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PubMed2006

Role of alloantibodies in the pathogenesis of graft arteriosclerosis in cardiac transplantation.

Graft arteriosclerosis (GA) remains the leading obstacle to long-term survival of cardiac allografts. The pathogenesis of this chronic disease, though perceived to be multifactorial, is most likely immune-driven. Based on clinical and experimental observations, the humoral arm of the immune system has long been suspected to play a pivotal role in the disease process. In this article, we shall review the evidence generated from key clinical and experimental studies on the role of alloantibodies in GA. We will argue that although the strong correlation between the presence of anti-donor antibodies in clinical and experimental GA is highly suggestive of a pathogenic role for alloantibodies, a direct causal link between GA and the humoral arm of the alloresponse cannot yet be established based on the currently available evidence, and may in fact be one of a number of pathogenic processes that potentiate this vasculopathy. Finally, in this article, we shall discuss some of the potential mechanisms by which alloantibodies may exert their pathogenic effect in GA.

Animals↗
PubMed1992

Cell-matrix interactions in the genesis of arteriosclerosis and atheroma. Effect of aging.

The progression of atheroarteriosclerosis was shown to be age dependent. This designation covers two separate entities: arteriosclerosis, the progressive and diffuse hardening of the walls of arteries with loss of elasticity, and atheromatous plaque formation, which can start early in life according to nutrition and genetic factors (LDL-receptor expression). Lipoprotein-receptor interactions play a crucial role in lipidic plaque formation. There is, however, no indication that the diffuse hardening of the vascular wall would also be influenced by these mechanisms. We described recently a high-affinity receptor for elastin peptides, present on smooth muscle cells, fibroblasts, and also on monocytes and PMNs. When activated, this receptor will increase intracellular calcium. Circulating elastin peptides were determined by a sensitive Elisa method and found to be between 0.1 and 20 micrograms/ml, in the range of activation of the elastin receptor. They increase in obliterative arteriopathies and type IIb hyperlipidemia. Elastolysis accompanies aging and vascular pathology; the sensitivity of this receptor changes with age, intracellular Ca++ increases, but the receptor appears to be uncoupled from its normal transmission mechanism. These results may well explain the increasing diffuse calcification of the vessel wall. The previously demonstrated potentiation of cholesterol deposition in elastic fibers by calcium is in agreement with simultaneous deposition of calcium and lipids. The recent demonstration of the efficient competition of fibronectin for LDL in proteoglycan-LDL complexes suggests that this reaction may be involved in foam cell formation by the opsonization of LDL for phagocytosis. Fibronectin was shown to accumulate in atherosclerotic plaques. Altogether these recent results confirm the importance of cell-matrix interactions in atherogenesis and lead to a better understanding of the age dependence of these disease processes.

Aging↗
PubMed1992

Homocystinuria, arteriosclerosis, methylmalonic aciduria, and methyltransferase deficiency: a key case revisited.

The original case of Cb1 C disease with homocystinuria, cystathioninuria, methylmalonic aciduria, and hypomethioninemia was reexamined because of its importance in the discovery of the homocysteine theory of arteriosclerosis. The vascular lesions in the case consist of proliferative fibrous intimal plaques and focal necrosis of the artery wall, which are attributed to effects of excess homocysteine thiolactone on aggregation of low-density lipoproteins (LDL) and on respiration of endothelial cells. Atrophic, metaplastic, and dysplastic changes within the gastric mucosa are attributed to effects of excess homocysteine thiolactone on synthesis of keratin, sulfomucins, and nucleoproteins within affected cells. The case illustrates how investigation of an inborn error of metabolism illuminates pathophysiological disease processes, normal metabolic pathways, and important aspects of cellular function.

Arteriosclerosis↗
PubMed1971

Effect of age and arteriosclerosis on the response of Parkinsonian patients to levodopa.

Twenty-four patients with Parkinsonism were treated with levodopa for up to one year. Ten were aged under 65, 12 were aged 65 or over, and two were specifically included because they were considered to have arteriosclerotic Parkinsonism. These two patients showed no response to treatment. The 10 younger patients showed less clinical evidence of arteriosclerosis than the older ones, and responded significantly better to treatment with levodopa. Mean improvement was 61% in the younger group after 12 months' treatment and 28% in the older group. Improvement was greatest within three months of starting treatment. Abnormal movements which resulted from treatment with levodopa could be reduced with only slight loss of therapeutic benefit by the addition of tetrabenazine.

Age Factors↗
PubMed2004

Association between apolipoprotein E e4 allele and arteriosclerosis, cerebral amyloid angiopathy, and cerebral white matter damage in Alzheimer's disease.

OBJECTIVE: To investigate the association between white matter damage, as evidenced by myelin loss (ML), the extent of cerebral amyloid angiopathy (CAA), or arteriosclerosis (Art), and apolipoprotein E (ApoE) e4 allele in Alzheimer's disease (AD), in order to understand the causes of damage to white matter in AD and its contribution to the pathogenesis of the disorder. MATERIALS AND METHODS: Brain tissues were obtained from 94 patients with AD confirmed by autopsy. ApoE genotyping was performed by PCR on DNA extracted from frontal cortex or cerebellum. CAA and Art were assessed on Weigert's haematoxylin and eosin stained sections in frontal, temporal, parietal, and occipital cortices; the extent of ML was scored on Luxol fast blue stained sections of these regions. RESULTS: The ApoE e4 allele frequency in the 61 patients with ML was not significantly different from that in the 33 patients without ML, nor did this differ in the 84 patients with Art from that in the 10 patients without Art. There were no significant differences in the proportions of patients with genotypes containing 0, 1, or 2 ApoE e4 alleles in the presence or absence of ML or Art. The mean ML, Art, or CAA scores within each region, and the total scores summed across all four brain regions, did not differ between patients with 0, 1, or 2 ApoE e4 alleles. However, the mean ML severity score in the occipital cortex was significantly greater than that in the frontal or temporal cortices in patients with 1 or 2 ApoE e4 alleles. The severity of CAA in the occipital cortex was significantly higher than that in other areas of cortex in patients with 0 or 2 ApoE e4 alleles. The mean Art score in the occipital cortex was greater than that in the temporal cortex in patients with two ApoE e4 alleles and was higher than that in the frontal cortex in patients with one ApoE e4 allele. CONCLUSIONS: The likelihood of patients with AD suffering from CAA, Art, or ML is not influenced by ApoE e4 allele, nor is the overall burden of these pathological changes in the brain. However, the distribution of ML, CAA, and Art within the brain is at least partly influenced by genotype and dosage of ApoE e4 allele, with the occipital cortex being more severely affected by all of these pathological changes in e4 allele bearers, particularly when two ApoE e4 alleles are present.

Aged↗
PubMed1994

Therapy of carotid arteriosclerosis.

Carotid arteriosclerotic disease is the most readily treatable type of lesion leading to stroke. Its management involves lowering those risk factors over which the patient has control. Patients should regulate hypertension, quit smoking, seek medical attention for treatable cardiac abnormalities, and take steps to reduce increased blood lipids. For symptomatic carotid disease, regardless of whether surgery is offered, platelet inhibitors are obligatory. The recommended dose is 650 mg aspirin per day (or up to 1300 mg, if tolerated). For patients whose symptoms continue despite aspirin therapy or who are aspirin intolerant, ticlopidine is the only recommended platelet inhibitor. Cerebral arterial bypass surgery is not an effective treatment for carotid arteriosclerosis. Carotid endarterectomy helps patients with > or = 70% stenosis as determined by strict arteriographic measurements. We do not yet have sufficient data to determine whether endarterectomy would benefit patients with lower levels of carotid stenosis or asymptomatic patients with any degree of stenosis.

Anastomosis, Surgical↗
PubMed2002

Arteriosclerosis of penile arteries: histological findings and their significance in the treatment of erectile dysfunction.

OBJECTIVES: In this pathomorphological study, location, distribution, and degree of arteriosclerotic stenoses in penile arteries from unselected cadavers are investigated. The findings are discussed in the context of penile revascularization and may explain the poor results of this form of surgery in older patients with general arteriosclerosis. MATERIALS AND METHODS: 120 penile specimens from 120 cadavers were examined histologically after van Gieson staining. Transverse sections were performed at the level of the pubic bone, in the middle of the penis, and at the sulcus coronarius. At these levels the dorsal and deep penile arteries were examined. RESULTS: We found arteriosclerotic stenoses of the penile arteries in 65% of the specimens. Of these stenotic lesions, 20.4% were situated proximally, 37.1% centrally, and 42.5% distally. CONCLUSIONS: In patients with arteriosclerotic stenoses of the penile arteries, microsurgical penile revascularization to the proximal part of the dorsal arteries at the base of the penis seems to be without any relevant long-lasting hemodynamic effect, because the blood flow will be impeded by the peripheral stenoses. This can explain the poor results of revascularization in this group of patients.

Adult↗
PubMed1982

Effect of cardiac glycosides on the release of adenylate kinase into cerebrospinal fluid of patients with cerebral arteriosclerosis.

48 patients with cerebral arteriosclerosis were found to have a manifest release of adenylate kinase (AK) into cerebrospinal fluid (CSF). This release was most probably due to an increased leak in the brain cells subsequent to a lowered adenylate charge potential followed by a diminished electrochemical potential in these cells suffering from disturbed oxygen supply. A further increase of AK release into CSF was noted for the 22 patients receiving cardiac glycosides compared to the 26 patients not treated with these drugs. The mean AK value of the former group was 0.119 +/- 0.028 U/l compared to that of the latter group, being 0.089 +/- 0.025 U/l, and this difference was significant (p less than 0.001). The effect of cardiac glycosides is most probably explained by an additional lowering of the membrane electrochemical potential in brain cells of these patients due to the direct action of cardiac glycosides on the Na+- and K+-dependent ATPase system in these cells, resulting in an increased leak in the plasma membrane.

Adenylate Kinase↗
PubMed1978

Smooth muscle cells in the development of plasmatic arterionecrosis, arteriosclerosis, and arterial contraction.

Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12-24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

Animals↗
PubMed1981

Arterial calcium metabolism, hypertension and arteriosclerosis.

Recent research emphasizes the importance of calcium transport in smooth muscle in the etiology of essential hypertension. Mönckeberg's arteriosclerosis may be due to the deposition of such calcium in the media of the large arteries, made ischemic and necrotic by a decrease in adventitial blood supply, as well as a decrease in luminal endothelial and intimal permeability; and also aided by chemicals derived from fragmented elastic tissue. In atherosclerosis, rupture of the internal elastica causes smooth muscle to migrate into plaques which become cholesterol- and lipid-filled and finally calcified. Endothelial cracks or ulcers cause the deposition of platelets which have internal calcium transport mechanisms similar to those of smooth muscle and so, on deterioration, contribute to the deposition of calcium. In arterioles, where there is no or minimal adventitial blood supply, where smooth muscle contraction counteracts lateral stretch and hence rupture of the internal elastica and where pressures are lower, plasmatic protein influx, as well as necrosis, causes hyalinization and connective tissue scarring rather than calcium deposition. In other words, calcification of blood vessels may occur because of the precipitation of this ion from the sources already mentioned, as well as because of a possible attraction of the ion into the lesion from the blood stream. If it is precipitated as calcium apatite, the lesion can resemble bone. In veins and in the pulmonary artery, calcium deposition is rare except when there is increased pressure or thrombosis.

Adult↗
PubMed1996

Increased antibody titers against mycobacterial heat-shock protein 65 in patients with vasculitis and arteriosclerosis.

Heat shock proteins (HSPs) are a group of highly conserved proteins that show extensive homology at the DNA and protein level among bacterial and mammalian species. Furthermore, bacterial HSPs induce specific cellular and humoral immune responses in mammals. Cross-reacting antibodies may therefore be induced in chronic infections. Recently, it has been claimed that patients with arteriosclerosis (AS) of the carotid arteries have significantly elevated antibody titers to mycobacterial HSPs. In this study, we extended the spectrum of vascular diseases and analyzed sera from patients with systemic vasculitis and systemic lupus erythematosus (SLE) for the presence of anti-HSP antibodies. Anti-HSP antibodies, tested in an ELISA with recombinant mycobacterial HSP 65, were significantly elevated in patients with vasculitis (n = 56; p < 0.01) and AS (n = 29; p < 0.0001), but only marginally in patients with SLE (n = 22; p > 0.05) compared to healthy controls (n = 90). These findings further support the concept of infection-induced immune reactions playing a pathogenic role in the development of both AS and vasculitis.

Adolescent↗
PubMed1988

Delusional parasitosis. A comparative study to late-onset schizophrenia and organic mental disorders due to cerebral arteriosclerosis.

Delusional parasitosis (DP) was found in about 7 of 10,000 psychiatric admissions. The comparison of patients suffering from DP (n = 20) with 170 cases of late-onset schizophrenia (LOS) and 120 patients diagnosed as organic mental disorder due to cerebral arteriosclerosis (CAS) showed more similarities of DP with organic than with schizophrenic disorders. In addition, the phenomenological analysis supports the classification of the majority of DP cases as organic mental disorders. Even careful analysis cannot always answer the question, whether the main symptoms of DP have to be classified as delusions, hallucinations or misidentifications.

Aged↗
PubMed2004

Autologous transplantation of peripheral blood stem cells as an effective therapeutic approach for severe arteriosclerosis obliterans of lower extremities.

Treatment of severe arteriosclerosis obliterans of lower extremities (ASOLE) remains a clinical challenge. To develop a more effective approach, we evaluated the clinical efficacy of autologous transplantation of mobilized peripheral blood stem cells (PBSCs) in 5 patients with ASOLE. The patients received recombinant human granulocyte colony-stimulating factor (rhG-CSF, 600 micro g/day) for 5 consecutive days. On day 5, PBSCs were collected, sorted from blood circulation of patients, and then intramuscularly injected into their ischemic lower limbs. A significant improvement of clinical manifestations including severe pain, skin temperature and ulcer, was observed, without obvious adverse effect. The patient's limb was successfully saved. Satisfactory remission was obtained 3 months after transplantation as shown by significant improvement in ankle-brachial pressure index (ABI), blood flow in personal vascular laboratory (PVL), laser Doppler blood perfusion, and the angio-graphic scores. Our data suggest for the first time that autologous transplantation of mobilized PBSCs provides a practical, safe, and effective method of treatment for lower limb ischemia.

Aged↗
PubMed2003

Origin of vascular smooth muscle cells and the role of circulating stem cells in transplant arteriosclerosis.

To date, clinical solid-organ transplantation has not achieved its goals as a long-term treatment for patients with end-stage organ failure. Development of so-called chronic transplant dysfunction (CTD) is now recognized as the predominant cause of allograft loss long term (after the first postoperative year) after transplantation. CTD has the remarkable histological feature that the luminal areas of intragraft arteries become obliterated, predominantly with vascular smooth muscle cells (VSMCs) intermingled with some inflammatory cells (transplant arteriosclerosis, or TA). The development of TA is a multifactorial process, and many risk factors have been identified. However, the precise pathogenetic mechanisms leading to TA are largely unknown and, as a result, adequate prevention and treatment protocols are still lacking. This review discusses the origin (donor versus recipient, bone marrow versus nonbone marrow) of the VSMCs in TA lesions. Poorly controlled influx and subsequent proliferative behavior of these VSMCs are considered to be critical elements in the development of TA. Available data show heterogeneity when analyzing the origin of neointimal VSMCs in various transplant models and species, indicating the existence of multiple sites of origin. Based on these findings, a model considering plasticity of VSMC origin in TA in relation to severity and extent of graft damage is proposed.

Animals↗
PubMed1993

Cytokeratins 8 and 18 in smooth muscle cells. Detection in human coronary artery, peripheral vascular, and vein graft disease and in transplantation-associated arteriosclerosis.

During development of atherosclerotic lesions, vascular smooth muscle cells (SMCs) undergo changes both phenotypically and in their cytoskeleton composition. An expression of cytokeratins 8 and 18 in SMCs in plaques of the human superficial femoral artery and of cytokeratin 8 in lesions of the aorta was recently described. Since cytokeratins are epithelial markers generally not found in normal adult vascular SMCs, we performed a detailed immunofluorescence microscopy study using a large panel of antibodies against the various cytokeratin polypeptides and other elements of the cytoskeleton. We included lesions of carotid, common and superficial femoral, iliac, and popliteal arteries; the abdominal aorta; and saphenous vein bypass grafts, as well as primary, restenotic, and transplantation-associated lesions of coronary arteries (n = 33). Cytokeratins 8 and 18 were present in myointimal cells of all pathological specimens. Colocalization with smooth muscle alpha-actin identified most cytokeratin-positive cells as SMCs. Only very few cells cosynthesized cytokeratin and desmin, whereas the majority of cytokeratin-positive cells were vimentin-positive. This pattern of cytoskeletal protein synthesis is similar to that found in some fetal and/or neonatal SMCs. These findings suggest that the synthesis of cytokeratins in a subset of SMCs of atherosclerotic lesions is a common phenomenon in coronary artery and peripheral vascular disease as well as graft disease and transplantation-associated arteriosclerosis and that the state of these SMCs is of a "dedifferentiated" fetal type.

Aorta↗
PubMedDate not supplied

Regional compliance of brachial artery and saline infusion in patients with arteriosclerosis obliterans.

Simultaneous brachial artery pressure and blood flow measurements were made in 15 patients with arteriosclerosis of the lower limbs (AOLL) and in controls of the same age and sex. Blood flow was evaluated by a pulsed Doppler device with a double-transducer probe. From analysis of the pressure-flow curves during diastole, regional arterial compliance (RAC) was determined by using as a model of the forearm arterial tree a system of tubes, each with a storage capacity, in series with the arteriolar resistance vessels. In AOLL patients, RAC was significantly reduced (102 +/- 13 vs 173 +/- 14.10(-4) ml/mm Hg, p less than 0.01), and systolic pressure was significantly increased. After saline infusion, systolic pressure continued to increase and arterial compliance, to decrease; brachial blood flow did not change. Study of the baroreflex sensitivity in AOLL patients under basal conditions indicated that a higher pulse pressure was required to obtain the same heart rate as in the controls. The study provided evidence that in AOLL patients: 1) compliance was reduced in the brachial artery (a regional circulation with no clinical evidence of arterial occlusion); 2) an increase in systolic pressure resulted from the decreased arterial compliance; and 3) saline infusion exaggerated the observed reduction in arterial compliance and increase in systolic pressure.

Aged↗
PubMedDate not supplied

Increased pulse pressure in patients with arteriosclerosis obliterans of the lower limbs.

Brachial blood pressure, ankle systolic pressure, calf blood flow before and after postocclusive reactive hyperemia, and treadmill exercise results were determined in 16 patients with arteriosclerosis obliterans disease (AOD) of the lower limbs. These values were compared with values from 16 controls matched for age and sex. For the same mean arterial pressure in controls, pulse pressure was significantly higher and resting calf blood flow, slightly lower in patients with AOD. Resting calf blood flow was positively correlated with mean arterial pressure and pulse pressure in patients with AOD but not in controls. In AOD patients, reduced walking distance was strongly and positively correlated with "vascular bed reserve" expressed as the ratio between peak blood flow after postocclusive reactive hyperemia and resting calf blood flow. Correlation studies indicated that the higher the pulse pressure, the more reduced the walking distance and the more altered the vascular bed reserve. The study provided evidence that: increased pulse pressure, rather than increased mean arterial pressure, is a characteristic feature of patients with AOD, and the pulsatile component of blood pressure, which reflects the alteration of the buffering function of large arteries, might influence the reductions in walking distance and vascular bed reserve observed in patients with AOD.

Adult↗