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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study was interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.
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PMID:Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. 776 Jan 96

Stroke is the third leading cause of death in the United States. Efforts directed at reversing acute cerebral ischemia are promising but are hampered by multiple logistic and physiologic barriers. Prevention of stroke, therefore, remains of critical importance. Primary prevention is accomplished through reduction of risk factors and the appropriate use of warfarin or aspirin in patients with cardiac sources of emboli such as atrial fibrillation. Secondary prevention is designed to reduce the risk of stroke in patients with known stroke precursors, including transient ischemia, reversible ischemic deficits, and completed stroke. Aspirin and ticlopidine are two antiplatelet agents with an established role in secondary stroke prevention. In a major North American clinical trial, ticlopidine demonstrated superior efficacy to aspirin for the prevention of recurrent stroke, particularly in the first year following a stroke. Dipyridamole has not been shown to be useful for stroke prevention. The role of warfarin in the prevention of recurrent noncardiogenic stroke remains controversial and is currently under investigation. Stroke prevention remains an important challenge, and therapy should be individualized to achieve optimal results.
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PMID:Stroke prevention therapies and management of patient subgroups. 788 86

Long-term management of patients following myocardial infarction requires assessment of both residual ischemia and left ventricular function, since these are the primary factors in determining the patient's prognosis. Most patients with uncomplicated hospital courses should undergo exercise testing and assessment of the ejection fraction. Aspirin and beta-adrenergic receptor blocking agents should be prescribed to most patients, and angiotensin converting enzyme inhibitors and cholesterol-lowering drugs should be administered when indicated. Psychologic issues unique to myocardial infarction must be addressed, and an appropriate exercise program should be prescribed. The goal is to help patients achieve the functional status they had before the infarction.
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PMID:Managing patients with myocardial infarction after hospital discharge. 781 77

The role of low-dose aspirin (3 mg/kg, i.v.) in attenuating ischemic reperfusion injury was studied in a canine model. Regional ischemia for 40 min was produced by temporary occlusion of the left anterior descending coronary artery and thereafter reperfusion instituted for 3 h. Mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), positive (+) LV dP/dtmax and negative (-) LV dP/dtmax were monitored along with myocardial adenosine triphosphate (ATP), creatine phosphate (CP), glycogen and lactate. Following reperfusion, there was a significant fall in (i) MAP, (ii) (+) LV dP/dtmax and (iii) (-) LV dP/dtmax. LVEDP was corrected after about 2 h of reperfusion. Replenishment of only myocardial CP occurred, without any change in ATP and glycogen, although lactate accumulation was corrected. Aspirin administered 15 min before reperfusion (post-treatment) caused normalisation of LVEDP within 15 min and prevented any deterioration in (-) LV dP/dtmax, although it had no effect on MAP and (+) LV dP/dtmax. After 3 h of reperfusion (post-treatment), myocardial ATP, CP, glycogen and lactate contents became normal. The number of premature ventricular complexes was significantly reduced after aspirin treatment. The present study indicates that low-dose aspirin post-treatment can ameliorate at least some of the deleterious consequences of reperfusion injury of the myocardium.
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PMID:Role of aspirin in modulating myocardial ischemic reperfusion injury. 794 22

Thrombolytic therapy markedly reduces mortality and improves left ventricular function in patients with acute myocardial infarction. Improvement may be even more substantial with adjuvant therapy. Aspirin has proved to be effective adjuvant therapy to thrombolysis. Other antiplatelet agents that may be even more effective or have an additive effect with aspirin are being studied. The role of antithrombotic agents, especially heparin, as adjuvant therapy remains unclear. Immediate cardiac catheterization with angioplasty has been used as adjunct therapy, but its routine use is not recommended. Instead, elective angioplasty (cardiac catheterization, with revascularization as indicated) should be undertaken in patients with recurrent ischemia. Angioplasty as an alternative to thrombolysis may be advantageous in certain patients, such as those presenting in cardiogenic shock or with contraindications to thrombolysis. The role of primary angioplasty in other groups (eg, the elderly, those with anterior myocardial infarction) remains unclear, and further trials are necessary before it can be recommended over thrombolytic therapy. Equipment needed for angioplasty limits its practicality, whereas thrombolytic therapy can be administered at most US hospitals.
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PMID:Adjuvants to thrombolysis after acute myocardial infarction. Does adding antiplatelet agents, antithrombotics, or angioplasty make a difference? 799 77

Carotid duplex ultrasonography is the noninvasive procedure of choice for evaluating ECAD. However, carotid angiography should be performed before doing carotid endarterectomy. Multivariate logistic regression analysis showed that significant prognostic variables for ECAD in an elderly population are (1) cigarette smoking, (2) serum total cholesterol, (3) serum HDL cholesterol (inverse association), (4) diabetes mellitus, and (5) prior CAD. Patients with 80-100% ECAD develop a higher incidence of ABI and TIA than patients with 40-80% ECAD. Patients with 40-80% ECAD develop a higher incidence of ABI and TIA than patients with 0-40% ECAD. Patients with ECAD have a higher prevalence of prior CAD and develop a higher incidence of new coronary events than patients without ECAD. In patients with ECAD, significant prognostic variables for new coronary events are (1) silent ischemia, (2) prior CAD, (3) serum HDL cholesterol (inverse association), and (4) cigarette smoking. Risk factors for ECAD and CAD should be treated in patients with ECAD. Cigarette smoking must be stopped. Hypertension, dyslipidemia, and diabetes mellitus should be treated. Aspirin, 325 mg/d, should be administered to patients with ECAD. Ticlopidine hydrochloride, 250 mg two times per day should be considered in patients with ECAD who are unable to tolerate aspirin or who develop cerebrovascular events on aspirin. Carotid endarterectomy should be considered in symptomatic patients with 70-99% ECAD.
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PMID:Extracranial carotid arterial disease. 818 62

The risk factors predominating in patients with peripheral arterial occlusive disease are cigarette smoking and diabetes. Moreover, hypertension and hyperlipidemia play an important role. Especially younger patients profit from elimination or treatment (primary or secondary prevention), whereas in elderly patients these measures are no longer crucial. In patients with intermittent claudication, the quality of life may be improved by physical training, vasoactive medicaments, optimal management of concomitant diseases and the different modalities of catheter therapy. According to the special situation in critical ischemia, surgical or catheter revascularization is preferred. If these two techniques cannot be used, intra-arterial or intravenous prostanoids are still promising. Aspirin and in second priority ticlopidine are suited for secondary prevention of arteriosclerosis not only in the extracranial, but also in the peripheral vascular region. After endarterectomy and catheter therapy, aspirin improves the long-term outcome by reducing the incidence of restenoses. Better results are obtained by oral anticoagulation in patients with emboli and after local thrombolysis.
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PMID:[Treatment strategies in arterial occlusive diseases]. 827 1

Since its introduction 40 years ago, the value of carotid endarterectomy has been controversial. In the early 1980s, several clinical trials were initiated to determine the efficacy of this operation in patients with carotid stenoses who were either symptomatic or asymptomatic for retinal or hemispheric ischemia. In 1991, interim results were published for the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST), both reporting efficacy for surgery in patients with symptomatic carotid artery stenosis of greater than 70%. Subgroup analyses revealed variable risk groups. The Veterans Administration (VA) Symptomatic Trial (Cooperative Studies Program 309 of the Department of Veterans Affairs) terminated early because of these results and its findings were consistent with the results of the larger trials. NASCET and ECST continue for symptomatic patients with carotid stenoses between 30% and 69%. The results of three trials in asymptomatic patients, the Mayo asymptomatic trial, the Carotid Artery Stenosis with Asymptomatic Narrowing: Operation Versus Aspirin trial, and the VA Asymptomatic Trial (Cooperative Studies Protocol 167 of the Department of Veterans Affairs), have been reported. None showed a statistically significant benefit for surgery in the prevention of stroke or death. However, none was sufficiently large to exclude such a benefit. The large Asymptomatic Carotid Atherosclerosis Study is in progress. Differences in the results and design of these trials are discussed as are restrictions in the applicability of their results.
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PMID:Carotid endarterectomy: trials and tribulations. 828 92

The susceptibility to ventricular arrhythmias under the conditions of cardiac ischemia and reperfusion was investigated in the Langendorff heart preparation of rats fed for eight weeks a standard chow enriched with 2% of pulverized wild garlic leaves. The isolated hearts were perfused with a modified Krebs-Henseleit solution. The incidence of ventricular fibrillation (VF) during 20 min occlusion of the descending branch of the left coronary artery (LAD) was significantly reduced in the wild garlic group as compared to untreated controls (20% vs 88%). The same holds for the size of the ischemic zone (33.6% vs 40.9% of heart weight). In the reperfusion experiments (5 min after 10 min ischemia), ventricular tachycardia (VT) occurred in 70% of the wild garlic group vs 100% in untreated controls and VF in 50% vs 90%. The time until occurrence of extrasystoles, VT or VR was prolonged. No significant alterations in cardiac fatty acid composition could be observed. Although the prostacyclin production was slightly increased in hearts of the wild garlic group, inhibition of cyclooxygenase by acetylsalicylic acid (ASA; aspirin) could not completely prevent the cardioprotective effects suggesting that the prostaglandin system does not play a decisive role in the cardioprotective action of wild garlic. Furthermore, a moderate angiotensin converting enzyme (ACE) inhibiting action of wild garlic was found in vitro as well as in vivo that could contribute to the cardioprotective and blood pressure lowering action of wild garlic. Whether a free radical scavenging activity of wild garlic is involved in its cardioprotective effects remains to be established.
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PMID:Cardioprotective actions of wild garlic (allium ursinum) in ischemia and reperfusion. 845 76

Eleven patients with ischemia heart disease (IHD) were treated with low dose aspirin (ASA, 50mg/day) for more than two weeks (ASA group). 29 cases with IHD not taking ASA served as patient control (NASA group) and 13 cases without IHD not taking ASA as normal control. Blood samples for measurement of plasma (serum) TXB2 and 6-keto-PGF1 alpha were simultaneously taken from aortic root (AO) and coronary sinus (CS). The results showed: ASA group had lower plasma TXB2 level in AO blood than NASA group (P < 0.05), but there was no significant difference in plasma 6-keto-PGF1 alpha level between the two groups. Both of plasma and serum TXB2/6-keto-PGF1 alpha ratios in AO blood in ASA group were significantly lower than those in NASA group (P < 0.05 and P < 0.0005 respectively). Plasma TXB2 CS/AO ratio and 6-keto-PGF1 alpha CS/AO ratio in ASA group were significantly lower than those in NASA group (P < 0.05), but not different from those in control group. Both ASA and NASA groups had lower serum TXB2 CS/AO ratios than control group (P < 0.05). The results suggest that low dose aspirin inhibits selectively TXA2 synthesis in systemic circulation and inhibits synthesis and/or release of TXA2 and PGI2 equally (no selectivity) in coronary circulation, but could not completely inhibit intracoronary platelet activation.
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PMID:[Effects of low dose aspirin on platelet function and prostaglandins metabolism in systemic and coronary circulation in patients with ischemia heart disease]. 869 24


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