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At least 1,117 records · Page 62Linked to original sources
PubMed2003

Update on vascular disease in systemic lupus erythematosus.

PURPOSE OF REVIEW: Young women with systemic lupus erythematosus have strikingly high rates of coronary heart disease. Current knowledge indicates that atherosclerosis is an active inflammatory and immune-mediated process. Therefore, the chronic inflammation and immune dysregulation characteristic of systemic lupus erythematosus undoubtedly contribute to the accelerated vascular disease seen in these patients. Carefully considering what is known about atherogenesis in the general population will provide clues to unraveling the complexity of why systemic lupus erythematosus and atherosclerosis are linked so frequently. RECENT FINDINGS: Inflammation is involved in all aspects of atherogenesis from the initial endothelial "response to injury," to foam cell formation leading to the atherosclerotic lesion, to the rupture of the "vulnerable" fibrous cap, resulting in the acute coronary syndrome and potentially in death. The authors review how factors commonly seen in systemic lupus erythematosus or inherent to the underlying disease mechanism may contribute to each of the stages of atherogenesis. SUMMARY: Our focus on the causes of vascular disease in systemic lupus erythematosus must now include nontraditional risk factors such as immune and inflammatory mediators. With the advent of noninvasive screening tools for atherosclerosis, we are better equipped to measure subclinical vascular disease and associated risk factors, including immune and inflammatory mediators. When considering strategies for preventing premature cardiovascular disease in systemic lupus erythematosus, modifying immune and inflammatory risk factors will likely become a major component of the program in addition to modifying the current traditional risk factors.

Adult↗
PubMed1995

Expression of receptors for advanced glycation end products in peripheral occlusive vascular disease.

The cellular interactions of advanced glycation end products (AGEs), which have been hypothesized to contribute to the development of vascular lesions, occur, at least in part, through their binding to a novel integral membrane protein, the receptor for AGEs (RAGE). Studies of human vascular segments show that endothelial RAGE expression at the antigen and mRNA level was variable and usually at low levels in samples from healthy individuals. In contrast, patients with a range of peripheral occlusive vascular diseases, with or without underlying diabetes, demonstrated prominent enhancement of endothelial RAGE expression. Smooth muscle cells and nerves in the vessel wall showed constitutively high levels of RAGE expression that were unchanged with aging (from 1 to 92 years) or by the presence of vascular disease. These data suggest that RAGE is likely to have ligands other than AGEs, and that multiple factors in addition to AGEs impact on its expression. Taken together, our findings suggest that RAGE may contribute to the pathogenesis of a range of vascular disorders.

Adult↗
PubMed2026

Investigation of the Causal Association Between Biological Aging Indicators and Vascular Disease Through Two-Sample Mendelian Randomization Analysis.

ObjectiveThis study used two-sample Mendelian Randomization to investigate the causal link between multiple biological aging indicators and vascular disease.MethodsSummary genetic data was obtained from genome-wide association studies (GWAS) focusing on aging-related exposures and various vascular disease outcomes. The exposures included granulocyte proportions, PAI-1 (plasminogen activator inhibitor-1), telomere lengths, and the Frailty Index. The primary analysis employed the Inverse Variance Weighted (IVW) method to estimate causal relationships, supported by MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses, including Cochran's Q test, MR-Egger regression, leave-one-out test, and the MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test, were conducted to evaluate heterogeneity and pleiotropy.ResultsThe analysis revealed distinct pathways after sensitivity adjustments. A higher genetically predicted Frailty Index was associated with an increased risk of abdominal aortic aneurysm (OR=2.5935, 95% CI: 1.3936-4.8268, P=0.0026, false discovery rate (FDR)=0.0475), atherosclerosis excluding cerebral and coronary sclerosis (OR=2.0262, 95% CI:1.5179-2.705, P=1.66×10-6, FDR=1×10-4), and arterial thromboembolic events (OR = 4.0306, 95% CI: 1.7133-9.4818, P = 0.0014, FDR = 0.0337). Conversely, longer telomere length demonstrated a strong, specific protective effect against abdominal aortic aneurysm (OR=0.5008, 95% CI:0.4111-0.6100, P=6.42×10-12, FDR=9.25×10-10), indicating that shorter telomere length is associated with an increased risk of AAA. Furthermore, a lower granulocyte proportion was causally linked to an increased risk of thoracic aortic aneurysm (OR=0.0181, 95% CI: 0.0014-0.2376, P=0.0023, FDR=0.0465).ConclusionThis study identifies three genetic pathways linking biological aging to vascular disease, offering new molecular targets for its prevention and treatment.

Humans↗
PubMed1989

Effects of taprostene, a chemically stable prostacyclin analogue, in patients with ischaemic peripheral vascular disease: a placebo controlled double-blind trial.

Thirty patients with ischaemic peripheral vascular disease and intermittent claudication were randomly allocated to receive either placebo or taprostene, a chemically stable prostacyclin analogue, intravenously at a rate of 25 ng/kg/min for 6 hours daily on 5 consecutive days. Taprostene produced a significant (p less than 0.05) increase in absolute walking time compared to placebo on one day after infusion and at 1, 4 and 8 weeks (14% vs 2.8%) later. Taprostene also produced a significant (p less than 0.05) increase in the pain-free walking time compared to placebo in the follow-up period (8 weeks after infusion: 23% vs 3.8%). During the infusion period systolic and diastolic blood pressure decreased (p less than 0.05) and heart rate was accelerated (p less than 0.05) in the taprostene treated group whereas no change was monitored in the placebo group. The ankle/brachial Doppler index was unaffected by taprostene. The platelet half-life was significantly (p less than 0.05) prolonged following taprostene-infusion (72.6 +/- 9.35 vs 77.9 +/- 7.44 hours). However, no change on platelet half-life was found in the placebo group (p less than 0.05). Various measures of platelet function parameters followed in vitro (ADP-induced aggregation, platelet sensitivity to PGI2, PGE1, PGD1 and taprostene, concentrations of platelet factor 4 and beta-thromboglobulin) showed no change with taprostene. Measures of circulating platelet aggregates and endothelial cells count showed no changes during the 2 months follow-up period too. It is assumed that taprostene may be of clinical benefit in patients with ischaemic peripheral vascular disease. However, future investigations have to be carried out to assess the optimal dose regime.

Alprostadil↗
PubMed1993

Imaging spectrum of thrombo-occlusive vascular disease associated with antiphospholipid antibodies.

The association of antiphospholipid antibodies with unexplained thrombo-occlusive vascular disease is well known but often remains unrecognized. The most well-studied clinical manifestation is venous thrombosis, but arterial occlusive disease involving multiple sites is also well documented. Twenty-six cases of thrombo-occlusive disease were observed in 22 patients over a 3-year period. Magnetic resonance imaging and angiography were used to make the diagnoses. None of the patients who underwent angiography or venography developed thrombolytic disease related to the puncture site. This group of patients with antiphospholipid antibody syndrome had a wide distribution of arterial and venous thrombotic disease. Radiologists should consider antiphospholipid antibody syndrome in the differential diagnosis when evaluating thrombo-occlusive vascular disease that is unexpected or occurs without risk factors. Knowledge of antiphospholipid antibody status has important implications for prognosis and therapy.

Adult↗
PubMed1991

Lower-extremity vascular grafts placed for peripheral vascular disease: prospective evaluation with duplex Doppler sonography.

Eighty-five men with 92 vascular grafts placed for peripheral vascular disease of the lower extremity underwent a total of 264 examinations with duplex Doppler over a 2.5-year period. In 64 patients who underwent more than one examination, the total follow-up encompassed 740 months. In 220 native femoral arteries (96.0%) the peak systolic velocity (PSV) was higher than that in the graft. Arteriovenous shunting was associated with a normal PSV and a markedly elevated diastolic component at spectral analysis. Focal fluid collections were common initially near the graft and usually disappeared uneventfully. An average PSV of 32 cm/sec or less was always associated with impending occlusion. The sensitivity of an average PSV of 40 cm/sec or less to indicate impending graft occlusion by the next visit was only 33%; the specificity, 94%. At initial examination, stenoses were associated with high PSV focally in the graft or low PSV with absent diastolic flow.

Aged↗
PubMed2001

Incidental renal artery stenosis in peripheral vascular disease: a case for treatment?

BACKGROUND: Renal artery stenosis (RAS) is frequently encountered as an incidental finding in peripheral vascular disease. We assessed whether revascularization is indicated to prevent the practical consequences of end-stage renal failure, that is, the need for renal replacement therapy. METHODS: In a retrospective study, a cohort of consecutive patients was followed who had undergone angiography 8 to 10 years previously for peripheral artery disease. Patients with untreated incidental RAS of > or =50% diameter stenosis (68.8 +/- 9.8 years, mean +/- SD) were compared with regard to the prevalence of renal replacement therapy to controls without RAS who were matched for age and gender. RESULTS: RAS was present in 126 of 386 evaluable patients (33%). None of these patients required renal replacement therapy during the 10-year follow-up. Serum creatinine values remained stable during follow-up. CONCLUSIONS: Incidental RAS is frequently seen in patients with peripheral vascular disease. If left untreated, incidental RAS seems not to result in end-stage renal failure or in a need for renal replacement therapy. Revascularization with the aim to prevent end-stage renal failure seems less indicated, and further prospective studies are indicated to elucidate this issue.

Aged↗
PubMed2006

Virulent strains of Helicobacter pylori and vascular diseases: a meta-analysis.

BACKGROUND: Cytotoxin-associated gene A (CagA)-positive strains of Helicobacter pylori are an etiological factor for peptic ulcer and gastric cancer. Studies on the role of these virulent strains in vascular diseases yield conflicting results. METHODS: We searched the MEDLINE database for relevant studies. Meta-analysis was performed using the random effects method. RESULTS: We found 10 retrospective case-control studies (with 1527 case patients and 1661 control subjects) and 3 prospective cohort studies (with 701 case patients and 1439 control subjects) on CagA status and ischemic heart disease and 4 retrospective case-control studies (with 513 case patients and 590 control subjects) on CagA status and cerebral ischemia. In the case-control studies, an association of ischemic heart disease with CagA-positive strains (OR 1.87, 95% CI 1.46-2.40) but no significant association with CagA-negative strains (OR 1.15, 95% CI 0.83-1.60) has been found; in the 3 prospective studies, association with ischemic heart disease was weaker but still significant (OR 1.26, 95% CI 1.05-1.51). In the 4 case-control studies, CagA-positive strains were significantly associated with cerebral ischemia (OR 2.43, 95% CI 1.89-3.13), again with no association for CagA-negative strains. CONCLUSIONS: We found a small but significant association between vascular diseases and virulent CagA-positive strains of H. pylori. The lack of association with CagA-negative strains further supports the hypothesis of an independent relationship between virulent strains of H. pylori and vascular diseases. The magnitude of the association with cerebral ischemia needs to be confirmed by prospective studies.

Antigens, Bacterial↗
PubMed1995

The influence of race on the use of surgical procedures for treatment of peripheral vascular disease of the lower extremities.

OBJECTIVE: To assess whether rates of amputation and leg-sparing surgery for peripheral vascular disease of the lower extremities differ between African-American and white patients. DESIGN: Retrospective cohort study using Medicare claims data for 1989 and 1990. SETTING: A total of 3313 hospitals in the United States. PATIENTS: Random sample of 19,236 Medicare Part A enrollees who underwent amputation and/or leg-sparing surgery for peripheral vascular disease. MAIN OUTCOME MEASURES: Adjusted odds of toe and/or foot amputation, below-knee amputation, above-knee amputation, lower extremity arterial vascularization, and percutaneous transluminal angioplasty for African American relative to whites, controlling for case-mix, region, and hospital characteristics. RESULTS: African-American patients were significantly more likely than white patients to undergo above-knee, below-knee, and toe and/or foot amputation and significantly less likely to undergo lower-extremity arterial revascularization and percutaneous transluminal angioplasty. These associations occurred for diabetic patients and nondiabetic patients but were more pronounced among patients who did not have diabetes. CONCLUSIONS: Potential explanations include unmeasured factors such as severity of disease and the technical expertise available at hospitals or other factors such as lack of compliance with medical treatment and race-specific treatment decisions by providers. Whatever the cause, interventions aimed toward reducing the number of amputations among African Americans are needed. Further work is required to determine where such interventions should be targeted.

Black or African American↗
PubMed2002

Optic disc hemorrhages and generalized vascular disease.

PURPOSE: To study the relationship between optic disc hemorrhages and four different groups of medications used in general vascular disease and diabetes. METHODS: The authors screened citizens of the city of Malmö, Sweden who were between 57 and 79 years old (32,918 subjects), in order to find individuals with undetected glaucoma. One set of optic disc photographs was taken of each participant and examined for optic disc hemorrhages. Logistic regression was used, with platelet aggregation inhibitors, antihypertensive agents, cholesterol-lowering medication, and antidiabetic agents as independent variables that were tested in isolation as well as in various combinations and adjusted for age and gender. RESULTS: Optic disc hemorrhages were significantly more common in individuals taking platelet aggregation inhibitors (OR 3.16, P < 0.0001). There was no significant association between ODH and the other three groups of medications. CONCLUSIONS: The significant relationship between platelet aggregation inhibitors and optic disc hemorrhages is a new and interesting finding that could indicate an association between optic disc hemorrhages and generalized vascular disease. Alternatively, it could mean that platelet aggregation inhibitors prolong resorption of or predispose to optic disc hemorrhages.

Aged↗
PubMed1999

[Vascular disease and cellular activation: exploration of cell adhesion phenotype by quantitative flow cytometry].

The pathogenesis of atheromatous and/or thrombotic vascular diseases involves rheological parameters, soluble mediators and cellular agents. The many studies that have tried to establish correlations between plasma factors, shear stress and the risk of ischemia have left some questions unanswered. Current exploration methods are now focusing on the determining role of cells. Activated cells express adhesion molecules on their membranes, which allow to communicate in a homo- or heterotypical manner. Quantifying adherence molecules on the surface of platelets, leukocytes and endothelial cells provides an assessment of the "adhesive phenotypical profile". Quantitative cytometry, using beads coated with a known amount of immunoglobulins as calibrators, is perfectly suited, through its multiple parameter analyses and the specificity provided by monoclonal antibodies, for the quantification of membrane antigens. Measuring the adhesive profile on the surface of cells that are implicated in vascular disease makes it possible to correlate that phenotype to the ischemic risk in such diversified pathologies or circumstances as intermittent angor, myocardial infarction, angioplasty, insulin-dependent diabetes or pre-eclampsia. In addition, that quantification permits monitoring the action of new therapeutical agents targeting adherence molecules.

Angioplasty, Balloon, Coronary↗
PubMed1987

Prostacyclin synthesis stimulating plasma factor in patients with peripheral vascular disease.

Human plasma contains a factor capable of stimulating vascular prostacyclin generation even in atherosclerotic vessels with minimal in-vitro capacity for PGI2-synthesis. The activity of this prostacyclin stimulating plasma factor (PSPF) has been reported to be elevated in renal failure and hepatic coma. We are not aware of any data as to whether this PSPF plays a role in maintaining hemostatic balance in patients with peripheral vascular lesions. Therefore, we examined 62 patients with peripheral vascular disease (PVD). This study group was subdivided into normo- and hyperlipemic subjects, patients with and without maturity onset diabetes, and plasma beta-thromboglobulin levels higher and lower than 50 ng/ml. 10 healthy sex and age matched persons served as controls. Vascular prostacyclin formation was studied in vitro after incubation of the patients' plasma and a buffer control with various tissue samples (human femoral artery, rat abdominal and thoracic aorta of healthy and of streptozotocin induced diabetic animals, swine endothelial layer and remaining tissue (media and adventitia) and cultured endothelial (EC) and smooth muscle cells (SMC) of minipig arota. In addition, 6-oxo-PFG1 alpha formation by cultured EC and SMC (minipig aorta source) after incubation with tris HCl-buffer or plasma were estimated by means of specific radioimmunoassays. In general, tissue samples and cells incubated in plasma exhibit a marked increase of in-vitro PGI2-formation as compared to buffer. No difference could be found between PSPF of CHD-patients and healthy controls. Similar findings were obtained using incubated vascular tissue and cultured cells by means of the bioassay and specific RIA, respectively. These findings indicate that the PSPF does not seem to be of any clinical relevance in hemostatic regulation in patients with advanced atherosclerosis.

Adult↗
PubMed1984

Exercise testing to evaluate patients with pulmonary vascular disease.

The maximal oxygen uptake and anaerobic threshold can be determined in patients with pulmonary vascular disease from noninvasive gas exchange measurements during progressive exercise. Maximal O2 utilization correlates directly with the maximal level of cardiac output and is inversely proportional to the pulmonary vascular resistance and the level of pulmonary arterial pressure. The accuracy of predicting the hemodynamic profile from noninvasive gas exchange measurements will obviously improve as more such patients are evaluated. Therefore, the determination of VO2 max has the potential of becoming a practical screening technique for detecting and predicting the severity of pulmonary vascular disease.

Adult↗
PubMed1998

Chlamydia pneumoniae and occlusive vascular disease: identification and characterization.

Chlamydia pneumoniae, a respiratory pathogen, has been associated with occlusive vascular disease, including atherosclerosis and intimal hyperplasia, through seroepidemiologic studies. Furthermore, using immunohistochemistry (IHC), polymerase chain reaction (PCR), transmission electron microscopy (TEM), and in situ hybridization, this association has been reconfirmed by detecting this organism in atherosclerotic vascular tissue. This review summarizes and critically analyzes these findings and also discusses various mechanisms of how Chlamydia pneumoniae could be involved in the pathogenesis of occlusive vascular disease. Although more studies are needed to reproduce these results and, possibly, uncover a mechanism, the current literature fails to include detailed methodologies for studying Chlamydia pneumoniae. Therefore, to provide a general standard, we have also outlined specific protocols for IHC, PCR, and TEM. These protocols incorporate essential components from various studies and are presented in a concise and easily adaptable format.

Arterial Occlusive Diseases↗
PubMed1992

Expansion of contracted visual fields following treatment with pentoxifylline in two patients with coexistent peripheral vascular disease--case reports.

Pentoxifylline, a hemorheologic drug reputed to reduce blood viscosity, can be used to improve the microcirculation in peripheral vascular disease. The authors report on 2 patients who were being followed up for possible glaucoma and whose visual field constriction became worse at about the same time as their peripheral vascular symptoms began to increase in severity. Following initiation of treatment with oral pentoxifylline, their peripheral vascular complaints decreased and their visual fields gradually expanded over the next several months. This dual effect seemed more than a coincidence. It may in fact indicate that the same mechanism said to aggravate the peripheral ischemia (ie, increased blood viscosity) in patients with peripheral vascular disease may also have been the basis for the visual field contraction in these 2 patients, possibly by producing retinal ischemia. The reversal of the contracted visual fields would then seem to be due to the ameliorative effect of the pentoxifylline treatment on the blood viscosity.

Aged↗
PubMed1980

Lung biopsy specimens in the evaluation of pulmonary vascular disease.

Open lung biopsy specimens in 72 patients were submitted for evaluation of pulmonary vascular disease. In nine instances, the specimens were inadequate for this purpose. Essentially, there were three indications for taking a lung biopsy specimen. The first was unexplained pulmonary hypertension with 40 patients in this category; plexogenic pulmonary arteriopathy was diagnosed in 14, and chronic pulmonary thromboembolism in 12. Others included pulmonary venoocclusive disease in two patients; two other patients had pulmonary vascular lesions in their lung biopsy specimens, indicative of chronic hypoxic pulmonary hypertension; and ten patients had severe arterial as well as venous alterations that could have been caused by obstruction to pulmonary venous flow as well as by fibrosis of lung tissue. Since we realized this possible source of error, we have submitted these two alternative possibilities to the clinician. In a heterogeneous group of eight patients, the nature of acquired or congenital heart disease remained doubtful in spite of extensive clinical investigation. In several instances, the biopsy specimen contributed to establishing the diagnosis of the cardiac condition. Finally, in a group of 15 patients with known congenital cardiac disease and pulmonary hypertension, whose state of pulmonary vasculature was considered borderline as far as the possibility of corrective surgery of the cardiac defect was concerned, lung biopsy specimens helped to determine the feasibility of surgery. The results show that in a restricted group of patients with pulmonary vascular disease, a biopsy of the lung has a place in establishing the nature and severity of the vascular alterations.

Adolescent↗