRI. After age-stratification(-29, 30-39, 40+ yrs), the subjects were classified into quartiles by coagulation-fibrinolysis parameters. The mean values of SBP and DBP and beta and PWV, the prevalence of brain infarctions were compared across these quartiles by means of analysis of variance, chi-square test, respectively. Multivariate analysis was also employed to adjust other risk factors. In conclusion, SBP and DBP and beta, PWV were elevated by increase of PAI1, TAT, respectively, in the 40+ years group even after adjustment for other possible risk factors. DD had no relation to any of the indicators of arteriosclerosis. None of the coagulation-fibrinolysis parameters had any relation to brain infarctions.

Adolescent↗

PubMed2000

[Ultrasonographic findings of carotid arteries in female patients with arteriosclerosis obliterans and aortic aneurysm].

To clarify carotid arterial changes in female patients with arteriosclerosis obliterans (ASO) and aortic aneurysm (AA), ultrasonographic (US) findings of the extra-cranial carotid arteries were studied in 26 patients with ASO (ASO group), and 31 patients with AA (AA group), compared to 38 controls (control group) with neither ASO nor AA. ASO was diagnosed with an ankle pressure index less than 0.9, while AA was done with computed tomography or angiography. Half of the patients with ASO were in stage II of the Fontaine clinical staging, and angiography, performed in 12, showed femoral arterial obstruction in 10. Most AA patients were abdominal aortic aneurysm. Using a high-resolution, real-time, B-mode US instrument, the diameter and wall thickness of the common carotids were measured bilaterally in the end-diastolic phase, and occlusive changes and plaque were estimated. As a risk factor for arteriosclerosis, hypertension, diabetes, hyperlipidemia, and cigarette smoking were assessed, in addition to the age, body height and weight. Mean ages of each group were 73 to 76.3 year-old. There was no significant difference between them in body height and weight. Diabetes, cigarette smoking, and cerebrovascular disease were frequent in the ASO group, whereas ischemic heart disease was frequent in the AA group. US findings revealed that carotid lesions were mostly plaque, and bilateral carotid lesions were significantly more frequent in the ASO and AA groups. The mean wall thickness of the carotids was greater in the AA and ASO groups, although dilated carotid arteries, namely arteriomegaly, was more frequent in the AA group than in the ASO and control groups. Stepwise regression analyses demonstrated that strong correlations were seen between carotid lesion and two variables [vessel diseases (ASO/AA) and cigarette smoking], between carotid diameter and three variables (age, AA, and wall thickness), and between the wall thickness and three variables (age, vessel diseases and diameter). These findings showed that atherosclerosis was not only frequent in female patients with ASO and AA, but arteriomegaly was characteristic in female patients with AA. Therefore, it suggested that circulatory disturbance in whole organs due to arteriosclerosis should be paid attention even in female patients with ASO and AA as well as male patients. Furthermore, it is considered that systemic fragility of the arterial media and ectasia could be present extensively in patients with AA.

Age Factors↗

PubMed1998

Signal transduction in arteriosclerosis: mechanical stress-activated MAP kinases in vascular smooth muscle cells (review).

Vascular smooth muscle cell (SMC) proliferation is a key event in the development of (spontaneous) atherosclerosis, hypertension-related arteriosclerosis, angioplasty-induced restenosis and venous bypass graft arteriosclerosis. Many factors or environmental stimuli are believed to be responsible for SMC growth or hypertrophy in the vessel wall. How these environmental stimuli or signals applied onto the surface of SMCs are transduced into the cell nucleus resulting in quantitative and qualitative changes in gene expression in SMCs of arterial walls is largely unknown. Mitogen-activated protein (MAP) kinases are rapidly activated in cells stimulated with various extracellular signals by dual phosphorylation of tyrosine and threonine residues. They are thought to play a pivotal role in transmitting transmembrane signals required for cell growth and differentiation. Recent studies have focused on the signalling events in vascular tissues in vivo and in cultured SMCs in vitro. It has been demonstrated that acute hypertension and angioplasty rapidly induced MAP kinase activation in the arterial wall. Kinase activation is followed by an increase in c-fos and c-jun gene expression and enhanced transcription factor AP-1 DNA-binding activity. A similar MAP kinase activation can be mimicked in in vitro cultured SMCs stimulated by either shear stress or cyclic strain stretch, suggesting direct effects of mechanical force. Interestingly, physical forces rapidly resulted in phosphorylation of platelet-derived growth factor (PDGF) receptor, an activated state, in cultured SMCs. Thus, mechanical stresses may directly perturb the cell surface or alter receptor conformation, thereby initiating signalling pathways usually used by growth factors. These findings have significantly enhanced our knowledge concerning the pathogenesis of arteriosclerosis and provide a basis for therapeutic intervention on vascular diseases.

Angioplasty↗

PubMed2000

[Cardiac allograft arteriosclerosis and myocardial necrosis].

OBJECTIVE: To study the development of myocardial necrosis, fibrosis, and arteriosclerosis in cardiac allograft in order to provide a theoretical basis for the prevention and treatment of anti-rejection. METHODS: The recipient was pretreated with inoculation of donor splenocytes (SPC) followed by cyclophosphamide (CP). Heterotopic cervical heart transplantation was performed. The allografts stained with Hematoxylin and eosin (HE), Masson and Van Gieson were studied about inflammatory cell infiltration, myocardial necrosis, fibrosis and arteriosclerosis. RESULTS: Preconditioning with SPC followed by CP prolonged the survival time of cardiac allograft. Inflammatory cell infiltration, myocardial necrosis, fibrosis, and arteriosclerosis in cardiac allograft were significantly decreased. CONCLUSIONS: The development of acute cardiac allograft rejection originated from the epicardial area to the intimal area of the heart in rat. The infiltration of collagenous fiber in the coronary arteries is one of the major causes of concentric stenosis. The pretreatment of SPC followed by CP can prevent and relieve the rejection.

Animals↗

PubMed1992

[Two thousand years of historical study on the words atheroma, atheromatosis, atherosclerosis, arteriosclerosis].

Renowned authors, when studying arterial diseases, use indifferently the words atheroma, atheromatosis, atherosclerosis or arteriosclerosis. The historical record of these words permits the justification of a selective choice. The word atheroma was created by Celsius, two thousand years ago; he have it the meaning of fatty tumor, which was kept till the middle of the nineteenth century. The word atheromatosis appeared on 1815, since J. Hodgson defined so the fatty arterial degeneration. Marchand, from Leipzig, proposed on 1904 the word atherosclerosis which has always been with us. The term arteriosclerosis was well defined on 1833 by Lobstein, from Strasbourg. The authors propose to reserve the word atherosclerosis to the arterial disease described by the WHO, to keep the words atheroma and atheromatosis to anatomical lesions well-defined. Arteriosclerosis is a disease which invades an extensive arterial network, with a particular anatomical image.

Arteriosclerosis↗

PubMed2004

[Clinical observation on effect of yangxue qingnao granule in treating patients with cerebral arteriosclerosis].

OBJECTIVE: To observe the efficacy of Yangxue Qingnao granule (YXQN) in treating cerebral arteriosclerosis and to explore its mechanisms. METHODS: One hundred and sixty-seven patients with arteriosclerosis were randomly divided into the treated group treated with conventional medical treatment plus YXQN and the control group treated with conventional medical treatment alone, to observe the changes before and after treatment in scores of chief symptoms, mean velocity of cerebral blood flow (VM), plasma nitric oxide (NO), calcitonin gene related peptide (CGRP) and endothelin (ET) levels. RESULTS: (1) After treatment in treated group, the scores of chief symptoms such as vertigo, headache and tinnitus were significantly lower than those in the control group (P < 0.05 or P < 0.01); (2) NO and CGRP level in the treated group after treatment obviously elevated, and ET and VM markedly reduced (P < 0.01), while no evident change of these parameters was found in the control group (P < 0.01). CONCLUSION: The efficacy of YXQN in treating cerebral arteriosclerosis is definite, modulating the level of vasoactive factors was its important mechanism.

Aged↗

PubMedDate not supplied

Comparison of arteriosclerosis, neoplasms and diabetes as the three main killers of man in the industrialized world.

Arteriosclerosis, neoplasms and diabetes are the three main killers in the industrialized world, complemented by infectious and parasitic diseases in the less developed countries. Neoplasms, the second most frequent killer in the industrialized world, exhibit the highest diversity of pathologic structures involved. Arteriosclerosis, the first killer in the industrialized world, is more complex, dealing with aberrations of the arterial wall. In contrast to neoplasms, cases are restricted to a closed circulatory system as noted in the various phyla. Neoplasms are also known from the kingdom of plants and fungi, whereas arteriosclerosis is restricted to specific animal phyla, at least theoretically. Even more restricted is the distribution of diabetes which is known only in certain vertebrates. All three disease groups have a substantial impact on man's health.

Animals↗

PubMed1992

Experimental graft arteriosclerosis. I. The Lewis-to-F-344 allograft model.

Progressive graft arteriosclerosis is responsible for the majority of late deaths occurring in cardiac transplant recipients. In order to define a model of this disease in the rat, we exchanged heterotopic cardiac allografts between MHC-compatible inbred strains. Lewis rats served as donors and F-344 rats as recipients. Twenty allografts were followed by daily palpation and removed at the time of terminal rejection or on the 120th postoperative day for pathologic study. Sixteen allografts (80%) survived at least three weeks, and five allografts (25%) survived indefinitely. The majority of arteries (greater than 90%) examined demonstrated significant intimal disease; histologic findings in lesions in allografts rejecting at early time points included intense mononuclear cell infiltration of the intima, while lesions in long-term-surviving allografts demonstrated fibrous intimal thickening, which is characteristic of graft arteriosclerosis seen clinically. A limited course of cyclosporine therapy in F-344 recipients increased the incidence of indefinite allograft survival from 25% to 86%, and was associated with a modest reduction in the amount of intimal disease observed. These results suggest that this model should be useful in future studies regarding the pathogenesis and therapy of cardiac graft arteriosclerosis.

Animals↗

PubMed2005

[The research on the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter with its effect of preventing ESRD patients from microinflammation and arteriosclerosis].

OBJECTIVE: We do this investigation in order to reveal the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter, and end stage renal disease (ESRD) patients microinflammatory state and arteriosclerosis (AS). METHODS: We used PCR-RFLP to measure the various kinds of distribution of IL-10 gene-1082A/G genotype and relevant indexes of microinflammatory state and AS of 870 ESRD patients and 1000 healthy persons of control group and to analyze the mechanism of its protection effect keeping ESRD patients away from microinflammation and arteriosclerosis. RESULTS: Compared with the control group, CRP, TNF-alpha, CH50, C3, IL-10 and Alb of ESRD group were in the normal range, but still significantly higher than those of the control group, while IL-10, Alb were significant lower (P < 0.05). The genotype distribution and allele frequency of IL-10A/G gene had no significant differences between the healthy group and the control group (P > 0.05). Levels of CRP, TNF-alpha, CH50 and C3 of ESRD patients with IL-10A/A genotype were significantly higher than those of ESRD patients with G/G and G/A genotype (P < 0.05), while IL-10 and Alb were significantly lower (P < 0.01). The production of IL-10 in serum from patients with IL-10A/A genotype was significantly lower than that of patients with G/G and G/A genotype (P < 0.01). The incidence rate of AS of patients with IL-10-1082A/A genotype was significantly higher than that of patients with G/G and G/A genotype (P < 0.01). The raise of AS incidence rate was correspondent with the decline of serum IL-10 and raise of serum CRP and Fib. CONCLUSION: The IL-10A/A genotype is a predictable factor of microinflammatory state and high AS incidence rate in ESRD patients. We use IL-10G/G genotype to modulate the high production of serum IL-10, to decline inflammatory reaction and to keep away from microinflammation and AS in ESRD patients. We should work hard on improving the dialysis membrane to reduce the anti-inflammatory factors in uremia for chronic renal failure patients with high arteriosclerosis risk.

Arteriosclerosis↗

PubMed1991

Chronic rejection of rat aortic allograft. II. Administration of cyclosporin induces accelerated allograft arteriosclerosis.

Rat aortic allografts immunosuppressed with cyclosporin--but not with azathioprine or steroids--develop an early inflammatory lesion in the subendothelial space. This "endothelialitis" is followed by an influx of proliferating smooth muscle cells into the intima, resulting in intimal thickening and accelerated arteriosclerosis. Administration of azathioprine and steroids largely ameliorates the development of the accelerated lesion. Similar endothelialitis and accelerated arteriosclerosis have been observed previously in the autopsy material of cardiac transplant recipients. Our results confirm the suggestion that the development of accelerated allograft arteriosclerosis is most likely linked to cyclosporin administration.

Animals↗

PubMed1979

[Does the concept for the prevention of chronic ischemic heart disease correspond to current ideas on etiology and pathogenesis of arteriosclerosis?].

A summarizing description of the essential relations between the existence of risk factors and the course of the morphologic changes in the arteriosclerosis in the intima is given. In this process the low density lipoproteins play an important role which together with further etiologic factors contribute to an increased permeability of the endothelium and to the stimulation of the proliferation and modulation of the smooth muscle cells, which are of central importance in the vascular reaction. Certain effects on the progression of the arteriosclerosis as well as a regression of adequate morphologic changes are to be expected from an elimination of risk factors, provided the necessary measures begin in the early stages of the arteriosclerosis, i. e. in the preatheromatous stage.

Adult↗

PubMed1985

The effect of HR (O-Beta-Hydroxyethylo-Rutoside, Venoruton) on the deformability of erythrocytes in patients with arteriosclerosis obliterans of lower limbs.

Deformability of red cells and plasma levels of cAMP and cGMP were studied in patients with arteriosclerosis obliterans of lower limbs. Deformability of red cells and plasma levels of cAMP were found to be decreased in these patients. Venous injection of HR (Venoruton) in one dose (1,000 mg) to patients, led to an increase of red cell deformability and normalisation of cAMP plasma level. The plasma level of cGMP was not changed. The beneficial effect of HR in arteriosclerosis obliterans depends, first of all, on improving the deformability of red cells. The decreased deformability observed in arteriosclerosis seems to be a result of disturbances in the rate of spectrin phosphorylation of the erythrocyte membrane. By normalising the plasma level of cAMP HR had a considerable influence on the appropriate state of elasticity of the red cell membrane.

Aged↗

PubMed1986

Arteriosclerosis risk in women and the role of oral contraceptive progestins.

UNLABELLED: Recent studies are reviewed to develop a perspective on the risk of arteriosclerotic heart disease occurring in women using various oral contraceptive (OC) formulations and postmenopausal estrogens. Evidence is provided in support of the following points: (1) arteriosclerosis risk increases in women after age 40 at a rate parallel to that in men; (2) arteriosclerosis risk is related to small changes in lipoprotein concentration, specifically LDL, HDL, and a subfraction of HDL, HDL2; (3) OC formulations alter LDL, HDL, and HDL2 concentrations in relation to the relative biologic effects (potency) of the estrogen and progestin components of the oral contraceptive pill, and/or the associated androgenic effect of the progestin component, with estrogen producing putatively favorable changes, and progestin, unfavorable changes; and (4) arteriosclerosis and myocardial infarction (MI) risk in young women using OC steroids is associated with increasing progestin potency, while postmenopausal women experience a reduced MI-related mortality and all-cause mortality, the latter attributable in part to an increase in HDL cholesterol concentrations. CLINICAL IMPLICATIONS: It is presently advisable to screen all subjects for hypercholesterolemia as a general measure, particularly those subjects who are contemplating the use of OCs. This national mandate is important in light of the data from the Lipid Research Clinics Coronary Primary Prevention Trial. This ten-year study showed that a 1% reduction in cholesterol yielded a 2% reduction in coronary risk. Therefore, small changes in a patient's lipid profile can have major ramifications later in life. OC steroids should be used with circumspection by women with existing cardiovascular disease risk factors and should be selected so as to minimize potentially adverse effects on lipoprotein physiology.

Arteriosclerosis↗

PubMed1987

Pathology of experimental pulmonary bone marrow embolism. II. Post-embolic pulmonary arteriosclerosis and pulmonary hypertension in rabbits receiving an intravenous infusion of allogeneic bone marrow.

The author investigated the morphogenesis of pulmonary arteriosclerosis in rabbits at 2 days to 3 months after the infusion of sliced fresh allogeneic bone marrow (500 mg) into the marginal ear vein of 87 rabbits. After 2 to 7 days, granulation tissue was formed in the embolized bone marrow, and new endothelial cells appeared on the surface resulting in recanalization. By 2 weeks, embolized bone marrow developed into fibrous and fibro-fatty plaques in the arterial wall. Moreover, from 4 weeks on, smooth muscle cells and elastic fibers proliferated in the emboli just beneath the new endothelial lining. The intima of non-embolized small arteries showed circumferential fibroelastosis, as the result of arteritis and followed by proliferation of medial smooth muscle cells, with narrowing of vascular lumen. The medial smooth muscle cells play an important role in the morphogenesis of pulmonary arteriosclerosis in bone marrow embolism. Pulmonary arterial pressure gradually increased 1 month as well as 3 months after the infusion. It is considered that narrowing of the vascular lumen resulted from post-embolic pulmonary arteriosclerosis may produce persistent pulmonary hypertension.

Animals↗

PubMed1986

[Arteriosclerosis and chelate therapy].

Based on a case history the therapeutic value of an iv-chelate therapy in arteriosclerosis is discussed. Ethylenediaminetetraacetate (EDTA) is used as a standard regime in the treatment of poisoning with heavy metals. The usefulness of EDTA in arteriosclerosis is doubtful: some authors suppose, that Ca-deposits are removed from arteriosclerotic lesions. This concept has not yet been proven by in-vivo experiments. Severe side effects such as hypocalcemia may cause the death of a patient under treatment. Therefore no real indications exist for treatment of arteriosclerosis with EDTA.

Aged↗

PubMed1986

[Significance of eicosanoids for arteriosclerosis and the effect of lipoproteins on prostanoid formation].

In a review the possible relevance of the eicosanoid system for arteriosclerosis is outlined. Particularly the interdependence between prostacyclin and thromboxane regarding the development of arteriosclerosis is discussed. Own findings show the influence of lipoproteins on the synthesis of prostacyclin or thromboxane in different biological material. On the one hand, HDL stimulates the synthesis of prostacyclin, whereas LDL inhibits it; both of them were sampled from human volunteers. On the other hand, the synthesis of thromboxane is inhibited by HDL and stimulated by LDL. The results indicate the close relationship between the lipoprotein and the eicosanoid hypotheses of arteriosclerosis.

Animals↗

PubMed1986

[Physiosclerosis--arteriosclerosis. Progression and regression then and now].

The clinical recognition of the physiosclerosis is still problematic even nowadays. This question seems not to be actual, since the disease arteriosclerosis with all its sequels is the superior epidemiological problem of mankind. Therefore, the inhibition of the progression and the regression of arteriosclerosis is of great interest. Now as ever, however, the coming forth of an atheromatous focus into the blood stream and the later change of the ulcer developed in such a way into fibrous connective tissue is the only regression of the arteriosclerosis in man up to now certainly made evident. A new course is adopted. Three approaches of intervention are represented with own results: favourable effects of multiply unsaturated fatty acid, importance of the trace element balance, particularly of selenium, the use of the classical risk factor concept at all ages.

Arteriosclerosis↗