Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombotic complications of heparin administration were observed in eight patients during a two year period. At sites of subcutaneous heparin injection, six patients developed areas of the skin and subcutaneous necrosis. Systemic thrombotic events and thrombocytopenia were observed in two of these patients when they received intravenous heparin and in two other patients who did not have primary skin necrosis. The complications included peripheral ischemia in three patients (two requiring amputation), myocardial infarction in two, and a cerebral infarction in one. All patients were receiving heparin for at least six days before complications occurred. Seven patients received heparin of bovine origin. Heparin-induced in vitro platelet aggregation was present in all six of the eight patients tested. (It was marked in four of these patients). It is theorized that skin necrosis and the other thrombotic complications observed are the result of heparin-induced in vivo platelet aggregation followed by intravascular thrombosis. Heparin-induced skin necrosis is a rare but serious hazard encountered with prophylactic heparin regimens. If heparin-induced thrombosis is present, the further use of heparin is contraindicated in most instances.
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PMID:Thrombotic complications of heparin therapy: including six cases of heparin--induced skin necrosis. 50 70

Skeletal muscle blood vessels from eight patients with documented Duchenne type muscular dystrophy were examined by light and electron microscopy, with particular attention to the capillary-venous bed. The characteristic lesions of vasoactive amine injury were not present. Endothelial degeneration and regeneration also were absent. Lamellation of capillary basement membranes was noted without true hypertrophy or evidence of discontunuities. Thrombus formation and platelet interaction were absent. Lumenal obliteration was not noted at the arterial level. Rarely, venous obliteration was present in association with nodular connective tissue overgrowth. The minimal abnormalities appear to be nonspecific and do not substantiate postulated vascular injury by vasoactive mediators or ischemia. The role of a nonspecific chronic inflammatory reaction with phagocytes derived from the vascular compartment should be considered with respect to those described basement membrane changes.
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PMID:Blood vessel structure in Duchenne muscular dystrophy. I. Light and electron microscopic observations in resting muscle. 56 43

Directional coronary atherectomy (DCA) was used in 74 patients with an average age of 56 years. They were categorized into three different groups depending on the indications for atherectomy. Group I included all patients who had atherectomy as their primary intervention (n = 26), because they were assumed to be unsuitable for PTCA. Group II consisted of patients in whom DCA was used after failed balloon dilatation with unsuccessful but uneventful treatment (n = 20). Group III (n = 28) included cases where DCA was performed as a "rescue" or "bail-out" procedure after failed PTCA resulted in critical ischemia (ECG changes, chest pain, hypotension, and shock). The target lesions were located in LM 2, LAD 52, RCA 16, ACVB 4. The mean length of lesion was 8 mm (2-25 mm). The overall success rate was 94%. The mean stenosis was reduced from 90.6 +/- 10% to 17.2 +/- 14.8% in cases with primary success. The presently available follow-up angiography (n = 31) showed six restenoses. Major complications occurred in seven cases (death: 0, myocardial infarction: 2, CABG within 24 h: 5). Histological analysis revealed highly cellular areal as a major characteristics of a coronary lesion and also of restenotic tissue. Tissue of the lamina elastica was present in 44% and of media in 14%. Thrombus was found only rarely. Ultrastructure showed a significant amount of extracellular matrix in the primary coronary lesions and isolated smooth muscle cells without gap-junctions. RER, mitochondria were typical for the synthesizing type of smooth muscle cell. In restenotic tissue a focal high density of smooth muscle cells with increased synthesizing activity and gap-junctions was present. Endothelial cells (and macrophages) were found only rarely. Furthermore, altered smooth muscle cells from restenotic tissue showed a significantly increased migration and proliferation. Our results show that DCA is a safe and effective technique that can extend the use of percutaneous procedures and provide a promising, nonsurgical option in cases of failed PTCA. Histological analysis revealed a proliferative process as a characteristics of restenosis development.
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PMID:[Current status of directional coronary atherectomy in interventional cardiology]. 179 47

The majority (greater than 75%) of major coronary thrombi are precipitated by a sudden rupture of the surface of an atherosclerotic plaque (plaque fissuring) causing platelet aggregation where thrombogenic subendothelial tissue has been exposed. Whether the thrombus remains mural and limited, just sealing the rupture, or evolves into an occlusive thrombus seems to depend on: (1) the amount and character of exposed thrombogenic material; (2) the actual thrombotic-thrombolytic equilibrium; and (3) local flow disturbances due to preexisting atherosclerotic stenosis. Thrombus formation may take place within the stenosis, where blood velocity and shear forces are highest, or it may take place or extend poststenotically, where flow separation, recirculation, and turbulence prevail. Platelet aggregation within the stenosis is responsible for the primary flow obstruction, but fibrin subsequently enmeshes the platelets and thus stabilizes the thrombus. Most thrombi have a layered structure, indicating an episodic growth that may alternate with thrombus fragmentation and peripheral embolization: thrombosis and thrombolysis are dynamic processes occurring simultaneously. If the platelet-rich thrombus at the rupture site evolves into an occlusive thrombus, the blood proximal and distal to the occlusion may stagnate and coagulate, giving rise to a secondarily formed red stagnation thrombosis consisting predominantly of erythrocytes held together by fibrin membranes. A ruptured plaque with a dynamic thrombosis superimposed (with or without spasm) seems to underlie the great majority of acute ischemic syndromes: unstable angina, acute infarction, and sudden death. The clinical presentation and the outcome depend on the severity and duration of ischemia: whether the obstruction is occlusive or nonocclusive, transient or persistent--modified by the magnitude of collateral flow.
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PMID:Coronary thrombosis: pathogenesis and clinical manifestations. 189 65

Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of ischemic coronary syndromes. Plaques that produce only mild-to-moderate angiographic luminal stenosis are frequently those that undergo abrupt disruption, leading to unstable angina or acute myocardial infarction. Plaques with increased lipid content appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages appear to play an important role in atherogenesis, perhaps by participating in the uptake and metabolism of lipoproteins, secretion of growth factors, and production of enzymes and toxic metabolites that may facilitate plaque rupture. In addition, the particular composition or configuration of a plaque and the hemodynamic forces to which it is exposed may determine its susceptibility to disruption. Exposure of collagen, lipids, and smooth muscle cells after plaque rupture leads to the activation of platelets and the coagulation cascade system. The resulting thrombus may lead to marked reduction in myocardial perfusion and the development of an unstable coronary syndrome, or it may become organized and incorporated into the diseased vessel, thus contributing to the progression of atherosclerosis. In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion. Release of vasoactive substances, arterial spasm, or increases in myocardial oxygen demand may contribute to ischemia. In acute myocardial infarction, plaque disruption results in a more persistent thrombotic vessel occlusion; the extent of necrosis depends on the size of the artery, the duration of occlusion, the presence of collateral flow, and the integrity of the fibrinolytic system. Thrombi that undergo lysis expose a highly thrombogenic surface to the circulating blood, which has the capacity of activating platelets and the coagulation cascade system and may lead to thrombotic reocclusion. Measurements aimed at reversing the process of atherosclerosis via cholesterol reduction and enhanced high density lipoprotein activity are encouraging. Active research is being focused on the development of new antithrombotic tools, such as inhibitors of thrombin, thromboxane, and serotonin receptor antagonists, and monoclonal antibodies aimed at blocking platelet membrane receptors or adhesive proteins. These compounds may prove useful when immediate and potent inhibition of the hemostatic system is desired. Intensive research is still needed in the areas of pathogenesis and therapeutic intervention in atherosclerosis.
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PMID:Atherosclerotic plaque rupture and thrombosis. Evolving concepts. 220 64

A 57-year-old man had subacute embolic ischemia of his right foot and subsequent acute embolic ischemia of his left foot after angiography. Thrombus removed at the time of the left femoral thromboembolectomy grew Histoplasma capsulatum confirming the diagnosis of disseminated histoplasmosis. Surgical revascularization of the right leg and parenteral amphotericin B was followed by chronic ketoconazole therapy for 16 months. The patient has remained asymptomatic at 30 months after operation. Effective treatment of endovascular infection with ischemic complications of Histoplasmosis requires surgical revascularization and intensive chemotherapeutic intervention. Histoplasmosis is a ubiquitous infection in endemic areas that often has an asymptomatic subclinical course. Involvement of the cardiovascular system is rarely reported. Previous case reports have described infected cardiac valves and aortic aneurysms. This report describes the uncommon presentation of disseminated Histoplasma capsulatum infection as a peripheral embolic event and the successful management with revascularization combined with systemic amphotericin B followed by ketoconazole therapy.
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PMID:Disseminated histoplasmosis with embolic endovascular complications: a case report. 223 70

A 36-year-old man with thoracic outlet syndrome, admitted to the hospital with digital ischemia from subclavian artery thrombosis and distal embolization, was given intra-arterial urokinase. Thrombus in the subclavian artery was lysed successfully and peripheral emboli were partially cleared, resulting in relief of digital symptoms. Although surgical decompression and vascular reconstruction at the thoracic outlet may be necessary, this technique provides a means of recanalizing small distal vessels.
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PMID:Treatment of a case of thromboembolism resulting from thoracic outlet syndrome with intra-arterial urokinase infusion. 335 71

The results of local low-dose thrombolytic treatments of 564 peripheral arterial occlusions were as follows: Embolic occlusions up to 6 weeks could be removed in 72.7%, the longer lasting occlusions in 42.3%. Thrombotic occlusions lasting up to 6 months were successfully treated in 58%, still older ones in 36.2%. The cumulative patency after 5 years was 89.5% in embolic and 58.8% in thrombotic occlusions. Therefore, the differential therapy of acute peripheral ischemia has to be thought over anew together with the vascular surgeons.
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PMID:[Local thrombolysis in the treatment of acute ischemia of the leg]. 343 Dec 83

Twelve patients with portal vein thrombosis (PVT) associated with various disorders were examined. In 11 the diagnosis of PVT was made primarily by ultrasound. Endovenous lesions that presented with a mainly homogenous texture pattern of different echodensity could be clearly displayed, but failed to disclose specific echographic features that allow conclusive discrimination between blood clots (n = 7; mean diameter 13 +/- 1.7 mm) and venous tumor invasion (n = 5; mean diameter 24 +/- 12 mm). Thrombus resolution on therapy as well as cavernous transformation of the portal vein following acute PVT may be visualized by serial sonograms. Secondary findings in PVT that can be displayed by sonography include splenomegaly and superior mesenteric vein obstruction with intestinal ischemia. Real-time sonography has proved to be a valuable noninvasive method for the early diagnosis and follow-up of PVT.
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PMID:Portal vein thrombosis: real-time sonographic demonstration and follow-up. 353 90

The in-vivo effects of the new antithrombotic compound nafazatrom on experimental thrombosis of the left circumflex coronary artery, on hemodynamics and on ultimate infarct size were studied in pentobarbital-anesthetized, open-chest dogs. Coronary artery thrombosis was induced by low amperage stimulation (150 microA, DC for 6 hr) of the circumflex artery intimal lining. The effects of oral pretreatment of 1%-Tylose suspension as drug diluent and 5 mg/kg nafazatrom plus vehicle were determined. Both agents were administered twice a day before onset of current stimulation. In the drug vehicle group, coronary thrombosis caused severe hemodynamic alterations, e.g. blood pressure and left ventricular pressure decrease, as well as reduction in the LV dP/dtmax associated with increases in end-diastolic filling pressure and heart rate. Time to coronary artery occlusion was delayed by nafazatrom (5.2 +/- 1.1 vs 3.1 +/- 0.4 hr, p less than 0.05). Smaller blood pressure and LV dP/dtmax reductions and minor heart rate and filling pressure increases around the time of thrombus formation suggested cardioprotection with the drug. Smaller R wave changes and S-T segment elevation indicated minor ischemia at the time of occlusive coronary artery occlusion in nafazatrom-treated hearts (24 +/- 0.5 vs 72 +/- 7% ST segment elevation, p less than 0.01). Thrombus wet weight was 18.4 +/- 2.6 mg in the nafazatrom group, but 63.7 +/- 3.1 mg in controls (p less than 0.01). Thus, ultimate infarct size was smaller in nafazatrom-treated hearts as related to left ventricular mass (8.4 +/- 1.4 vs 32.3 +/- 3.1%, p less than 0.02) or to the occluded artery perfusion area at risk for infarction (16 +/- 3.4 vs 53 +/- 6.2%, p less than 0.05). No ex-vivo effect of nafazatrom on collagen-induced platelet aggregation was observed. These results may indicate efficacy of the drug in prevention of acute coronary artery disease as one cause of ischemic jeopardy of the myocardium and/or therapeutic value in coronary artery spasm.
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PMID:The effects of oral nafazatrom (= BAY g 6575) on canine coronary artery thrombosis and myocardial ischemia. 661 99


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