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

A 79-yr-old man with previously documented atherosclerotic vascular disease presented with acute abdominal pain, signs of peritoneal irritation, and guaiac-positive stool. A mesenteric arteriogram showed high-grade stenosis of the superior mesenteric artery with a pressure gradient of 70 mmHg and complete occlusion of the inferior mesenteric artery. Percutaneous transluminal angioplasty of the superior mesenteric artery was performed with immediate reduction of the pressure gradient, increase in vessel caliber, and relief of abdominal pain. The patient went on to complete recovery and remains pain-free 6 mo after discharge from the hospital. To our knowledge, this is the first report of percutaneous transluminal angioplasty used to treat acute mesenteric ischemia.
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PMID:Treatment of acute mesenteric ischemia by percutaneous transluminal angioplasty. 294 29

Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.
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PMID:Platelet activation and secretion associated with emotional stress. 298 76

The clinical and histopathologic findings in 13 patients with lipomembranous changes in the subcutaneous adipose tissue as part of the inflammatory reaction are presented. Nine patients had clinical evidence of vascular disease and four had clinical evidence of connective tissue disease. Histopathologic evidence of endarteritis obliterans, venous stasis, and hemorrhage was present in more than half the patients, and the clinical lesion of liposclerosis was frequently present. These findings suggest that the histologic changes of lipomembranous panniculitis may be the result of an inflammatory reaction in patients who have the liposclerosis of venous insufficiency with connective tissue disease or previous leg ischemia or both.
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PMID:Lipomembranous changes in chronic panniculitis. 304 17

Studies on animal models demonstrate that platelet products contribute to vascular spasm in ischemic syndromes and that this is reversible with administration of ketanserin and thromboxane synthesis inhibitors. Laboratory animals (dogs, rabbits, and rats) that had femoral artery ligations exhibited supersensitivity to serotonin within days in their collateral blood vessels. This supersensitivity lasted at least 6 months. The response to serotonin was reversed by ketanserin, but not by 5HT-1 antagonists. Supersensitivity does not extend to norepinephrine, and alpha blockers do not influence the response to serotonin. It appears that platelet activation by endothelial injury contributes to ischemia through blood vessel occlusion and vascular spasm. When platelet activation occurs in vivo, blood vessel occlusion and vascular spasm are reversible in part by using ketanserin or agents that block thromboxane synthesis or its action. Combining both classes of agents reverses spasm completely. These findings support existing evidence that platelet products contribute to vascular disease, and provide an approach to improved management with currently available pharmacologic agents.
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PMID:Serotonin, atherosclerosis, and collateral vessel spasm. 304 34

The evaluation of clinical reports on vascular disease is often made difficult by variations in descriptive terms, clinical classification, and outcome criteria. In 1983 the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery created the Ad Hoc Committee on Reporting Standards to address these problems and recommend solutions. Some general problems were addressed in the initial report dealing with lower extremity ischemia. This article concerns clinical standards for reports dealing with cerebrovascular disease, suggests a scheme for clinical classification, and recommends standardized reporting practices for grading risk factors, angiographic and other diagnostic findings, and the results and complications of therapeutic intervention.
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PMID:Suggested standards for reports dealing with cerebrovascular disease. Subcommittee on Reporting Standards for Cerebrovascular Disease, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery. 276 Oct 2

The impending release of erythropoietin (EPO) is expected to result in a dramatic increase in hematocrit (Hct) for most hemodialysis (HD) patients. Our studies indicate that as Hct rises, dialyzer mass transport for some clinically critical solutes will be adversely affected. When whole blood clearances are corrected for solute-specific blood-water flows (QBH2O), the effect on the surrogate molecule, urea, used in urea kinetic modeling (UKM) is deceptively minimal, because only urea can diffuse almost instantly from red cells into blood water. For the critical solutes, potassium and phosphate, QBH2O is reduced to Q (plasma water). With a KoA of 690 ml/min at QB = 300, clearance of potassium falls at least 19.3% as Hct rises from 20 to 40% so that steady-state predialysis potassium could rise from 6.0 to 6.95 mEq/L. Already inadequate phosphate clearance falls at least 10% and additional loss results from physical interference by RBCs with solute diffusion. Hcts are further increased with rapid weight losses during high-efficiency dialyses (0.15 per 5% weight loss in 3 hours, r = 0.82) resulting in blood-side pressures such that most dialysis machines cannot provide adequate dialysate pressures to maintain low ultrafiltration rates (UFRs) at the high QB levels. The combination of pre-existing diffuse vascular disease, postdialysis hypovolemia, hypotension, decreased cardiac output, and increased blood viscosity has and will produce disastrous syndromes of organ ischemia, thrombosis, and infarction. Predialysis hypertension can worsen. Extreme caution and adjustment of dialysis regimen is necessary as patient Hct rises above 36%.
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PMID:Erythropoietin alert: risks of high hematocrit hemodialysis. 319 6

We report here two autopsied cases of patients who had been in a longstanding bedridden state from cerebrovascular dementia. They showed a clinical history of persistent hypertension, a history of acute strokes, a lengthy clinical course with long plateau periods and a gradual accumulation of focal neurological symptoms and signs, including dementia and prominent motor disturbances and pseudobulbar palsy. They had been in a bedridden state for the last several years and had to be fed. The pathology seemed to predominently affect the perforating vessels to the subcortical gray and white matter. Demyelination, loss of axons, patchy gliosis and infiltration by macrophages were noted in the involved regions. The long penetrating vessels of the white matter showed advanced arteriosclerotic changes. There was a relative sparing of the cortex. The low attenuation of the white matter with moderate to severe atrophy, and an infarction might well be significant features on a CT-scan of these conditions. One of the possible mechanisms on the pathogenesis of chronic vascular disease includes diffuse ischemia related to hypertensive vasculopathy.
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PMID:Diffuse white matter involvement seen in patients in longstanding bedridden state from cerebrovascular dementia. 324 76

Hypertension can directly damage blood vessels, and leads to renal failure, intracranial bleeds, and lacunar infarctions. Of equal importance is the effect of hypertension on the development of atherosclerosis. Specific changes in both the microvasculature and macrovasculature vary depending on the degree and rapidity of blood pressure elevation. Changes in the intima and media can lead to significant narrowing of vessels and ischemia in various tissues. In addition, changes in small-resistance vessels contribute to changes in peripheral-vasculature resistance and thus affect blood pressure regulation. Treatment of moderate to severe elevation in blood pressure clearly results in a decrease in the incidence of stroke. However, evidence that treating mild hypertension reduces coronary events is less convincing. Antihypertensive therapy may result in partial regression of vascular changes, especially fibrinoid necrosis seen in malignant hypertension, but more work needs to be done to clearly define the roles of specific drugs in preventing or regressing hypertensive vascular disease.
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PMID:Vascular changes in hypertension. 330 5

Fibromuscular dysplasia is a nonatherosclerotic, noninflammatory vascular disease that involves primarily the renal and internal carotid arteries and less often the vertebral, iliac, subclavian, and visceral arteries. Although its pathogenesis is not completely understood, humoral, mechanical, and genetic factors as well as mural ischemia may play a role. The natural history is relatively benign, with progression occurring in only a minority of the patients. Typical clinical manifestations are renovascular hypertension, stroke, subarachnoid hemorrhage, abdominal angina, or claudication of the legs or arms. In patients with symptoms, percutaneous transluminal angioplasty has emerged as the treatment of choice in most involved vascular beds.
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PMID:Arterial fibromuscular dysplasia. 330 88

Blood flow and transcutaneous oxygen tension was measured by venous occlusion plethysmography and a transcutaneous oxygen electrode before and after 5 min of arterial occlusion in the forearm of young adult subjects with type I (insulin-dependent) diabetes without overt evidence of angiopathy. In control subjects (n = 21), the forearm blood flow increased by greater than or equal to 2.8-fold at 30 s after ischemia. Diabetic subjects with glycosylated hemoglobin (GHb) less than or equal to 9.5% (n = 15) exhibited a blood flow response that was not statistically different from normal control subjects. Diabetic subjects with GHb greater than or equal to 12.5% (n = 23) did not exhibit an increase in the postischemic blood flow. When blood flow patterns for the first 14 diabetic subjects were examined regardless of GHb value, four patterns of response were noted: 1) normal pattern (n = 3), 2) normal postischemic rise in blood flow with a prolonged elevation (n = 3), 3) no postischemic rise (n = 4), and 4) variable baseline blood flow with a decrease in blood flow postischemia (n = 4). This approach indicated that a comparison of means obscured potentially meaningful abnormal patterns. Abnormalities in the response of the transcutaneous oxygen tension to ischemia were observed in both groups of diabetic patients, but the difference between diabetic patients in good and poor control was less obvious. We have defined an abnormal response of blood flow and transcutaneous oxygen tension to ischemia that may correlate to glycemic control and have identified several patterns of blood flow after ischemia that may be important in defining the etiology and natural history of diabetic angiopathy.
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PMID:Early detection of vascular dysfunction in type I diabetes. 337 62


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