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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A thirty-year-old man who had sudden onsets of unconsciousness, right hemiparesis and conjugate deviation to the left side, was admitted to our clinic. The clinical symptoms were similar to an apoplexic attack. The neurologic examination showed right hyperactive knee and ankle reflexes, and left inferior temporal retinal arterial occlusion. The serial left carotid angiography, performed immediately after admission, showed the occlusion of left middle cerebral artery at the location of trifurcation. We diagnosed this case as a cerebral vascular disease, and then the large amount of Urokinase and Heparin were injected immediately after the diagnosis. The clinical symptoms were improved tremendously after the injection. Three days later, the second left carotid angiography showed the complete recanalization of the occlusion, and further did a tumor stain at the distal portion of the occlusion. The brain scintigram revealed an increased up-take of 99mTc in the left parieto-temporal region. We finally diagnosed brain tumor, and the tumor was subtotally removed by the left parieto-temporal craniotomy. The histological findings of the tumor showed angioblastic meningioma. The cerebral arterial occlusion secondary to the brain tumor should be caused by the compression of the vessels and the hemorrhage of the tumor. This case is rarely reported.
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PMID:[Middle cerebral arterial occlusion secondary to brain tumor -- case report (author's transl)]. 57 68

One unit (500 ml) of 10% Intralipid (an intravenous soy bean oil-egg yolk lecithin preparation) was infused into 20 normal subjects over 4 hr. Serum triglyceride concentration and plasma optic density (at 700 nm) increased to maximal levels of 339 +/- 102 mg/100 ml and 1.14 +/- 0.41, respectively, at the completion of the infusion, and returned to basal levels in most subjects within 4 hr. Pulmonary membrane diffusion was decreased in six subjects at rest and with exercise at 25 and 50% maximum oxygen uptake. Only one subject showed a minor change in PO2 and none showed clinical signs of ischemia. The changes in pulmonary diffusion reverted to basal levels when serum lipids were cleared. Heparin (60 IU/kg) prevented the marked increase in serum lipids and, as a consequence, the changes in pulmonary function. Changes in pulmonary function from Intralipid-induced lipemia are similar to those known to result from diet-induced lipemia. The findings suggest that in the presence of normal vasculature and pulmonary function, Intralipid-induced lipemia should cause no clinical consequences. However, patients with preexisting pulmonary or vascular disease may be at greater risk after Intralipid-induced lipemia.
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PMID:Relationship between Intralipid-induced hyperlipemia and pulmonary function. 81 3

Arterial emboli were extracted from 79 patients between 1955 and 1963 with polyethylene catheter suction systems and/or retrograde flushing and from 149 patients between 1963 and 1973 with Fogarty catheters. The Fogarty-era patients were older, had a greater incidence of ischemic heart disease, and presented with a greater degree of preoperative peripheral ischemia. The limb salvage rate of 87 percent after Fogarty catheter embolectomy was not statistically different from the salvage rate of 79 percent after suction catheter embolectomy, but the number of limbs with distal pulses postoperatively was significantly greater after Fogarty treatment, 64 vs. 42 percent. Delay in treatment and the presence of prior occlusive vascular disease adversely affected results in both eras. The in-hospital embolic recurrences occurred in 9 percent of the patients anticoagulated postoperatively and in 31 percent of those not anticoagulated. Heparin and warfarin were equally effective in preventing recurrences, but wound complications were seen in 33 percent of the heparinized patients, compared with 7 percent of those receiving warfarin and 4 percent of those not anticoagulated.
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PMID:Arterial embolectomy before and after the Fogarty catheter. 110 16

Platelet function and thromboxane A2 release were measured in 71 patients admitted to a coronary care unit with a provisional diagnosis of acute myocardial infarction (AMI). All measurements were carried out within twenty-four hours of admission. Of these, 35 patients had the diagnosis of AMI confirmed. The remainder (n = 36), who did not have AMI (NMI), were divided into two groups: those (n = 18) with an unequivocal history of previous vascular disease and those without vascular disease (n = 18). Platelet aggregation and thromboxane A2 (TXA2) release were significantly increased in the AMI group when compared with those in the NMI without vascular disease group or a healthy control group with similar age and sex distribution. Aggregation and TXA2 release in the NMI patients with vascular disease were greater than those in controls and did not differ significantly from those in the AMI group. Patients in the AMI or NMI with vascular disease groups who were taking beta-blockers or calcium channel antagonists at the time of admission showed significantly less platelet aggregation than those who were not taking these drugs. Heparin, added in vitro at therapeutic concentrations, induced significantly more aggregation in patients in the AMI and NMI with vascular disease groups than in the NMI without vascular disease group. We conclude that: platelets obtained from patients with AMI are hyperaggregable and release more TXA2; platelets from patients with significant vascular disease are hyperaggregable, even in the absence of AMI, although they are not as hyperaggregable as those from AMI; treatment with nifedipine and beta-blockers protects these patients from platelet hyperaggregability; heparin induces significant aggregation of platelets from patients with AMI and NMI with vascular disease. These observations are of importance in considering the pathogenesis and treatment of AMI and ischemic heart disease.
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PMID:Platelet function in patients admitted with a diagnosis of myocardial infarction. 288 May 35

Arterial embolism is usually caused by cardiac disease, and atherosclerotic coronary vascular disease is the primary precursor. Other cardiac states, as well as several uncommon causes, are part of the etiologic spectrum. The earliest signs are pain, paresthesias, pallor, and pulselessness. Severe ischemia is indicated by paralysis, a late feature. Arterial embolism and acute thrombosis can be difficult to distinguish, and deep venous thrombosis may also be suspected in the differential diagnosis. To restore arterial flow, anticoagulation treatment with heparin (Lipo-Hepin, Liquaemin) is given and surgical embolectomy is performed. Heparin infusion is continued until the patient is ambulatory, and then warfarin sodium (Coumadin, Panwarfin) is given over the long term. Fibrinolysis has also been used to treat acute arterial occlusion. Complications of embolism must be carefully guarded against, and additional procedures are sometimes necessary.
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PMID:Management of arterial emboli. Gleanings from 20 years of experience. 357 97

Proliferative angiopathy represents the morphological basis of delayed cerebral vasospasm. The initial vasoconstriction and endothelial damage of the vasospastic arteries leads to an exaggerated response of the smooth muscle cells within the media leading to subintimal thickening and myonecrosis. Heparin reduces the exposure of the media to platelet derived growth factor, a mitogen from aggregating platelets responsible for the migration and proliferation of the myofibroblasts. Since systemic heparin in the setting of a subarachnoid haemorrhage would be unacceptable, we have tested the effect of heparin on proliferative angiopathy by injecting autologous non-heparinized blood into two groups of rats (N = 12 each) and then inject the heparin into the spinal fluid of one group after one hour. We were able to show histologically that intracisternal heparin injection after the subarachnoid haemorrhage has reduced the vascular wall changes to a great degree. Heparinization of the cerebrospinal fluid carried out in conjunction with early operation for aneurysms may be a promising approach to prevent the morbid complications of SAH in the clinical setting.
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PMID:Preventive effect of intracisternal heparin for proliferative angiopathy after experimental subarachnoid haemorrhage in rats. 752 76

Physiological changes occurring during pregnancy and puerperium may increase the risk of stroke. However, the incidence rate of ischemic stroke is of 3.8 to 5 in 100,000 pregnancies, i.e. quite similar to that of ischemic strokes occurring in non pregnant women of child bearing age. Whereas eclampsia, choriocarcinoma and amniotic emboli occur only during pregnancy or puerperium, peripartum cardiomyopathy and benign cerebral angiopathy are less specific. All other causes of cerebral ischemia may also occur during pregnancy and puerperium. The management of an ischemic stroke should not differ between pregnant and non pregnant women of child bearing age. Strokes associated with pregnancy require a complete diagnostic work-up including angiography if necessary. Low doses of aspirin (60-80 mg/d) can be used after 3 months of pregnancy. Heparin is the anticoagulant of choice during pregnancy, but warfarin may be used between 13 and 36 weeks of gestation; heparin and warfarin can be used during breast feeding. There is no neurological reason to recommend a systematic use of cesarean section. Subsequent prescription of oral contraceptive therapy is not recommended except in patients with a definite cause of ischemic stroke which is not influenced by hormones.
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PMID:Arterial ischemic strokes associated with pregnancy and puerperium. 910 39

A 30-year-old healthy woman was involved in a road traffic accident. She sustained a fracture dislocation of T11/12 with a complete Frankel A paraplegia below T11. She had no associated injuries. High Dose Methylprednisolone was administered according to the NASCIS III protocol (48 h) together with low molecular weight Heparin and gastroprotected medication. Complete transection of the spinal cord and an anterior haematoma from T11 to T12 were confirmed on X rays, CT's and MRI scans. Posterior surgical stabilisation was performed using Isola instrumentation, starting 8 h post injury. Her post surgical period was uneventful except for some episodes of low blood pressure (85/60 mmHg) from which she had no symptoms. On the 12th post operative day, while in the physiotherapy department, she complained of right scapular pain. This occurred every time she was sat up and was associated with paraesthesia of both upper limbs. Two days later she deteriorated neurologically and her level ascended initially to T8 and then to T3. MRI of the spine with and without gadolinium showed spinal cord oedema between C3 and T1. There was no evidence of haemorrhage or syringomyelia. The authors discussed this case making different hypotheses. They are mainly the following: (1) Gradually ascending ischaemia due to a vascular disorder; (2) Double spinal trauma; (3) Ischaemia related to repeated hypotensive episodes; (4) Low grade intramedullary tumour; and (5) Thrombus of the Radicularis Magna artery. The case has been recognised as being very rare and interesting. In the conclusions, the presenting author stresses the importance of adopting MRI-compatible instrumentation for the surgical stabilisation of the spine, and careful monitoring of blood pressure during the acute phase of spinal cord injury. Dr Aito agrees with Mr El Masry about the opportunity of forming a group of clinicians in order to discuss protocols to cope with this devastating complication.
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PMID:Ascending myelopathy in the early stage of spinal cord injury. 1049 Aug 52

We have assessed the prevalence of heparin-platelet factor 4 antibodies in a group of 100 patients on chronic intermittent hemodialysis with repeated exposure to heparin in order to establish the clinical significance of an immunological response to heparin. Heparin-induced platelet reactivity was studied in a subgroup of 86 patients. Routine laboratory parameters such as plasma C-reactive protein, albumin and immunoglobulins were included. Clinical endpoints were thrombosis in blood access, change of blood access, other thromboembolic events, bleeding complications, falling platelet count, and ischemic vascular disease or death within 1 year of blood sampling. Blood access thrombosis was a frequent complication (26%), often leading to change of dialysis blood access (21%). Antibodies were detected in 3-6% of hemodialysis patients and antibody levels correlated to blood access thrombosis and change of access (p<0.05). An unexpected finding was that of increased heparin-induced platelet reactivity in 36% of the control group of 24 uremic patients prior to dialysis or exposure to heparin. The findings suggest that antibodies to heparin-platelet factor 4 may contribute to hypercoagulability during hemodialysis, leading to thrombotic complications in affected patients.
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PMID:The presence of heparin-platelet factor 4 antibodies as a marker of hypercoagulability during hemodialysis. 1191 67

Coagulation times and protamine titration values for heparin are apt to be lower than average in patients with allergic disease, particularly asthma. Severe asthma is commonly treated with gluco-corticoids or ACTH. Prolonged high dosage of gluco-corticoids, either endogenous or exogenous, depresses mast cell function and heparin production. Thrombo-embolic phenomena occur frequently in severe cases of asthma so treated, particularly if predisposing vascular disease is present. Heparin can be used to treat and prevent these complications. Adjuvant antiasthmatic effects under these conditions are noted in addition to the desired anticoagulation.
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PMID:Thrombo-embolic phenomena in severe asthma. Use of heparin for prevention and treatment in patients receiving ACTH or gluco-steroids. 1395 39


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