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Symposium on Peripheral Vascular Diseases. Foreword.
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[Differential diagnosis of peripheral vascular diseases].
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Revascularization in peripheral vascular disease: stents, atherectomies, lasers, and thrombolytics.
Peripheral vascular disease affects a significant number of individuals. Signs and symptoms may develop because of partial or total vessel occlusion due to plaque, dissection, or thrombus. Percutaneous transluminal angioplasty is effective as an independent intervention to open occluded vessels and also may be combined with other nonsurgical therapies such as stents, atherectomy, or laser treatments. Thrombolytics also are used to treat acute or chronic occlusions. The nurse's role in treating and monitoring the patient is key in minimizing complications during and after intervention.
Circulating immune complexes and complement C4 null alleles in patients in patients operated on for premature atherosclerotic peripheral vascular disease.
Circulating immune complexes can lead to vascular inflammation and premature atherosclerosis and the fourth component of complement, C4, plays an important role in the removal of immune complexes. The objective of this study was to analyze the relation between circulating immune complexes and C4 null alleles in patients operated on for peripheral vascular disease before the age of 50. The prevalence of circulating immune complexes and null alleles of C4 (C4Q0) was determined in 62 patients with peripheral atherosclerosis requiring surgery before 50 years of age and in a matched control group. C4A and C4B null alleles (C4A*Q0, C4B*Q0) were determined by electrophoresis of plasma, followed by immunofixation. C4A and C4B concentrations were measured by ELISA. Circulating immune complexes were determined by sucrose density gradient centrifugation and gel filtration. There was no difference in the distribution of C4Q0 between patients and controls. The patients had higher prevalences and levels of circulating immune complexes. This was correlated with the presence of C4Q0, especially C4A*Q0. There was an inverse correlation of concentration of circulating immune complexes with C4A levels and with ratio of C4A/B levels. Thus, a significant proportion of patients with premature peripheral atherosclerosis had circulating immune complexes and C4A*Q0 enhanced the propensity to immune complex formation. This might represent one mechanism for vascular damage in this patient group.
Magnesium, lipids and vascular diseases. Experimental evidence in animal models.
The possible role of Mg in the pathogenesis of vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked hypertriglyceridemia and a decrease in the percentage of cholesterol transported by high-density lipoprotein. The decreased clearance of circulating triglycerides appears to be the major mechanism contributing to hyperlipemia. The same animals were found to have a reduced insulin response after intravenous glucose challenge and a slight reduction in heparin release lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the fatty acid pattern of total plasma lipids, as shown by decreased levels of stearic acid, increased of oleic acid and linoleic acid, and decreased levels of arachidonic acid. Platelets from Mg-deficient rats become more sensitive to thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and vascular disease.
To what extent does peripheral vascular disease and hypertension predict renal artery stenosis?
The incidence of renal artery stenosis (RAS) was prospectively evaluated by aortofemoral angiography in 100 patients with peripheral vascular disease (PVD) to find whether RAS was a more common finding in hypertensive than in normotensive patients. For a possible association with RAS, risk factors, clinical and angiographical variables were evaluated. Nephrotoxicity of the contrast medium Iohexol was elucidated. A follow-up of six month was performed in patients with severe stenosis or total occlusion of the renal arteries. Of the 49 patients with a renal artery lesion 26.5% were normotensive and 73.5% hypertensive. Hypertension was significantly correlated to RAS. Reconstructive vascular procedures were during the follow-up performed in 47.3% of the patients with severe RAS or occluded renal arteries, two patients underwent a renal artery revascularization, none of them got a postoperative blood pressure decrease. Hypertension in patients with peripheral vascular disease is predictive for renal artery stenosis and a possible renovascular hypertension should be evaluated. Surgery for renal artery stenosis in peripheral vascular diseased patients should, however, probably be performed firstly to reduce the risk for occlusion. The effect on the blood pressure can not be predicted without a more careful analysis that the blood pressure is renin-dependent. Iohexol showed low nephrotoxicity, also in patients with renal artery disease.
Quantitative blood flow measurements with cine phase-contrast MR imaging of subjects at rest and after exercise to assess peripheral vascular disease.
OBJECTIVE: The purpose of this study was to determine whether cine phase-contrast MR volume flow measurements can identify patients with peripheral vascular disease. SUBJECTS AND METHODS: We performed MR measurements of volume blood flow in the popliteal artery of subjects at rest and after 5 min of plantar flexion exercise in 10 volunteers (mean age, 28 years old), in five patients suspected of having peripheral vascular disease (mean age, 58 years old), and in five other volunteers of a similar age (mean age, 57 years old). RESULTS: Volume blood flow at rest was similar in volunteers and in patients. Four patients who had abnormal ankle-brachial indexes had lower flow increases after exercise (2.6-fold) compared with the five older normal volunteers (4.8-fold; p < .03, t test). These flow increases correlated well with ankle-brachial indexes: r = .97. The four patients with abnormal ankle-brachial indexes had monophasic resting waveforms, whereas all other subjects had triphasic waveforms. CONCLUSION: MR volume blood flow measurement may aid in evaluating peripheral vascular disease. Studies of larger patient groups will be necessary.
Neurologic complications of collagen vascular diseases.
Despite the importance of neurologic manifestations of the collagen vascular diseases, it is clear that there are more questions than answers. The use of in vitro culture systems, in vivo models, and clinical and laboratory study of patients that attempt to correlate these findings with immunologic abnormalities, including parallels with animal models, should increase our understanding of these syndromes.
Ultrastructural and capillary adaptation of gastrocnemius muscle to occlusive peripheral vascular disease.
The effect of chronic occlusive peripheral vascular disease (PVD) on the histochemistry and capillarity of the gastrocnemius muscle was studied in 129 biopsies taken from 93 subjects. Sixty-three patients underwent biopsy during surgical procedures, and data related to walking distance and ankle systolic pressure. Thirty biopsies taken from normal subjects post mortem served as a control group, and data were analyzed for fiber type distribution, fiber area, fiber type grouping, and fiber capillarity. Fiber type distribution did not alter significantly between the patients with PVD and the control group, but the mean fiber area of the type 1 fiber in male patients with intermittent claudication (IC) was reduced when compared to that in age-matched controls (4608 +/- 1181 mu 2, IC +/- 1 SD; 5795 +/- 1771 mu 2, controls +/- 1 SD) (P less than 0.05). When bilateral biopsies were taken from the gastrocnemii of patients with unilateral occlusions, the type 2 fibers in the diseased leg were significantly smaller than fibers of the control group (2821 +/- 953 mu 2, IC +/- 1 SD; 4318 +/- 1504 mu 2, controls +/- 1 SD) (P less than 0.02). Fiber type grouping, evidence of denervation and reinnervation of muscle, appeared to be more common in patients with more severe limb ischemia. Overall capillary numbers did not appear to alter with degree of ischemia, but fiber shrinkage appeared to compensate for any loss of capillaries in the more ischemic muscle. These data suggest that the limb of the untrained patient with IC does not adapt to ischemia by adjusting its exercise capacity but merely shows evidence of disuse. These adaptations suggest that there may be much to be gained by nonsurgical methods of treating IC.
Evaluation of indirect blood pressure measurement as a method of assessment of peripheral vascular disease.
In over 200 patients with peripheral vascular disease, pressure index (formula: see text) was compared with radiological grade; although calf P.I. had a better correlation, there was wide overlap between the groups. In 28 patients, resting calf P.I. was compared with functional impairment measured on a treadmill. At two rates of exercise, calf P.I. correlated poorly with functional impairment. In 35 patients, reproducibility of indirect pressure measurement was assessed; coefficients of variation ranged 0-10%; coefficient of variation of calf P.I. ranged 0-8%; coefficient of variation of calf P.I. ranged 0-8%. In 12 patients, indirect thigh systolic pressure was compared with and nearly always exceeded direct common femoral artery pressure; this was due to an effect of the cuff which reduced blood flow and reduced the pressure gradient. This methodological error has not previously been described and reduces the clinical value of the measurement.
The value of segmental pressure measurement in the assessment of peripheral vascular disease.
In 60 patients with symptomatic peripheral vascular disease a study was performed to evaluate the reliability of segmental pressure measurement in detecting and localizing vascular lesions. Five groups of limbs with different pressure patterns were identified: normals, distals disease (diabetics), aorto-iliac disease, aorto-iliac and superficial femoral disease, superficial femoral and distal disease. The comparison with angiography showed the high efficacy of this method (when combined with Doppler study of the arteries) to localize and quantify the lesions. The combination with femoral intraarterial pressure measurement allows to predict exactly the segmental pressure after segmental vascular reconstructions. It is concluded that segmental pressure measurement (with the described technique) selects patients for angiography and surgery and can predict the outcome of vascular reconstruction.
Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease.
OBJECTIVE: To determine whether endothelial cell injury would be produced by factor(s) released into the fetal circulation, manifested by altered messenger RNA expression of nitric oxide synthase. DESIGN: Case-control study. SETTING: University teaching hospital. SAMPLES: Fetal plasma was collected from 34 normal pregnancies, 44 pregnancies with umbilical placental vascular disease identified by an abnormal umbilical Doppler and 11 pregnancies with maternal pre-eclampsia but with normal umbilical Doppler studies. METHODS: Aliquots from a common culture of human umbilical vein endothelial cells (HUVECs) were incubated with fetal plasma from the members of the three patient groups. The total RNA was extracted from the endothelial cells and mRNA for nitric oxide synthase was measured by reverse transcription and semi-quantitative polymerase chain reaction (RT-PCR). This was standardised by comparison of the amplified inducible nitric oxide synthase (iNOS) or endothelial constitutive nitric oxide synthase (ecNOS) to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). MAIN OUTCOME MEASURE: Endothelial cell gene expression of iNOS and ecNOS. RESULTS: The mRNA expression of iNOS and ecNOS were significantly higher (P < 0.05) in HUVECs stimulated by fetal plasma from pregnancies with umbilical placental vascular disease [iNOS 1.12 (0.16); ecNOS 1.78 (0.18)] when compared with normal pregnancies [iNOS 0.56 (0.06); ecNOS 1.06 (0.10)]. In the maternal pre-eclampsia group, the NOS expression [iNOS 0.76 (0.11); ecNOS 1.39 (0.26)] did not differ from normal pregnancy. In the vascular disease group, there was no difference in NOS expression between the subgroups with and without maternal pre-eclampsia. CONCLUSIONS: Our study demonstrates that umbilical placental vascular disease is associated with a factor(s) in fetal plasma that produces an increase in the expression of iNOS and ecNOS mRNA by endothelial cells. Our findings raise the possibility that the release of factors causing an up-regulation of iNOS and ecNOS in the endothelium in the fetal placenta may occur as part of an inflammatory response of the vascular endothelium to injury.
Lumbar neurolytic sympathetic blockades provide immediate and long-lasting improvement of painless walking distance and muscle metabolism in patients with severe peripheral vascular disease.
Thirty patients with angiographically proven peripheral vascular disease (PVD) and intermittent claudication were treated with percutaneous lumbar neurolytic sympathetic blockade (NSB) using 1.5 mL ethanol 95%. Claudication had been progressive in all patients during conservative treatment. Median (range) painless walking distance increased from 95 (10-200) meters (m) before to 355 (25-1003) m immediately after NSB. Further improvement was seen during the 1-year follow-up, with two exceptions: one patient lost a leg after acute arterial embolism and another patient deteriorated after 6 months. In the latter case, a second NSB improved the walking distance again. One case of transient mild neuralgia of the L3 dermatome occurred. 31P-magnetic resonance investigations of the calf muscles before, during, and after a treadmill exercise were performed in seven patients: 1 week after NSB, the postexercise recovery of phosphocreatine was accelerated in all patients compared to the pre-NSB values. The accelerated recovery suggests an improved post-ischemic metabolic situation after chemical sympathectomy.
Is snoring a cause of vascular disease? An epidemiological review.
Eight studies that examined the relation between snoring and vascular disease were identified. The prevalence of habitual snoring, measured by questionnaire or interview, varied from 3% to 29% of adults and was dependent on age, sex, obesity, and smoking habit. In men, habitual snoring was associated with hypertension and ischaemic heart disease, with adjusted relative risks in the range 1.3-2.0. For women, only one study provided adjusted estimates of relative risk, which were 2.8 for hypertension and 1.2 for angina. Adequately adjusted relative risks for cerebrovascular disease have not been reported, but unadjusted estimates varied from 1.6 to 10.3. These studies had several limitations, including the lack of a standard definition of snoring, the use of unvalidated questionnaires, and failure to account for confounding variables and the possibility of reporting bias. Only one study was prospective. Epidemiological criteria for a causal association between snoring and vascular disease have not been satisfied. The apparent excess risk is probably due to the consequences of sleep apnoea rather than snoring itself.
Diabetes mellitus and peripheral vascular disease: is aspirin effective in preventing vascular events?
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Thrombocytopenia and lupus-like anticoagulant in a patient with peripheral vascular disease: response to infusion of prostacyclin.
A 46 year old man with intermittent claudication due to severe peripheral vascular disease had a circulating lupus like anticoagulant (LLAC), thrombocytopenia (79 X 109/1), markedly reduced platelet survival and a normal bone marrow. He was treated with intravenous prostacyclin (PGI2) infusions which resulted in improvement of the patient's exercise tolerance and normalisation of his platelet count (300 X 109/1) and platelet aggregation could then be assessed. The platelets were markedly hyperaggregable and generated supranormal quantities of thromboxane A2. A diagnosis of consumptive thrombocytopenia secondary to peripheral vascular disease and platelet hyperaggregability was made. Despite therapy with aspirin and dipyridamole, gradual and progressive reduction in platelet count followed and his exercise tolerance declined over the next three months. Immunoglobulin prepared from the patient's serum did not inhibit vascular PGI2 synthesis in vitro. To our knowledge this is the first reported case of consumptive thrombocytopenia due to severe peripheral vascular disease and platelet hyperaggregability. PGI2 administration caused a transient resolution of these features which was not sustained by aspirin and dipyridamole.
Mild hyperhomocysteinemia is an independent risk factor of arterial vascular disease.
Evidence of a positive association between mild hyperhomocysteinemia and arterial vascular disease has been accumulating in the last decade. Mild hyperhomocysteinemia acts as an independent vascular risk factor with equal strength as hypercholesterolemia and smoking. If jointly present with hypertension and smoking, its effect seems synergistic. This could make the outcome of homocysteine-lowering intervention beneficial, particularly in cases with concomitance of conventional vascular risk factors. So far, however, data on the clinical outcome of homocysteine-lowering treatment with a simple, safe, and cheap vitamin regimen are lacking. Trials investigating a beneficial clinical effect of homocysteine-lowering treatment using folic acid in a dose ranging from 0.2 to 5 mg daily, alone or in combination with vitamin B12 with or without vitamin B6 versus placebo, are ongoing. Furthermore, exploration of the unifying mechanism by which increased homocysteine levels may lead to both arterial and venous occlusions is warranted. These lines of investigations have to provide the ultimate proof of causality of hyperhomocysteinemia in vascular disease in the near future.