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

Ten patients with circulating lupus anticoagulant who presented with cutaneous vascular disease and cerebrovascular disease are presented. Cutaneous manifestations were gangrene, thrombophlebitis, ulcers, and livedo reticularis. All 10 patients had cerebral infarction. The relationship between the cerebral and cutaneous vascular changes and the presence of lupus anticoagulant is supported by a common noninflammatory vascular thrombosis histologically in these patients and by the presence of similar pathologic and clinical findings in patients with the lupus anticoagulant syndrome.
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PMID:Cutaneous thrombosis, cerebrovascular thrombosis, and lupus anticoagulant--the Sneddon syndrome. Report of 10 cases. 210 36

Treatment of hypertension may prevent many of the complications attributable to blood pressure elevation, particularly those that are "pressure-related," such as stroke. However, the atherosclerotic complications of hypertension, e.g., coronary artery disease manifested as coronary morbidity and mortality, have not been reduced significantly with antihypertensive therapy. This disappointing outcome may reflect the adverse metabolic effects of the traditional therapies, diuretics and beta blockers, and their lack of specific vasoprotective properties. Increasing attention is thus being paid to the newer antihypertensive agents, which typically have fewer adverse effects and perhaps more physiologic mechanisms of antihypertensive action. Since calcium plays a key role in the genesis of atherosclerosis, calcium antagonists may positively affect the course of vascular disease. Investigators have observed that calcium antagonists display clear antiatherosclerotic properties in experimental as well as clinical studies. In one recently published clinical study, coronary artery disease was shown to develop more slowly, with a slower progression of individual stenoses, higher regression rate and less frequent occurrence of new lesions in patients treated chronically with verapamil compared to those receiving conventional therapies. Other similar investigations are currently under way to evaluate the antiatherogenic properties of calcium antagonists, including the Frankfurt Isoptin Progression Study (FIPS), the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS), the International Nifedipine Trial on Atherosclerosis Coronary Therapy (INTACT), and the large-scale Montreal Heart Institute Study. Results of these studies, which use precise end points such as myocardial infarction, cerebral infarction and peripheral vascular disease, may revolutionize the treatment of hypertension by identifying therapeutic approaches that control both the pressure-related and atherosclerotic complications of the disease.
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PMID:Anti-atherosclerotic and vasculoprotective actions of calcium antagonists. 225 66

Of 1721 consecutive autopsies performed on patients over 60 years of age in Tokyo Metropolitan Geriatric Hospital, 550 (32% of all autopsied cases) revealed symptomatic cerebrovascular lesions. Among the 550 patients, intracranial hemorrhage was found in 19%, cerebral infarction in 75%, and coexisting cerebral hemorrhage and cerebral infarction in 6%. Twenty-eight percent of the cerebral infarctions were embolic infarctions of cardiac origin, half of which were caused by nonvalvular atrial fibrillation, and 69% were non-embolic infarctions of cardiac origin. Progressive subcortical vascular encephalopathy accounted for 15% of the cerebral infarctions. Two-thirds of all lobar cerebral hemorrhages were amyloid angiopathy-related. Nonvalvular atrial fibrillation is the most important cardiac source of embolic stroke. Progressive subcortical vascular encephalopathy is one of the characteristic features of ischemic lesions, and cerebral amyloid angiopathy is an important cause of lobar cerebral hemorrhage in the aged.
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PMID:Subtypes and proportions of cerebrovascular disease in an autopsy series in a Japanese geriatric hospital. 228 May 80

Using immunohistochemical staining methods with antibodies to amyloid beta protein and human cystatin C, we examined cerebrovascular amyloid protein in the brains from 46 cases with cerebral amyloid angiopathy (seven with Alzheimer's disease, one with Down's syndrome, 18 with intracranial hemorrhage, 10 with cerebral infarction, and 10 elderly patients without any neurologic disorder). All cerebrovascular amyloid deposits in these 46 cases were consistently immunoreactive to anti-beta protein antibody. However, in nine cases some vascular walls with strong beta protein immunoreactivity also reacted less intensely with the anti-cystatin C antiserum. Of these nine cases, seven showed relatively heavy cerebrovascular amyloid deposition, and all seven had suffered a fatal subcortical hemorrhage presumably caused by cerebral amyloid angiopathy. Previous limited studies have suggested that the amyloid protein seen in elderly individuals with cerebral amyloid angiopathy is composed of beta protein. However, subcortical hemorrhage rarely occurs in such individuals. Our study shows that aged patients with different brain disorders commonly suffer from beta protein-type cerebral amyloid angiopathy, and we also suggest that the severity of beta protein-type cerebrovascular amyloid deposition is a fundamental factor in cerebral amyloid angiopathy-induced brain hemorrhage in the elderly. The nature of the cystatin C-immunoreactive substance in some of these vascular lesions is uncertain, but it might conceivably play an additional important role in the pathogenesis of brain hemorrhage in these cases.
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PMID:Immunohistochemical characterization of cerebrovascular amyloid in 46 autopsied cases using antibodies to beta protein and cystatin C. 221 20

80 patients with transitory ischemic attacks (TIA) and 30 patients with cerebral infarction (CI) were investigated regarding hemostatic disturbances to evaluate selected coagulation test methods for routine laboratory use. The patients were studied a few days after the first appearance of symptoms and at defined times subsequently. The study included measurements of circulating platelet aggregates; platelet adhesiveness, factor-VIII-related antigen (VIIIR:Ag), fibrinolytic activity after venous stasis, alpha-2-antiplasmin activity, and antithrombin III activity. Platelet aggregates and/or adhesiveness were increased in the acute stage in most patients as well as in patients with recurrent attacks. Increased platelet adhesiveness was also found in some patients with nonvascular neurologic diseases. Factor VIIIR:Ag was increased especially in the acute stage and more in patients with recurrent attacks. Diminished fibrinolytic response after venous stasis was found in about 40% of the TIA and in 50% of the CI patients as well as in all patients who died from vascular disease. Antiplasmin activity was increased especially in women. Antithrombin activity was increased during warfarin treatment. The effect of acetylsalicylic acid (ASA) treatment on platelet function was registered only in women but ASA seemed to influence mechanisms other than platelet function, e.g. normalization of factor VIIIR:Ag. Our findings indicate that with methods available for the routine laboratory the measurement of fibrinolytic response to venous stasis, factor VIIIR:Ag and platelet reactivity would be of value in selecting risk patients and following the effect of treatment.
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PMID:Value of blood coagulation tests in ischemic cerebral disease. 243 Aug 7

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
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PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99

In 75 patients with acute cerebral vascular disease (infarction 43, TIA 4, cerebral hemorrhage 25, subarachnoid hemorrhage 3), the plasma levels of Antithrombin-III (AT-III) and plasminogen (Plg) were measured within one week stroke patient and with 27 non-stroke patient as controls. The results showed: the plasma AT-III level was of no significant difference between the patients with hemorrhagic or ischemic cerebral vascular disease group and control group; the plasma plg level was a significant decrease in ischemic cerebral vascular disease groups (cerebral infarction. TIA), and it was of significant difference between the cerebral infarction group, or the TIA group and those of the control group (P less than 0.001 and P less than 0.01) respectively. In view of these results suggest that measuring of Plasma Plg level is a valuable unspecific assays indicator for ischemic cerebral vascular diseases. Finally, the relationship between high coagulation and acute cerebral vascular disease was discussed.
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PMID:[Observation of plasma levels of antithrombin-III and plasminogen in acute cerebrovascular disease]. 262 May 88

Records of perioperative complications following 407 consecutive carotid endarterectomies performed in 366 patients in the 18-year period have been presented. The complications are categorized according to the clinical stage of vascular disease, that is, according to the indications for the surgery. Out of the total number, 46 (11.3%) operations were done in the 1st, asymptomatic stage of disease, for the haemodinamically significant stenoses and ulcerated plaques; 173 (42.5%) in the 2nd clinical stage for hemispheral and nonhemispheral transient ishemic attacks (TIA) and reversible neurologic deficits (RIND); 3 (0.7%) in the 3rd stage which is a progressive cerebrovascular stroke and 185 (45.5%) in the 4th clinical stage of the disease, in patients with previous cerebral infarction and a permanent neurologic deficit. The rate of a temporary and permanent neurologic deficit, as well as mortality in the first stage of the disease equals zero. In the second stage of the disease, the rate of a temporary neurologic postoperative morbidity increases to 1.7%, of a permanent neurologic morbidity to 1.2%, while the rate of mortality is 1.2%. In the 3rd and 4th stage, those rates amount to 66.7%, 0% and 33.3%, and 1.1%, 3.8% and 1.6%, respectively. The rates of perioperative morbidity and mortality are in proportion to the scope of preoperative brain dysfunction. Results of this work suggest the necessity of categorization of patients, candidates for carotid endarterectomy, according to the clinical stage of the disease, which will enable a better comparison with other authors' results, give a more reliable view on the efficacy of the surgical treatment and justify the surgeons' attitude towards indications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Perioperative complications in carotid endarterectomy with respect to the stage of the cerebrovascular disease]. 263 89

Auditory brainstem evoked potentials (BAEPs) reflect activities of the brainstem auditory pathway and the influence of activities of structures surrounding the pathway. It is said that BAEPs are reliable in predicting the outcome of patients with severe brain damage. The author studied the relationship between initial BAEP findings, particularly interpeak latencies of waves I to V and waves III to V, and mortality as based on the cause of each disorder. BAEPs were sequentially recorded in 241 cases of various neurological diseases resulting in severe brain damage (GCS less than 8) during the first few days after onset. BAEPs were graded into four groups based on initial findings. Group A: all waves I to V were recorded (159 cases). Group B: waves IV & V absent (11 cases). Group C: either wave I or waves I & II only were recorded (28 cases), Group D: all waves absent. Prognosis in Group B & C was poor, only two patients surviving in a vegetative state. There were no survivors in Group D. The relationship in Group A between interpeak latencies (I-V ipl, III-V ipl) and prognosis is discussed. This group consisted of 41 cases subarachnoid hemorrhage, 29 cases hypertensive intracerebral hemorrhage, 5 cases severe cerebral infarction, 21 cases infratentorial cerebral vascular disease, 49 cases supratentorial severe head injury, and 14 cases infratentorial head injury. In deceased cases of subarachnoid hemorrhage and supratentorial head injury, there was significant prolongation of I-V ipl and III-V ipl over the mean latency of 20 normal subjects plus 2SD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prognostic evaluation of severe brain damage by auditory brainstem evoked potentials (BAEPs)]. 275 41

Fifty unselected patients undergoing open heart surgery (OHS) were examined by duplex and transcranial Doppler sonography. Two high degree (greater than 75%) carotid stenosis were found in 70 carotid arteries of 35 patients with coronary artery disease. Fourteen vessels had unmistakable signs of extracranial vascular disease whilst 54 carotid arteries were identified as normal. Two high degree (greater than 75%) carotid stenosis were found in 30 vessels of 15 patients with valvular disease. Seven other vessels had a low grade stenosis or excessive atheroma, whereas 21 were identified as normal. The rate of about 5-10% asymptomatic high grade carotid stenosis in patients undergoing OHS justifies routine noninvasive examination of the cerebral circulation by duplex and transcranial Doppler sonography. Patients with high grade stenosis are offered a follow-up preventive programme against cerebral infarction, which consists of 3 steps: 1. anti-platelet aggregating drugs, 2. periodic control examinations by duplex and transcranial Doppler sonography, and 3. continued evaluation of indication for carotid endarterectomy.
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PMID:[Duplex and transcranial sonography in the preoperative evaluation of cerebrovascular circulation before heart operations]. 278 9


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