[Sense of taste in Menière's disease and cochleo-vestibular disorders during vascular diseases and brain trauma].
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Brain Injuries↗
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A pilot double-blind study of sodium-magnesium EDTA in peripheral vascular disease.
Ten male patients with peripheral vascular disease, Type 2 (LaFontaine), were randomly assigned in a double-blind study to receive either Na2 ethylene diamine tetra acetic acid (EDTA) plus MgSO4, B complex, and vitamin C, or a placebo of MgSO4, B complex, and vitamin C in Ringer's lactate solution. A total of 20 intravenous infusions were planned for administration to each patient. Clinical and laboratory (noninvasive) tests showed dramatic improvements after 10 infusions in some patients, and thus was broken the code indicating who was receiving EDTA and who was receiving placebo. The group that improved had been receiving EDTA; there was no change in the placebo group. The trial was then completed in a single-blind fashion. Patients originally assigned to receive placebo then received 10 EDTA infusions, while the group originally assigned to EDTA received 20 EDTA infusions. The group that had formerly received placebo showed improvements comparable to those seen in the first EDTA group after 10 treatments.
Adult↗
Plasma lipid profiles and vascular disease in type 2 (non-insulin dependent) Nigerian diabetic patients.
Although ischaemic vascular disease is uncommon in Nigerians (diabetic and nondiabetic), foot gangrene of vascular origin still causes considerable morbidity in Nigerian diabetics. One known cause of vascular disease is lipid abnormalities. We therefore measured plasma lipid levels in diabetic patients with foot gangrene of vascular origin and compared those results with values in diabetics without gangrene and nondiabetic subjects, in relation to other variables such as glycaemic control, disease duration and body mass index. 45 noninsulin dependent diabetics (10 with foot gangrene) and 22 nondiabetic control subjects were studied. Those diabetics with gangrene had poorer (p less than 0.001) short-term glycaemic control (as assessed from fasting blood glucose levels) than those without, although longer-term control (HBA1C) was similar in both groups. Plasma triglyceride levels were significantly elevated in diabetics with or without gangrene (p less than 0.001) compared to nondiabetic subjects, while total cholesterol levels were high only in those with gangrene (p less than 0.02) who also had a longer disease duration. Plasma phospholipid and HDL-cholesterol did not differ significantly from control values. We therefore conclude that the raised plasma cholesterol and longer duration of diabetes in those diabetics with foot gangrene may have contributed to the genesis of vascular disease in those subjects.
Adult↗
Donor PAI-1 expression inhibits the intimal response of early allograft vascular disease.
BACKGROUND: The development of allograft vascular disease (AVD) may be related to altered expression of the fibrinolytic system. We determined the extent to which plasminogen activator inhibitor type 1 (PAI-1) expression in donor tissue influences intimal proliferation (IP) in a mouse model of AVD. METHODS: We utilized an end-to-end abdominal aortic transplant model in mice to investigate the development of IP in 3 groups of 6 recipients. Group A (negative control) utilized C57BL/6J strain mice as both donors and recipients. In Groups B (positive control) and C, C57BL/6J mice were vessel donors and CBA/J mice were recipients. Both groups received intraperitoneal anti-CD4 and anti-CD8 monoclonal antibodies (250 microg/week for 5 weeks). Group C recipients, however, were transplanted with vessels from C57BL/6J PAI-1 knockout mice. Animals were killed at 50 days. Transplanted aortas were removed and intimal areas calculated using morphometric analysis. RESULTS: Group A (mean intimal area 6421 +/- 8507 microm(2)) demonstrated very little IP in comparison to the other groups. IP was significantly higher in Group B (mean intimal area 56357 +/- 35629 microm(2)) than Group A (p = 0.008). Group C (mean intimal area 288195 +/- 123279 microm(2)) demonstrated significantly more intimal proliferation than either Groups A or B (vs B, p = 0.003; vs A, p < 0.001). The significance of these results is maintained if intimal thickness is measured as a stand-alone reference for the intimal response. CONCLUSIONS: Lack of PAI-1 expression in donor tissue greatly exaggerates the extent of IP after allogeneic transplantation and suggests that PAI-1 is important in limiting the early phase of AVD.
Animals↗
Pivotal role of plasminogen-activator inhibitor 1 in vascular disease.
Fibrinolysis plays a crucial role in the development of vascular disease. The interface between the plasminogen activators and inhibitors determines the fibrinolytic potential of human blood. In addition to fibrin degradation, fibrinolytic system components modulate several complex biological events such as angiogenesis, tumorigenesis, arteriosclerosis and cellular migration. Recent experimental and clinical data indicated that PAI-1 as a novel vascular risk factor. In this concise review, we will examine the accumulating evidence suggesting that there is an intricate relationship between these systems which may provide new therapeutic strategies for prevention of vascular disease.
Arteriosclerosis↗
Rate of decline of GFR and progression of vascular disease in type 2 diabetic patients with diabetic or vascular nephropathy during the last three years before starting dialysis therapy.
BACKGROUND: The progression of chronic renal insufficiency depends on the type of primary renal disease and blood pressure (BP) levels. We investigated the rate of decline of glomerular filtration rate (GFR) during 3 years prior to the start of dialysis therapy in type 2 diabetic patients with diabetic nephropathy (dNP) or vascular nephropathy (vNP). The aim of the study was to determine differences in the progression of renal insufficiency and the prevalence of vascular diseases in the two patient groups. METHODS: In a retrospective study, we investigated type 2 diabetic patients with chronic renal insufficiency who were undergoing regular controls in our outpatient care unit for at least 3 years prior to the start of dialysis. We evaluated only patients who had already died under chronic dialysis therapy, and whose diagnosis of primary renal disease was histologically conformed at autopsy. A total of 40 type 2 diabetic patients were included in the study. Of these, 28 patients had dNP (age 62 +/- 8 years) and 12 had vNP (age 70 +/- 7 years). The following parameters were determined at 3- to 6-month intervals: body weight, BP, HbA1c, serum creatinine (Cr), Cr clearance (Cockroft formula), cholesterol and triglycerides. The prevalence of vascular disease in the two groups was also assessed. RESULTS: The average decrease in Cr clearance was 7.7 +/- 2.4 ml/min/year in patients with dNP and 7.7 +/- 2.1 ml/min/year in those with vNP (NS). During the entire observation period, mean HbA1c values (7.0 +/- 0.8 vs. 6.8 +/- 0.6%), systolic BP (137 +/- 8 vs. 138 +/- 11 mm Hg) and diastolic BP (86 +/- 4 vs. 87 +/- 7 mm Hg), cholesterol and triglycerides did not differ significantly in the two groups. The prevalence of vascular disease 3 years prior to and at the start of dialysis therapy was similar in patients with dNP and vNP. CONCLUSION: The progression of dNP and vNP is similar at least during 3 years before the start of dialysis therapy. Vascular risk factors and the prevalence of vascular diseases were not significantly different in the two patient groups. However, diabetic patients with ESRD secondary to dNP were significantly younger than those with vNP.
Aged↗
Microalbuminuria as predictor of vascular disease in non-diabetic subjects. Islington Diabetes Survey.
The relation between urinary albumin excretion rate (AER) and vascular disease was studied in 187 subjects aged over 40 selected from 1084 cases attending a diabetic screening project. AER exceeded 20 micrograms/min in 3 of 13 newly diagnosed diabetic subjects (23%) and 16 of 171 non-diabetic subjects (9.4%). There was a weak relation between AER and both systolic and diastolic blood pressures. Coronary heart disease was found in 54 of 164 (32.9%) subjects with AER of 20 micrograms/min or less and in 14 of 19 (74%) with AER above this. Peripheral vascular disease was present in 16 of 165 (9.7%) subjects with AER of 20 micrograms/min or less and 8 of 18 (44%) with a high AER. Logistic regression, including diabetes, impaired glucose tolerance, systolic and diastolic blood pressures, smoking, age, sex, ethnic origin, and body mass index, demonstrated the independence of this relation between AER above 20 micrograms/min and coronary heart disease (odds ratio [OR] 6.38, 95% confidence interval 1.91-21.4) and peripheral vascular disease (OR 7.72, 2.14-27.8). After a mean of 3.6 (SD 0.19) years, 167 subjects (89.3%) were traced. There had been 9 deaths, 3 (2.0%) among 149 subjects with normal AER and 6 (33%) among 18 microalbuminuric subjects (OR 24.33, 5.40-109.7).
Adult↗
Lp(a) lipoprotein, vascular disease, and mortality in the elderly.
BACKGROUND: As compared with what is known about predictors of vascular events in middle-aged persons, less is known about these events in the elderly. Lp(a) lipoprotein, which plays an important part in atherothrombogenesis, has been associated with an increased risk of vascular disease. We investigated this relation among older U.S. adults. METHODS: In a prospective study of 5888 community-dwelling older adults (65 years of age or older) in the United States, 2375 women and 1597 men who were free of vascular disease provided base-line serum samples for analysis for levels of Lp(a) lipoprotein. These 3972 subjects were followed for a median of 7.4 years to evaluate the development of stroke and to track deaths from vascular causes and all causes. The men and women were divided into quintile groups according to the Lp(a) lipoprotein level at base line. RESULTS: Using Cox proportional-hazards models, we determined the risk associated with each quintile level of Lp(a) lipoprotein, with the lowest quintile serving as the reference group. As compared with those in the lowest quintile, men in the highest quintile had three times the unadjusted risk of stroke (relative risk, 3.00; 95 percent confidence interval, 1.59 to 5.65), almost three times the risk of death associated with vascular events (relative risk, 2.54; 95 percent confidence interval, 1.59 to 4.08), and nearly twice the risk of death from all causes (relative risk, 1.76; 95 percent confidence interval, 1.31 to 2.36). Adjustment for age; sex; the levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides; carotid-wall thickness; smoking status; the presence or absence of diabetes and systolic and diastolic hypertension; body-mass index; and other traditional risk factors had little effect on the final assessments. Similar analyses for women, which also included adjustment for estrogen use or nonuse, revealed no such relation. CONCLUSIONS: Among older adults in the United States, an elevated level of Lp(a) lipoprotein is an independent predictor of stroke, death from vascular disease, and death from any cause in men but not in women. These data support the use of Lp(a) lipoprotein levels in predicting the risk of these events in older men.
Aged↗
Concurrent lumbar spinal stenosis and peripheral vascular disease. A report of nine patients.
Intermittent claudication from peripheral vascular disease is sometimes difficult to distinguish from neurogenic claudication secondary to lumbar spinal stenosis. Of 172 patients with symptoms of claudication and lumbar spinal stenosis proved by myelography or computed tomography (CT), nine had peripheral vascular disease identified with ultrasonography and arteriography. All of the nine patients had a laminectomy performed to decompress the narrow spinal canal, and two had an additional posterolateral fusion. Two patients were treated with an excision of their abdominal aortic aneurysm, while one of those patients later required a bypass graft for iliac stenosis. One patient had had an aortofemoral bypass graft, one a femoropopliteal graft, and one a lumbar sympathectomy. Follow-up study ranged from three to eight years, with an average of five years after their last surgical procedure. Paresthesias generally dissipated after the spinal surgery. The cramping-type discomfort associated with walking was not easily attributed either to vascular or a neurogenic etiology. Five patients had initial weakness, which invariably improved. A secondary etiology contributing to claudication must be excluded in those patients with persistent discomfort following previous lumbar spinal or vascular surgery for arterial insufficiency.
Aged↗
Three-dimensional topographic angiography in chorioretinal vascular disease.
PURPOSE: To evaluate a new angiographic technique that offers three-dimensional imaging of chorioretinal vascular diseases. METHODS: Fluorescein (FA) and indocyanine green angiography (ICGA) were performed using a confocal scanning laser ophthalmoscope. Tomographic series with 32 images per set were taken over a depth of 4 mm at an image frequency of 20 Hz. An axial analysis was performed for each x/y position to determine the fluorescence distribution along the z-axis. The location of the onset of fluorescence at a defined threshold intensity was identified and a depth profile was generated. The overall results of fluorescence topography were displayed in a gray scale-coded image and three-dimensional relief. RESULTS: Topographic angiography delineated the choriocapillary surface covering the posterior pole with exposed larger retinal vessels. Superficial masking of fluorescence by hemorrhage or absorbing fluid did not preclude detection of underlying diseases. Choroidal neovascularization (CNV) appeared as a vascular formation with distinct configuration and prominence. Chorioretinal infiltrates exhibited perfusion defects with dye pooling. Retinal pigment epithelium detachments (PEDs) demonstrated dynamic filling mechanisms. Intraretinal extravasation in retinal vascular disease was detected within a well-demarcated area with prominent retinal thickening. CONCLUSIONS: Confocal topographic angiography allows high-resolution three-dimensional imaging of chorioretinal vascular and exudative diseases. Structural vascular changes (e.g., proliferation) are detected in respect to location and size. Dynamic processes (e.g., perfusion defects, extravasation, and barrier dysfunction) are clearly identified and may be quantified. Topographic angiography is a promising technique in the diagnosis, therapeutic evaluation, and pathophysiological evaluation of macular disease.
Choroid↗
Association of mild hyperhomocysteinemia with cardiac graft vascular disease.
In non-transplant patients mild hyperhomocysteinemia is an independent risk factor for vascular disease. The aim of this study was to determine whether hyperhomocysteinemia is associated with graft vascular disease. Fasting total plasma homocysteine was assessed in 18 patients with graft vasculopathy and 18 transplanted patients without graft vasculopathy matched for age, sex and the time since transplant. All were on cyclosporin. Graft vasculopathy was defined at coronary angiography as stenoses > or = 25%, or aneurysms. We found that hyperhomocysteinemia ( > or = 15 micromol/l) is common among transplanted heart recipients and significantly more frequent in the patients with graft vasculopathy (17/18 versus 11/18). Accordingly, the mean homocysteinemia was significantly higher in the group with graft vasculopathy (23.6+/-7.8 versus 16.9+/-7.1 micromol/l, P=0.01). The elevation of homocysteine plasma levels in the heart transplant recipients has probably multiple causes. The main cause seems to be renal failure. Additional causes could be azathioprine treatment or genetic polymorphisms. These results suggest that besides the immunological factors, homocysteine can play an additional role in the pathogenesis of graft vascular disease.
Adult↗
Glucose and diabetic vascular disease.
The central therapeutic problem in diabetes mellitus is prevention and treatment of the chronic vascular disease associated with this disorder. Prolonged exposure to hyperglycemia is the primary factor associated with the development of diabetes-specific microvascular disease, and the relationship between deranged glucose metabolism and arterial disease is complicated by many other factors that influence atherogenesis in nondiabetics. Until relatively recently, knowledge about diabetic vascular disease was limited mainly to clinical description. New information about abnormal vascular physiology, ultrastructure, biochemistry, cell biology, and molecular biology now makes it possible to understand in an integrated fashion the major specific mechanisms by which hyperglycemia damages diabetic vessels. Continued progress in this area will further optimize the development of safe and effective drugs for the treatment of diabetic vascular disease.
Animals↗
[Remote results of tetraethylammonium chloride therapy of occlusive vascular diseases of the extremities].
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Cardiovascular Diseases↗
Aspirin, platelets and prevention of vascular disease.
Aspirin inhibits thromboxane and prostaglandin formation in platelets and in vascular cells. It prevents platelet aggregation by irreversible acetylation of cyclooxygenase, a key enzyme in arachidonic acid metabolism. On the basis of its antiplatelet effect, aspirin has been assessed during the past two decades in patients with a history of myocardial infarction, stroke, transient ischemic attack or unstable angina. A meta-analysis of randomized controlled trials of long-term aspirin treatment for the secondary prevention of vascular disease indicated that aspirin (300-1500 mg daily) significantly reduced fatal and non-fatal vascular events. More recently aspirin (160 mg daily) produced a significant reduction in hospital vascular mortality and in non-fatal events in patients with suspected acute myocardial infarction. The combination of aspirin and streptokinase was significantly better than either drug alone. On the other hand, two primary prevention trials of aspirin in healthy doctors did not show any modification of vascular mortality despite an overall reduction of non-fatal myocardial infarction. Resolution of some problems related to the mechanism of action of aspirin and to selection of trial populations will possibly increase the benefit/risk ratio of aspirin treatment for the prevention of vascular disease.
Aspirin↗
Effect of transdermal nitroglycerin on inflammatory mediators in patients with peripheral atherosclerotic vascular disease.
OBJECTIVE: To demonstrate that nitroglycerin improves biological markers of arterial inflammation in patients with peripheral vascular disease. BACKGROUND: Atherosclerosis is an inflammatory disease in which there is an increase in active inflammation markers such as C-reactive protein and other factors released by endothelial cells. Nitroglycerin acts by a chemical liberation of nitric oxide. We have previously published the results from several controlled clinical trials confirming an anti-inflammatory action of nitroglycerin. METHODS: Forty patients with peripheral vascular disease entered a randomized, double-blind, placebo-controlled pilot study for 6 weeks. Twenty-one patients were treated with continuous application of a transdermal nitroglycerin patch (15 mg/24 hours) on the anterior face of the thigh. Venous blood samples were obtained before treatment and 2 and 6 weeks after. We measured plasma levels of C-reactive protein, cGMP (also intraplatelet cGMP), E-selectin, ICAM, VCAM-1, IL-6, and nitrites/nitrates. RESULTS: No biological parameter was modified in the placebo group. On the contrary, nitroglycerin significantly reduced plasma levels of C-reactive protein and sE-selectin and increased the levels of intraplatelet cGMP. CONCLUSIONS: The results of this preliminary study show that nitroglycerin has an anti-inflammatory action in patients with peripheral vascular disease. This may provide a new therapeutic approach to understanding the efficacy of nitrovasodilators in the improvement of atherosclerotic syndromes.
Administration, Cutaneous↗
Cholesteryl ester transfer protein as a protective factor against vascular disease in hemodialysis patients.
Cholesteryl ester transfer protein (CETP) may promote reverse cholesterol transport. An elevated concentration of high-density lipoprotein cholesterol (HDL-C) is a protective factor against atherosclerosis. However, the effects of CETP itself and its interaction with HDL-C have not been investigated in hemodialysis patients, who are at high risk for atherosclerosis and generally considered to have decreased reverse cholesterol transport. We investigated the independent or synergistic influence of postprandial serum CETP and HDL-C concentrations on apparent atherosclerotic complications in 202 hemodialysis patients aged 40 to 80 years. Patients with vascular disease (n = 39) had significantly lower concentrations of CETP than those without vascular disease (n = 163). When all study subjects were divided into four groups according to CETP and HDL-C concentrations based on median values, we found significant differences in the prevalence of vascular disease (test for trend, P < 0.005): 28.8% in group I (HDL-C < 48 mg/dL; CETP < 2.2 microgram/mL); 25.0% in group II (HDL-C < 48 mg/dL; CETP >/= 2.2 microgram/mL); 17.8% in group III (HDL-C >/= 48 mg/dL; CETP < 2.2 microgram/mL); and 6.9% in group IV (HDL-C >/= 48 mg/dL; CETP >/= 2.2 microgram/mL). Multiple logistic regression analysis retained the interaction term between HDL-C (in milligrams per deciliter) and CETP (in micrograms per milliliter), but not HDL-C or CETP itself, as inversely associated with vascular disease in the entire patient group. In patients with HDL-C levels at the median value or greater, CETP had an independent odds ratio of 0.31 (95% confidence interval, 0.1 to 0.97; P < 0.05) after adjusting for age. These results suggest that CETP may serve as a protective factor against vascular disease in hemodialysis patients, especially those with normal or elevated HDL-C concentrations.
Adult↗
PERIPHERAL VASCULAR DISEASE.
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Angiography↗
Associations of urinary albumin excretion rate with vascular disease in europid nondiabetic subjects.
Microalbuminuria and its association with vascular disease has previously been reported in nondiabetic individuals. The aims of this study were to determine whether there is a cross-sectional relationship between urinary albumin excretion rate and cardiovascular disease in nondiabetic subjects and to investigate hereditary predisposition to microalbuminuria by studying offspring of the main study population. Europid patients, aged 40-70 years, were randomly selected from a large inner-city general practice; there was a 62.6% attendance rate, and a study population of 959 remained after exclusions. Blood pressure, ankle systolic pressure, height, and weight were measured. Albumin excretion rate was calculated from overnight and morning urine collections. Venous blood was taken for lipids, fibrinogen, and factor VII; and resting electrocardiograms were carried out. Offspring (aged 15-40 years) of those found to be microalbuminuric were invited to attend for the same tests, and controls were selected by age and sex matching the parents. There was no association between parents' albumin excretion rate with that of their offspring, and there were no significant differences in albumin excretion rate between offspring subjects and their controls. There were no statistically significant associations of prevalent coronary heart disease (CHD) with albumin excretion rate or microalbuminuria in either sex [CHD in women: odds ratio (OR) 1.85; 95% confidence interval (CI) 0.19,9.0] [CHD in men: OR 2.13; 95% CI (0.64, 6.59)]. In women, there were significant associations between albumin excretion rate and peripheral vascular disease (positive) and fibrinogen (negative). Because established risk factors may not be as strongly associated with CHD in cross-sectional studies, we intend to follow this group prospectively.
Adult↗