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At least 19 recordsLinked to original sources
PubMed2001

Clinical picture of arteriolosclerosis.

Arteriolosclerosis is a generalised systemic vascular disease which is characterised by hyalinisation of intima (hyalinosis) as well as proliferation and hypertrophy of the media in the arteriolar part of the arterial system (so-called benign arteriolosclerosis). However, the patients suffering from accelerated and malign hypertension develop also fibrinoid necrosis (so-called malign arteriolosclerosis, arteriolonecrosis). Arteriolosclerosis as well as other similar stenotic (obliterating, obstructive, occlusive) diseases of the arterial system, have one single common consequence--ischemia. Currently, angio-organic ischemic syndromes in the whole world most frequently result from atherosclerosis which, however, is not the only nosologic unit of the group of arterial diseases having the tendency to develop arterial wall sclerosis. The latter group is briefly referred to as arteriosclerosis. In addition to atherosclerosis, this group includes also Mönckeberg's medial arteriosclerosis, diabetic angiopathy and arteriolosclerosis. The authors of this study, on the basis of their analysis of their own large set of patients (71,662 angiologic consultant examinations performed during the period of 25 years of the existence of the Angiologic Department of the Medical Faculty Hospital of Comenius University in Bratislava) attract attention to the fact that the clinical picture of this disease is multiform, and that it occurs frequently in clinical practice. Therefore, angiology is a separate specialisation which is above the structure of internal medicine.

Arterioles↗
PubMed1996

Diffuse vacuolization (spongiosis) and arteriolosclerosis in the frontal white matter occurs in vascular dementia.

OBJECTIVE: To examine quantitatively white-matter changes at different sites in patients with definite vascular dementia and Alzheimer's disease. DESIGN: Prospective clinical and neuropathological series. SETTING: University Hospital clinics (Helsinki, Finland and London, Ontario). SUBJECTS: Twenty-two patients with a clinical and neuropathological diagnosis of vascular dementia and 20 patients with Alzheimer's disease. MEASURES: The frequencies of focal white-matter lesions, arteriolosclerosis, and cerebral amyloid angiopathy were assessed. Validated ratings and cell counts were done in the subcortical U-fiber, centrum semiovale, and periventricular areas of the frontal white matter. Degrees of abnormality (none, mild, moderate, severe) were rated for spongiosis (vacuolization of white matter), état criblé (widening of perivascular spaces), myelin loss, oligodendrocyte density, axonal loss, and overall. Densities of oligodendrocytes and astrocytes (cells per square millimeter) were determined. RESULTS: Patients with vascular dementia showed focal white-matter lesions and arteriolosclerosis more often than patients with Alzheimer's disease. The patients with vascular dementia also had significantly greater spongiosis (P<.001), état criblé (P=.004), myelin loss (P<.005) and overall white-matter abnormality (P<.001). Arteriolosclerosis was found in association with spongiosis but not with état criblé. Cerebral amyloid angiopathy did not appear to be related to any of the white-matter changes in patients with either vascular dementia or Alzheimer's disease. The U-fiber area showed fewer changes, and the periventricular area tended to be most affected. CONCLUSION: In addition to focal infarcts, patients with vascular dementia showed widespread diffuse changes, including spongiosis and arteriolosclerosis, along with état criblé and myelin loss. White-matter changes in patients with Alzheimer's disease could not be related to infarction. Pathologic changes in small blood vessels are associated with diffuse white-matter changes and may have a distinct role in the genesis of vascular dementia.

Aged↗
PubMed1992

Myoendothelial contacts in arteriolosclerosis.

Human renal biopsies were examined electron microscopically to investigate close contacts between endothelial and smooth muscle cells in small arterioles. These myoendothelial contacts were seen in the form of cytoplasmic projections passing through fenestrae in the basal lamina. Most of these cell processes seem to arise from the endothelial cells. In the control vessels, the separation between the endothelial cells and smooth muscle cells of the tunica media is 0.09-0.27 microns. With arteriolosclerosis there is an increasing separation between the elements of the intima and the media, from 1.0 to 2.42 microns. In spite of this increasing separation, myoendothelial contacts maintain an intercellular space of 10-15 nm, as observed in the control vessels. At 2.42 microns of separation, the amount of extracellular material accumulated is such that the cells can no longer keep in contact. Break up of the myoendothelial contacts may be responsible for impairment of communication between the tunica intima and media in the vessel wall in arteriolosclerosis.

Aged↗
PubMed1978

Histophysical and histochemical investigations on muscle arterioles in hypertensive arteriolosclerosis; an interference microscopical, polarization optical and histophotometrical study.

In 50 formol fixed biopsies from the m. quadriceps femoris normal and hypertensive arteriolosclerotic arterioles were characterized by quantitative histophysical and histochemical methods. The interference microscopical measurements showed a real increase of dry mass concentration in the pathologically changed vessels. Additional histophotometrical results are interpreted as an increase of proteins with higher isoelectric point (globulins, actomyosin). An augmentation of actomyosin is compatible with the medial hyperplasia demonstrated histologically. Likewise a positive correlation was found between the fibrin incorporation proved histochemically and the quantitatively evaluated protein reaction with Fast green; Glycosaminglycans do not carry weight quantitatively. The polarization optical measurements yielded an alteration of the submicroscopical structure in arteriolosclerosis. It consists in a diminution of the submicroscopical volum of gaps and in a diminished orientated dye binding of Congo red. Thereby the pathogenesis of hypertensive arteriolosclerosis of skeleton muscle is above all characterized by an increase of heterogeneous proteins (blood plasma proteins, actomyosin) in the arteriolar wall, leading to a diminution of the submicroscopical volume of gaps and to an elevation of the dry mass concentration.

Arteries↗
PubMed1991

Periventricular lesions in the white matter on magnetic resonance imaging in the elderly. A morphometric correlation with arteriolosclerosis and dilated perivascular spaces.

Magnetic resonance imaging (MRI) was performed postmortem on the brains of 40 patients aged over 60 yrs who had died from causes other than brain disease. Periventricular lesions of increased signal intensity on T2-weighted images, graded as moderate or severe, were found in 10% of the patients in the age group between 60 and 69 yrs, and in 50% between 80 and 89 yrs. Macroscopic and microscopic whole-brain sections were studied in 19 brain specimens (8 with normal white matter, 4 with moderate lesions and 7 with severe lesions of the white matter on MRI). The presence or absence of periventricular lesions on MRI correlated well with the severity of demyelination and astrocytic gliosis. Demyelination was always associated with an increased ratio between wall thickness and external diameter of arterioles (up to 150 microns). A variable degree of axonal loss in Bodian-stained sections was present in the white matter of all brains with demyelination. Dilated perivascular spaces were found and studied morphometrically in 9 brain specimens; their presence correlated strongly with corrected brain weight, but incompletely with demyelination and arteriolosclerosis. Our findings suggest that arteriolosclerosis is the primary factor in the pathogenesis of diffuse white matter lesions in the elderly. This is soon followed by demyelination and loss of axons, and only later by dilatation of perivascular spaces.

Aged↗
PubMed2000

Adverse effect of donor arteriolosclerosis on graft outcome after renal transplantation.

INTRODUCTION: In recent years less strict criteria for renal graft donors have been applied. Our study was designed to investigate whether the histological picture, with special reference to vascular changes of the donor kidney, has an effect on the development and level of graft function, and on 48-month graft survival. METHODS: Three morphologically distinct groups were formed from 150 consecutive cadaveric kidneys donors transplanted into 290 recipients. A control group (C) consisted of kidneys with a completely normal histological picture. Group M1 included kidneys with mild arteriolosclerosis and group M2 (n=122) was comprised of kidneys showing significant arteriolosclerosis. The onset of graft function was assessed by the need for dialysis treatment post-transplantation and the levels of serum creatinine and creatinine clearance at 6, 12, 24 and 36 months post transplant. RESULTS: The proportion of sclerotic glomeruli (P<0.001) and the incidence and severity of interstitial fibrosis was greater in groups M1 and M2 than in the control group (M1, P<0.01; M2, P<0.001). The incidence of vascular fibrinoid necrosis in M2 was greater than in controls (P<0.001). The onset of graft function did not differ significantly between the groups. Group M2 showed a significantly lower level of graft function (P<0.001). The 4-year graft survival rate of group M2 was 74.2%, significantly lower than in the combined group C+M1 (P=0.03). CONCLUSION: Significant vascular lesions in the donor kidney should be taken into account when predicting graft function and survival.

Acute Disease↗
PubMed2002

Significance of white matter high intensity lesions as a predictor of stroke from arteriolosclerosis.

OBJECTIVES: To determine whether the extent of white matter high intensity lesions (WML) on magnetic resonance imaging (MRI) is an independent predictor of risk for stroke from arteriolosclerosis, and whether serial evaluation of WML can be used to identify patients who are at risk of strokes. METHODS: Prospective follow up with serial MRI scans was done in 89 patients who were either diagnosed as having symptomatic lacunar infarcts or were stroke-free, neurologically normal individuals with headache or dizziness. None had significant stenosis of major cerebral arteries or atrial fibrillation. Multivariable analysis with the Cox proportional hazards model was used to test the predictive value for subsequent stroke of risk factor status at entry and during follow up, lacunar infarction, and the extent of WML (scored from 0 to 16) on the baseline scans. RESULTS: During follow up (mean (SD), 51 (19) months), seven strokes occurred (five lacunar infarcts and two haemorrhages): four in nine patients with severe WML (score 9-16), and three in 40 patients with mild WML (score 1-8) (log-rank test; p < 0.005). None of 40 patients without WML experienced stroke. The extent of WML was an independent predictor of subsequent stroke (relative risk for a 1 point score increase, 1.60; 95% confidence interval, 1.02 to 2.54; p < 0.05). In three strokes among 80 patients without severe WML, two occurred in four patients with an increase in WML score during follow up, and one occurred in the other 76 patients without an increased score (p < 0.0001). CONCLUSIONS: Severe WML at baseline is an independent predictor of risk for stroke from arteriolosclerosis, while progression of WML during follow up may be associated with subsequent stroke in patients with initially mild WML.

Adult↗
PubMed1985

Significance of renal hyaline arteriolosclerosis in focal segmental glomerulosclerosis.

The renal biopsy findings of 60 adults with idiopathic focal segmental glomerulosclerosis (FSGS) were reviewed in order to determine the clinicopathological significance of renal hyaline arteriolosclerosis (HA) in FSGS. 36 biopsies (60%) exhibited a definite HA [HA (+)] in association with high levels of proteinuria (p less than 0.0024) and serum creatinine (p less than 0.0316) and a high frequency of global sclerosis (p less than 0.0014) when compared to the remaining 24 biopsies without definite HA [HA (-)]. 14 (39%) of these HA (+) biopsies showed continuity of afferent arteriolosclerosis with hyalinosis of the adjacent glomerular axial segmental sclerosis. These results suggest that HA (+) patients with FSGS show more severe disease than HA (-) patients, and there is a possible relationship between FSGS and HA.

Adolescent↗
PubMed1999

Brain arteriolosclerosis and hemodynamic disturbance may induce leukoaraiosis.

OBJECTIVE: To investigate whether internal carotid artery (ICA) occlusive disease-induced hemodynamic disturbance is associated with extensive white matter high-intensity lesions (WMLs) on T2-weighted MR images in the hemisphere with lacunar infarct in the basal ganglia. BACKGROUND: Hemodynamic disturbance in the brain with arteriolosclerosis may be one of the mechanisms by which ischemic injury induces extensive WMLs. METHODS: The authors used MRI and PET to study 21 patients with unilateral ICA occlusion or stenosis and lacunar infarct in the bilateral basal ganglia. In hemispheres with ICA disease, the association of WMLs with the mean hemispheric values of oxygen extraction fraction (OEF)-an index of hemodynamic compromise-measured with the 15O-labeled gas steady-state technique was analyzed. Twenty-five patients with ICA occlusive disease without lacunar infarct were studied as control subjects. RESULTS: In the hemispheres with ICA disease, patients with lacunar infarct had a significantly greater severity of WMLs than control subjects, although the mean hemispheric values of the OEF showed no significant difference. The severity of WMLs correlated significantly with the mean hemispheric values of the OEF in patients with lacunar infarct, but not in control subjects. Multivariate analysis revealed that lacunar infarcts and increased OEF were independent predictors of extensive WMLs, with lacunar infarcts the most heavily weighted factor. CONCLUSION: Internal carotid artery occlusive disease-induced hemodynamic disturbance is associated with extensive WMLs in hemispheres with lacunar infarct. Hemodynamic disturbance may contribute to the development of extensive WMLs, although brain arteriolosclerosis may be a major contributing factor.

Aged↗
PubMed1977

Quantitative studies of the renal corpuscles IV. Determination of normal values in various age categories, and an analysis of the possible influence of physiological degrees of arteriolosclerosis.

A quantitative study including total and differential counts of nuclei and determination of mesangial and total glomerular area was carried out on kidney tissue from 21 persons without renal disease, in order to determine the normal values of glomerular parameters and to estimate the possible influence of age and physiological degrees of arteriolosclerosis. No age dependency was found to exist for the glomerular parameters within the age category of 17 to 45 years. Above the age of forty-five a rise in mesangial area per cent of total area and mesangial nuclei per cent of total nuclei was found on increasing age, while a decline on increasing age was demonstrated for epithelial nuclei per cent of total nuclei. The mean value of mesangial nuclei per 1000 micron2 of mesangial area was found to be significantly higher in the older age category than in the younger. Arteriolosclerosis did not appear to influence the parameters. The study also attempted to describe the three variance components: interrenal, interfocal and interglomerular variation. Interfocal variation was the smallest part of the total variation, and interrenal plus interfocal variation was at most of the same size os interglomerular variation.

Adolescent↗
PubMed1977

[Factor analysis in hypertension. Risks of coronary heart disease and hypertensive arteriolosclerosis (author's transl)].

Based upon factor analysis, initial findings of the risk factors for coronary heart disease are reported, following invesitgations performed on a large number of patho-anatomical cases which were selected for specified criteria. The so-called hypertensive form of arteriosclerosis was demonstrated in the spleen, pancreas, and adrenal gland. It was shown that diabetes mellitus is an influencing factor in arteriolosclerosis in the liver. Several types of arterial hypertension can be differentiated according to clinical features and findings in the heart. Renoparenchymatous and renovascular sclerosis, pyelonephritis, diabetes mellitus, and age are the factors correlated or associated with various types of hypertension. Primary (?) renal hypertension can be differentiated from the secondary (?) TYPE. The discussion suggests that the morphological findings of arteriosclerosis and its complications may be explained, to a certain extent, by the known risk factors of coronary diseases defined by the methods described.

Adrenal Glands↗
PubMed2000

Coronary reserve and arteriolosclerosis in hypertensive heart disease.

Hypertensive heart disease leads to left ventricular hypertrophy, structural and functional alterations of the myocardium, and to wall thickening and sclerosis of intramural coronary arteries and arterioles, called arteriolosclerosis, that increase myocardial stiffness and cause diastolic dysfunction right from the beginning. Especially, increased content of collagen in the periarteriolar region contributes to impaired coronary reserve that predisposes to myocardial ischemia even in the absence of coronary artery disease and may be an important factor for diastolic and finally systolic dysfunction. Antihypertensive therapy should additionally aim at inducing repair of myocardial and vascular structure.

Animals↗
PubMed1987

Significance of renal hyaline arteriolosclerosis and tubulo-interstitial change in IgA glomerulonephropathy and focal glomerular sclerosis.

The relationship between glomerular sclerosis and hyaline arteriolosclerosis (HA) or tubulo-interstitial (T-I) change was investigated in 66 patients with IgA glomerulonephropathy (IgA-GN) and in 12 patients with idiopathic focal segmental glomerulosclerosis (FGS). More than a 10% incidence of global sclerosis was noted in 15 patients with IgA-GN and in 9 patients with FGS. There was no significant discrepancy of age between patients with IgA-GN and those with FGS (IgA-GN: 37.5 +/- 12.5; FGS: 35.7 +/- 10.3). In patients with IgA-GN, 7 out of 15 were HA-positive (46.7%), whereas in patients with FGS, 7 out of 9 were HA-positive (77.8%). However, a close correlation was observed between glomerular sclerosis and T-I change only in patients with IgA-GN (r = 0.82; p less than 0.001). The results suggested that in the case of IgA-GN, T-I change was related to the prognosis of glomerular sclerosis. In addition, it is assumed that a possible correlation exists between FGS and HA.

Adolescent↗
PubMed2001

A clinical investigation on 30 cases of senile benign renal arteriolosclerosis treated by huang qi gu jing yin.

Huang Qi Gu Jing Yin (HQGJY[symbol: see text]decoction of Astragalus root for Strengthening the Essence) was used in a controlled clinical trial for treatment of senile benign renal arteriolosclerosis. In the therapeutic group (n = 30), cure, marked effect and no effect were obtained respectively in 18 (60%), 9 (30%) and 3 (10%) cases with the total effective rate being 90%; the corresponding figures in the control group (n = 30) were 10 (33.3%), 9 (30%) and 11 (36.7%) with the total effective rate being 63.3%. The significant difference (P < 0.01) between the two groups demonstrated that HQGJY is an effective agent for treatment of the disease.

Aged↗
PubMed1986

The pathogenesis of hyaline arteriolosclerosis.

Although hyaline arteriolosclerosis is very common and has been of interest to pathologists for well over 100 years, its pathogenesis has never been determined. This study demonstrates that iC3b bound via an ester linkage to hydroxyl groups on the repeating disaccharide units of hyaluronic acid is a major component of arteriolar hyaline. The deposition of iC3b within the walls of arterioles appears to be due to slow spontaneous activation of the alternative complement pathway and random binding of metastable C3b to proximate hyaluronic acid within the arteriolar wall. Since hyaluronic acid does not activate the alternative complement pathway, bound C3b is rapidly inactivated by factors I and H to iC3b, which, along with factor H, remains bound to hyaluronic acid. The hyaline in some hyalinized arterioles also contains IgM and early and late classical complement pathway components. Indirect evidence suggests that the IgM represents immunoconglutinin, an autoantibody to neoantigens on iC3b and that their interaction results in activation of the classical complement pathway. The gradual accumulation of iC3b, factor H, and, at times, IgM and classical complement pathway components within the walls of arterioles is considered to be a physiologic consequence of aging and probably cannot be prevented, because interruption of the initial binding of metastable C3b to hyaluronic acid would require abrogation of the critically important functions of the alternative complement pathway.

Adolescent↗