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)

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63

Between August 1983 and December 1987, 23 patients received a 30-minute intraoperative, intraarterial infusion of streptokinase (seven patients) or urokinase (16 patients) because of residual thrombus or persistent ischemia or both after thromboembolectomy. Ages ranged from 21 to 77 years (mean, 58 years). In 15 patients intraoperative lytic therapy was part of the initial operation, whereas in eight patients intraoperative lytic therapy was performed during a secondary operation to treat thrombosis of a recently placed graft. Seven patients in the latter group had hypercoagulable conditions (five had heparin-induced thrombosis; one had protein C deficiency; one had polycythemia with thrombocytosis). Improvement after intraoperative lytic therapy was seen on angiography performed after infusion in 13 of 17 (76%) patients in whom angiography was performed both before and after intraoperative lytic therapy. Grafts in 12 of these patients remained patent without additional intervention, and in one graft thrombus formed again. In contrast, among four patients without angiographic evidence of improvement, thrombus formed again in four grafts (p less than 0.004). Intraoperative lytic therapy was considered successful in 74% of instances (17/23), including four of seven patients with hypercoagulable states. Three of six patients whose grafts failed had major amputations, whereas there were no amputations after successful infusions. Twelve patients were heparinized after intraoperative lytic therapy. Ten patients in this group were considered treatment successes, and two were considered treatment failures. Three of 11 patients not heparinized after intraoperative lytic therapy were considered treatment failures. Four hematomas occurred in the former group and none in the latter (p less than 0.03). No hematomas occurred in the heparin-induced thrombosis group in spite of anticoagulation with sodium warfarin (Coumadin). Only one hematoma occurred within 6 hours of intraoperative lytic therapy, and thus it was attributable to the infusion. We conclude that intraoperative lytic therapy is an effective adjunct to manage residual thrombus or persistent ischemia or both after lower extremity revascularization. Postinfusion angiography is of prognostic value. Heparinization after intraoperative lytic therapy seems beneficial but significantly increases the risk of bleeding complications.
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PMID:Intraoperative infusion of lytic drugs for thrombotic complications of revascularization. 279 66

The Authors report a series of 21 cases of heparin induced thrombocytopenia (HIT) observed in a Department of Cardiovascular Surgery. The indication for heparin treatment was a cardiac procedure in 12 cases, peripheral arterial reconstructive surgery in 3 cases and in 6 cases a prevention of embolism. Two routes were used for heparin administration: subcutaneous and intravenous injections. The diagnosis was biological on low platelet counts (p.c.) in 4 cases, in 7 cases a deep venous thrombophlebitis and in 9 cases an acute arterial ischemia complicated the heparin treatment. From the 7th to 15th day after heparin treatment the p.c. had risen to the average value of 46,857/mm3. The diagnosis was clinical in 3 cases, biological with a positive aggregation test in the presence of heparin in 11 cases out of 14 biological tests performed and pathological with observation of white clots in 11 cases. The related mortality rate to HIT was 28.5% of the cases (6 cases). HIT is a rare but severe complication often associated with thrombo-embolic complications. The routine check of p.c. before and after the first week of heparin treatment is reasonable. The negative aggregation test in the presence of heparin does not permit to confirm this diagnosis. The drop in the p.c. between the 6th to 10th day after heparin treatment required an immediate arrest of this type of anticoagulation and replacement with Coumadin. The low molecular weight Heparin may induce cross matching reactions with heparin and therefore is not used as treatment for HIT. In emergency, cardiac surgery with the use of the extra-corporeal circulation device can be performed with success with heparin (2 cases).
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PMID:Cardiovascular surgery and heparin induced thrombocytopenia. 319 76

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

Clinical experience with aortic saddle embolus (ASE) is not extensive due to the relative infrequent lodging of emboli at the aortic bifurcation. During the period 1962-1982, 26 patients (mean age, 56 years) were treated at the UCLA Medical Center for ASE and followed from 2 to 158 months (mean, 45 months). These cases were reviewed in order to identify features of diagnosis, anticoagulation, and operation which impact on results. All 26 patients presented with bilateral lower extremity ischemia with or without extension of clot to the iliac bifurcation. Ninety-six per cent of emboli were of cardiac origin and one-third occurred in patients who had previous symptoms of chronic lower extremity ischemia. Rest pain and motor/sensory deficits were main complaints in 92% of the patients, but did not become manifest until more than 6 hours, unlike more distal emboli which have an earlier presentation. Preoperative angiography, even in the patient with a history of claudication, has a small role in planning the surgical approach to patients with ASE and, although performed in 11 patients, it influenced operation in only two. Operation within the "golden period" of 6 hours after embolization did not significantly influence outcome after ASE, since 20 patients were operated on more than 6 hours after embolization, with results similar to six patients who were operated on less than 6 hours after embolization. Early high-dose heparinization, used in all patients and maintained for a mean of 12 days, may have contributed to this effect. In 22 patients (85%) Forgarty catheter extraction via bilateral groin approaches was used with a mortality of 14%; only one death was directly attributed to the catheter embolectomy. In 15% of patients, a direct approach on the aorta was selected with a zero mortality rate. Postoperative functional result was excellent with an amputation rate of only 2% (one limb). Re-embolization occurred in seven patients (27%) after discharge, five of whom had not been maintained on Coumadin and two who were not anticoagulated adequately. The authors conclude that the keys to successful treatment of ASE include high dose heparin which is maintained through the perioperative period, embolectomy without preoperative angiography, and maintenance of long-term oral anticoagulation.
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PMID:Aortic saddle embolus. A twenty-year experience. 685 79

Coronary artery bypass operations are associated with increased morbidity and mortality in the elderly. Similarly, it has been shown that coronary angioplasty is associated with a higher risk of complications in the elderly than in younger patients. The purpose of this study was to evaluate the 1-month outcome of elderly patients (>75 years old) who were included in the Stenting without Coumadin French Registry. From December 1992 to March 1995, 2,900 patients (mean age 61+/-11 years) were included in this registry. All patients were treated with ticlopidine (250 to 500 mg/day) for 1 month from the day of percutaneous transluminal angioplasty, aspirin (100 to 250 mg/day) for >6 months, and low-molecular-weight heparin (antiXa 0.5 to 1 IU/ml) for 1 month in phase II, 15 days in phase III, and 7 days in phase IV. No heparin was given in phase V. The study group included 233 patients (8.0%) > 75 years old (mean age 79+/-4), 44 (18%) of whom were women. All patients underwent dilatation of a native coronary vessel. One hundred seventeen had unstable angina (50.2%), 20 had postmyocardial infarction ischemia (8.6%), and 6 had acute myocardial infarction (2.6%). Indications for stenting were de novo lesion in 63 patients (27.0%), restenosis in 38 (16.3%), suboptimal result in 48 (20.6%), nonocclusive dissection in 56 (24.0%), and occlusive dissection in 28 (12.0%), respectively. Stented coronary arteries were the left anterior descending in 109 (46.8%), the right in 80 (34.3%), the left circumflex in 40 (17.2%), and the left main in 4 (1.7%). Palmaz-Schatz stents were used in 228 patients (82.0%), AVE microstents in 38 (13.7%), and other stents in 12 (4.3%). More than 1 stent was used in 48 patients (17.3%). The mean diameter of the balloon used for stenting was 3.31+/-0.38 mm and maximal inflation pressure was 12.2+/-2.9 atm. At one-month follow-up, vascular complications occurred in 5 patients, requiring surgery in 2 (1.3%), acute closure occurred in 1 (0.4%), subacute closure in 3 (1.3%), emergency or planned coronary artery bypass graft surgery in none, acute myocardial infarction in 4 (1.7%), stroke in 1 (0.4%), and death in 8 (3.4%). The composite end point of a major cardiac event was observed in 13 cases (5.6%). Coronary stenting using ticlopidine and aspirin appears to be a particularly safe approach in this high-risk subset.
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PMID:One-month results of coronary stenting in patients > or = 75 years of age. 967 Oct 2

Coronary angioplasty is used to treat coronary atherosclerotic disease in many patients. One problem with coronary angioplasty is the phenomenon of restenosis. Restenosis appears to be a universal response to arterial wall injury. The biological events that underlie restenosis are characterized by: platelet adhesion and aggregation at sites of damaged endothelium, and within dissections into the medial layers, release of platelet derived growth-promoting substances, inflammation of the injured medial zone, transformation, migration, and proliferation of smooth muscle cells of the media following their activation by growth-promoting substances, secretion of copious amounts of extracellular matrix material, and finally, termination of the growth process following regrowth of endothelium over the damaged area. More than a decade of research work has helped identify clinical correlates of restenosis after coronary angioplasty. Patient-related correlates include male gender, unstable angina, diabetes, and continued smoking after angioplasty. Lesion-related correlates include multilesion and multivessel procedures, higher post-angioplasty residual stenosis, proximal vessel location, location in the left anterior descending coronary artery, location in a vein graft, long lesions, and total occlusions. However, for the purposes of individual patient care, clinical correlates are not particularly helpful. No group of variables has predicted complete freedom from restenosis, and conversely no group of variables has reliably indicated its presence. All patients undergoing angioplasty will require some form of follow-up evaluation. Symptom status by itself has not been found to be useful for predicting restenosis. However, when symptom status is combined with exercise thallium-201 scintigraphy, performed 4-6 months after angioplasty, it is less than ideal, but has a negative predictive value of over 90%. This means that over 90% of patients who are asymptomatic and have no evidence of ischemia by thallium-201 scintigraphy, will not have angiographic restenosis. Numerous clinical trials have been performed in order to reduce or prevent restenosis. Almost all have been disappointing, while a few have been encouraging. Studies of antiplatelet agents such as aspirin, dipyridamole (Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT, USA), and Ticlopidine (Syntex, Humgcao, Puerto Rico) have not shown efficacy, yet studies of an inhibitor of platelet-derived growth factor have been provocatively encouraging. No reduction in restenosis rates was found with the anticoagulants Coumadin (Du Pont Pharmaceuticals, Wilmington, DE, USA) and Heparin (Wyeth-Ayerst, Philadelphia, PA, USA). Fish oils (omega fatty acids) have been found in several clinical trials to provide modest, but encouraging, reductions in restenosis, but await further confirmation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Restenosis after coronary angioplasty. 1015 Oct 16

Dissection of the carotid artery in the neck is a relatively common condition. Most dissections are spontaneous, likely related to activities that cause sudden stretch of the pharyngeal portion of the carotid artery. Many patients do not develop brain ischemia but have a triad of neck and head pain, Horner's syndrome, and pulsatile tinnitus. Others present with transient or persistent brain ischemia. Strokes are due to the embolization of thrombus material from the lumen of the dissected artery to the intracranial arteries, most often the middle cerebral artery. Although there have been no randomized therapeutic trials in patients with carotid artery dissection, experience shows that standard anticoagulants in the form of heparin followed by Coumadin (Du Pont Pharma, Wilmington, DE) are effective in preventing further artery-to-artery emboli.
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PMID:Carotid Artery Dissection. 1509 17

Cerebral vasospasm is a well-known consequence of aneurysmal subarachnoid hemorrhage (SAH) triggered by blood breakdown products. Here, we present the first case of cerebral vasospasm with ischemia following a spontaneous spinal SAH. A 67-year-old woman, who was on Coumadin for atrial fibrillation, presented with chest pain radiating to the back accompanied by headache and leg paresthesias. The international normalized ratio (INR) was 4.5. Ten hours after presentation, she developed loss of movement in both legs and lack of sensation below the umbilicus. Spine MRI showed intradural hemorrhage. Her coagulopathy was reversed, and she underwent T2 to T12 laminectomies. A large subarachnoid hematoma was evacuated. Given her complaint of headache preoperatively and the intraoperative finding of spinal SAH, a head CT was done postoperatively that displayed SAH in peripheral sulci. On postoperative day 5, she became obtunded. Brain MRI demonstrated focal restricted diffusion in the left frontoparietal area. Formal angiography revealed vasospasm in anterior cerebral arteries bilaterally and right middle cerebral artery. Vasospasm was treated, and she returned to baseline within 48 hours. Spontaneous spinal SAH can result in the same sequelae typically associated with aneurysmal SAH, and the clinician must have a degree of suspicion in such patients. The pathophysiological mechanisms underlying cerebral vasospasm may explain this unique case.
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PMID:Cerebral Vasospasm with Ischemia following a Spontaneous Spinal Subarachnoid Hemorrhage. 2347 68