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)

Nine cases of microemboli of arterial origin to the upper extremity are reported. The source of emboli in five of these cases was in the subclavian artery compressed by osseous anomalies in the thoracic outlet. Three aneurysms, one in a subclavian vein graft and two traumatic false aneurysms in the hand, were also noted to be the sources of distal emboli. One unproved case of emboli from an atherosclerotic plaque of the subclavian artery is also reported. Chronicity of symptoms and delay in operation are often noted and lead to difficulties in surgical management. The compressing osseous structures causing the vascular lesion in the thoracic outlet syndrome must be resected, along with removal of the source of emboli. Cervicodorsal sympathectomy is often needed in cases of extensive thrombosis and/or long-standing ischemia. Embolectomy is usually a futile procedure when the main arterial trunk contains old, organized thrombus. Differential diagnostic problems between collagen vascular disease, vasculitis, vasospastic disease, and microembolic disease in cases of unilateral Raynaud's phenomenon are pointed out.
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PMID:Ischemia of the upper extremity due to noncardiac emboli. 56 Jan 30

In advanced ischemia of the lower extremity, the deep femoral artery is rarely completely occluded, but may have a hemodynamically significant occluding plaque at its origin. Detection of this lesion requires biplanar arteriographic views. As indicated in this report, the related simple procedure of femoral artery profundaplasty may salvage limbs and lower amputation sites, and it is suitable for poor risk patients.
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PMID:Femoral artery profundaplasty. 70 5

From many observations made at autopsy it is apparent that thrombosis in a coronary artery is usually, if not always, associated with rupture of an atheromatous plaque. The sequelae of such rupture include hemorrhage into the plaque with further narrowing of the lumen, formation of an occlusive thrombus or of a non-occlusive thrombus. A developing thrombus in an artery undergoes fragmentation with showering of the distal microcirculation by aggregates of platelets possibly with some admixture of fibrin. In many cases of sudden cardiac death associated with severe atherosclerotic stenosis of the coronary vessels, an occlusive thrombus is not found and the myocardium shows no morphological lesion or else focal patchy early damage in the subendocardial region. One possible mechanism that might explain these findings is microembolism from mural nonobstructing coronary thrombus. Such a mechanism is well established in transient ischemia of the brain and retina related to ulcerated atheroma of the internal carotid artery. Experimental observations indicate that platelet aggregates in the myocardial circulation cause arrhythmias, sudden death, vasculitis, and myocardial ischemic damage. Induction of an occlusive coronary artery thrombus is associated with development of an infarct involving the full thickness of the myocardium. A nonocclusive thrombus is associated with either no myocardial damage or focal subendocardial ischemic injury. It is possible that further aggregation of platelets may facilitate the extension of infarction subsequent to an occlusive event, although there is little evidence on this point. A number of clinical studies show increased platelet reactivity to agents causing aggregation, such as norepinephrine or collagen, in subjects experiencing thromboembolic episodes. It seems unlikely, however, that in vitro tests of platelet function can identify or predict clinical arterial thrombotic disease, although studies of platelet survival and turnover may be more helpful. There is also evidence that platelet survival may be prolonged by drugs having a therapeutic benefit in coronary artery disease and arterial thromboembolism. There is a need for better designed and coordinated clinical trials and for better experimental approaches to explore the relationships among coronary thrombosis, embolsim of the myocardial microcirculation, myocardial ischemia, and sudden death.
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PMID:Platelet aggregation secondary to coronary obstruction. 76 18

Electroencephalographic monitoring of a patient during carotid endarterectomy demonstrated severe ipsilateral voltage suppression with preservation of rhythms when the common carotid artery was clamped. Because the atheromatous plaque extended almost to the base of the skull, it was impossible to insert a shunt. Occlusion time was 19 minutes. After carotid flow was re-established, there was a rapid recovery of voltage. The patient awoke with a profound hemiparesis, but this cleared almost completely within a week. The EEG changes indicated severe ischemia, but, though function was transiently impaired, there was no apparent cerebral necrosis. This case represents the most severe yet reversible episode of ischemia during carotid clamping reported to date. Preservation of EEG rhythms, even in the face of voltage suppression, may have been a favorable sign.
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PMID:Cerebral Ischemia during carotid endarterectomy with severe but reversible changes. 84 33

Two patients with retroperitoneal fibrosis demonstrated symptoms of peripheral vascular ischemia. Arteriolysis to free the distal aorta and iliac vessels was successful in both patients. Aortography in the posteroanterior view was equivocal, but the accompanying urologic abnormalities and a history of methysergide ingestion helped establish the etiology of the ischemia. The most direct approach to the treatment of the vascular obstruction caused by retroperitoneal fibrosis is complete arteriolysis. Most previous reports indicate that it is relatively easy to establish a dissection plane between the fibrotic plaque and the vessel wall. We found that the fibrotic process invaded the vessel wall. Accordingly, the surgeon must anticipate a difficult, tedious dissection when performing arteriolysis for the treatment of vascular compression secondary to retroperitoneal fibrosis.
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PMID:Peripheral ischemia due to retroperitoneal fibrosis. 87 Nov 93

Forty-two patients developed signs of acute arterial insufficiency following percutaneous femoral angiography. Three responsible mechanisms were recognized: 1. Occlusion of the femoral artery due to stripping off of thrombus formed on the intra-arterial catheter (22 cases). 2. Distal embolization of thrombus formed at the puncture site in the femoral artery (12 cases). 3. Subintimal dissection of an atherosclerotic plaque with secondary thrombosis (8 cases). Vasospasm was not an adequate explanation for the resulting symptoms and signs of ischemia. Such a diagnosis caused delay in proper surgical therapy. Early heparinization and thrombectomy were necessary. It was successful in all but one of 35 cases. Of seven delayed cases there were complications in three.
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PMID:Femoral artery occlusion caused by percutaneous angiography. Mechanisms and management. 89 66

At present, percutaneous peripheral ultrasound angioplasty should be considered in those patients with symptoms of claudication or resting limb ischemia. With the development of an over-the-wire system, we treat patients with suprageniculate or infrageniculate lesions. It is expected that the over-the-wire probe will allow application of ultrasound angioplasty not only to lesions below the knee but to contralateral vascular occlusions as well. An intraoperative device for plaque ablation and arterial recanalization is in development for use in less accessible sites such as the coronary arteries. Experimental studies have shown that catheter-delivered therapeutic ultrasound recanalizes complete occlusions, reduces stenoses, dissolves thrombus, vasodilates, and enhances arterial distensibility. The potential clinical applications of therapeutic ultrasound include recanalizing total arterial occlusions, dissolving thrombi, facilitating balloon angioplasty by increasing arterial compliance, and as a stand-alone angioplasty device.
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PMID:Ultrasound recanalization of diseased arteries. From experimental studies to clinical application. 138 89

Two types of myocardial infarction, transmural and subendocardial, were macroscopically examined, and the gross and microscopic findings were correlated. The transmural type usually consisted of yellowish-brown coagulation necrosis in the center of an infarcted focus and coagulative myocytolysis at the marginal zone. The subendocardial type was characterized by coagulative myocytolysis throughout the entire focus. Wavy fiber and colliquative myocytolysis of non-specific ischemic lesions were seen only microscopically in both peripheral and subendocardial areas of infarcted foci. Coagulation necrosis was associated with obstructive thrombus formation in 79% of cases as a result of absolute ischemia in the transmural type. Coagulative myocytolysis was associated with obstruction by plaque hemorrhage in 27% of cases, and multivessel disease was frequently encountered in the subendocardial type due to insufficient blood supply. Based on histochemical and immunohistochemical examinations, the ischemic lesions were graded in descending order of coagulation necrosis, coagulative myocytolysis, wavy fiber, and colliquative myocytolysis. The close relation between coagulation necrosis and the transmural type as well as that of coagulative myocytolysis with the subendocardial type suggests two different pathogenetic mechanisms of transmural and subendocardial infarction.
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PMID:Characterization of transmural and subendocardial infarction by typing and grading of ischemic lesions in autopsied human hearts. 141 57

Recent studies have shown that the principal component of the senile plaque in Alzheimer's disease (AD), beta-amyloid protein (beta AP) can exert direct and indirect neurotoxicity in vitro. Because of the studies that demonstrated potentiation of excitatory amino acid toxicity by beta AP, we decided to test whether beta AP was able to potentiate damage in an in vivo model where excitotoxic damage is thought to be important. The present study evaluated the in vivo effects of beta AP implants in the brain of rats before and after being subjected to 10 min of transient global forebrain ischemia by 4-vessel occlusion (4-VO). Implants of either synthetic beta AP or prolactin (PRL), which was used as a control protein, were made into the striatum and the hippocampus of either the left (beta AP) or the right (PRL) cerebral hemisphere. The implants were made in a lipophilic, non-toxic vehicle so as to try and achieve sustained beta AP exposure. One group of animals was evaluated for direct in vivo effects within 1 week following implantation; the other group was subjected to 4-VO 3-4 days post-implantation for evaluation of potential indirect effects. This latter group was compared to the histopathology of animals subjected to 4-VO without prior implantation. In the group of animals evaluated for direct effects, no evidence of neurotoxicity was observed. Bielschowsky silver staining and immunostaining for ubiquitin were unremarkable in all lesions. beta AP was detected by immunocytochemistry in the parenchymal tissue that received beta AP implants. Marked glial activation was observed to be associated with experimental and control implants. Under the experimental conditions employed in this study, significant protection from ischemia rather than potentiation of damage was observed. These results suggest that beta AP may not be neurotoxic in rodents in vivo and that the lesions and/or trauma produced by the implantation procedure 3-4 days prior to 4-VO may have induced factors that were protective against ischemia-induced damage.
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PMID:In vivo effects of beta-amyloid implants in rodents: lack of potentiation of damage associated with transient global forebrain ischemia. 152 Nov 57

Duplex-derived velocity measurements were used to assess the hemodynamics of 64 femoropopliteal arterial sites in 59 patients after angiographically successful percutaneous transluminal balloon angioplasty. With use of angiography as the gold standard, percutaneous transluminal balloon angioplasty was judged to be successful if (1) evidence existed of a "split" caused by intimal dissection and splitting of atherosclerotic plaque; and (2) no significant diameter-reducing residual stenosis was observed at the percutaneous transluminal balloon angioplasty site. At 1 month, 55 limbs (86%) were hemodynamically and clinically improved by SVS/ISCVS clinical criteria for chronic limb ischemia. Of the 55 percutaneous transluminal balloon angioplasty sites, duplex scanning had identified 40 (63%) sites with a less than 50% diameter-reducing stenosis and 15 (27%) sites with a greater than 50% diameter-reducing stenosis within a week after percutaneous transluminal balloon angioplasty. Independent review of the 55 angiograms taken after percutaneous transluminal balloon angioplasty identified 39 sites (71%) with a split and 16 sites (29%) without. By life-table analysis, a greater than 50% diameter-reducing stenosis predicted a worse clinical outcome (15% at 1 year) compared with the presence of a less than 50% diameter-reducing stenosis (84% at 1 year) (p less than 0.001; log rank test). The presence or absence of an angiographic split was not a predictive factor of percutaneous transluminal balloon angioplasty outcome (split, 61% at 1 year; no split, 62% at 1 year) (p = 0.832; log rank test). The detection of a functional residual stenosis by duplex scanning did not correlate with angiographic appearance, but was predictive of clinical failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of duplex scanning versus angiography in predicting outcome after balloon angioplasty in the femoropopliteal artery. 153 85


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