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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evaluating the use of antithrombotic drugs in artery disease has been a long and difficult process, which is far from complete. The aims of treatment have ranged from the primary prevention of myocardial infarction or stroke, through the restoration of blood flow to ischaemic organs in order to salvage threatened tissue, to the prevention of recurrent vascular occlusion. Drugs studied in depth by clinical trial include the oral anticoagulants, antiplatelet drugs (especially aspirin), and thrombolytic agents. Their results are considered under the headings of coronary artery disease, cerebral ischaemia, and peripheral vascular disease. Aspirin, with or without dipyridamole, prevents progression of unstable angina to myocardial infarction or death, probably reduces long-term mortality after myocardial infarction, and prevents aortocoronary bypass graft occlusion. It decreases the risks of stroke or death in patients with transient cerebral ischaemia, diminishes cardiovascular morbidity after a thrombotic stroke, and may improve the outcome after some kinds of surgery for peripheral vascular disease. The benefits of oral anticoagulant treatment to prevent artery occlusion remain poorly defined. Oral anticoagulants prevent systemic embolism in many groups of high-risk patients, and probably reduce the risk of recurrence after embolism has occurred. Whether their long-term use to prevent reinfarction in patients with a previous myocardial infarct can be justified remains uncertain. They are of little or no proven value in patients with transient cerebral ischaemia or thrombotic stroke. On the other hand, there is increasing support for early thrombolytic treatment after myocardial infarction, especially since two multicentre trials have now shown reduced mortality in patients treated with intracoronary streptokinase within 4-6 hours of infarction and a further large multicentre study also demonstrated reduced mortality in patients treated with early intravenous streptokinase. In addition, the local infusion of streptokinase leads to recanalization in a high proportion of patients with a recent peripheral artery occlusion who are poor candidates for surgery.
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PMID:The use of antithrombotic drugs in artery disease. 352 34

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children. 360 47

Many strokes are thought to develop as a consequence of platelet aggregation on areas of arterial endothelial damage, with subsequent embolism or thrombus formation. Aspirin prevents platelet adhesion and aggregation by inhibiting the formation of thromboxane A2 by platelets. This suggests that aspirin could be used to prevent stroke. However aspirin also inhibits endothelial formation of the anti-aggregatory substance prostacyclin, though probably only in a slightly higher dose than that just capable of inhibiting platelet aggregation. Consequently, too high an aspirin dose may defeat its purpose. The effect of aspirin on platelets lasts for as long as they survive, whereas the effects of aspirin on endothelium are shorter. Theoretical considerations suggest that aspirin, given in brief pulses just to reach platelet inhibitory concentrations in plasma, and administered at the maximum interval that will maintain inhibition of platelet aggregation, should offer the most favourable balance between altered platelet and altered endothelial function from the viewpoint of stroke prevention. Data are presented showing that rapid rather than slow or delayed release aspirin preparations are necessary to achieve suitable plasma aspirin concentration-time profiles in humans, and that a peak plasma aspirin concentration of around 1.2 mg/L is necessary in vivo to inhibit aggregability of previously untreated platelets.
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PMID:The basis for aspirin dosage in stroke prevention. 366 79

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.
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PMID:Circulatory effects of isoflurane during acute hypercapnia. 368 95

The biochemistry of platelets is surprisingly complex, and offers the opportunity for numerous platelet-aggregation inhibiting ("antiplatelet") drugs to interfere with different aspects of their metabolism and function. Thus, aspirin inhibits platelet aggregation by irreversibly inactivating cyclo-oxygenase, a key enzyme in platelet prostaglandin metabolism, while the other nonsteroidal anti-inflammatory drugs and sulphinpyrazone cause reversible and dose-dependent inhibition of the same enzyme. Dipyridamole can inhibit both platelet adhesion and aggregation by raising the platelet cyclic AMP level through phosphodiesterase inhibition. The use of aspirin, sulphinpyrazone, and dipyridamole as antithrombotic agents has now been extensively evaluated. In general, treatment with these drugs has been more likely to prevent arterial than venous thromboembolism, and aspirin or the combination of aspirin and dipyridamole has been more effective in this respect than has sulphinpyrazone. Recent evidence strongly suggests that aspirin reduces the risk of non-fatal myocardial infarction in patients with unstable angina, and that the administration of aspirin in combination with dipyridamole significantly improves graft patency after aortocoronary bypass. Aspirin also appears to reduce the likelihood of stroke or death in men with transient cerebral ischaemic attacks.
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PMID:Aspirin and other platelet-aggregation inhibiting drugs. 388 Aug 61

Data from the Aspirin in Transient Ischemic Attack (AITIA) study, an ongoing study of two platelet antiaggregant drugs, and other published therapeutic trials were reviewed to determine whether the severity of stroke is reduced in patients taking platelet antiaggregants. Data from three of four studies suggest that strokes in treated patients are less severe than those in untreated patients. Further studies evaluating platelet antiaggregant therapy should include assessment of the severity as well as the incidence of stroke.
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PMID:Does platelet antiaggregant therapy lessen the severity of stroke? 388 10

The only well established, clinically useful platelet inhibiting drug is aspirin, though the optimal dose is unknown. Experimental findings, the virtual absence of side effects and, so far, four clinical studies favour a dose of 100-300 mg per day. The majority of clinical studies, however, and particularly those involving patients with cerebrovascular diseases, have employed doses of aspirin of 1000-1200 mg per day. Aspirin reduces mortality and infarction rates in patients who have already had myocardial infarction by 0-30%. The efficacy of additional dipyridamol or of sulfinpyrazone is not proven either. So far the effects of aspirin in patients with unstable angina and in patients after aortocoronary bypass surgery are more favourable. The best evidenced indication for aspirin treatment is transient ischemic attacks and status post stroke. The beneficial effect of aspirin in these conditions may also extend to women. Additional dipyridamol is also useless in this condition.
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PMID:[Controversy on platelet-inhibiting drugs]. 389 59

The feeding of large amounts of fish or fish oils to healthy volunteers has been shown to reduce plasma triglycerides and platelet aggregation, and prolong the skin bleeding time. To determine whether a commercially available marine oil (MaxEpa) would have similar effect in stroke patients, we performed a double-blind, placebo-controlled study in 11 patients (7 men, 4 women) with completed stroke (7) or transient ischemic attacks (TIA's) (4). Ten 1 ml opaque capsules containing either MaxEpa or olive oil were given daily for 6 weeks, and then the patients were crossed-over. Aspirin was avoided during the trial. The data were analyzed by paired-sample t-tests. A significant reduction was found in serum triglycerides, but total serum cholesterol and HDL cholesterol were unaffected. The bleeding time was modestly prolonged after 3 weeks of treatment, but the differences between MaxEpa and olive oil treatments were not significant at 6 weeks. Aside from an increase in collagen-stimulated malondialdehyde formation no other statistically significant changes in hemostatic factors were observed. We conclude that the ingestion of up to 10 MaxEpa capsules daily for 6 weeks has little influence on such established risk factors as cholesterol concentration and platelet function in patients with stroke or TIA's.
Stroke
PMID:A double-blind, placebo-controlled trial of fish oil concentrate (MaxEpa) in stroke patients. 389 95

The aim of therapy of carotid artery stenosis is to reduce the number of cerebral ischemic accident complications, but marked uncertainty exists at the present time as to the spontaneous course of these stenotic lesions and the efficacy of the different treatments proposed. After a transient ischemic accident (TIA) there is a 37% risk of a vascular accident (CVA) of a more definite type occurring within 5 years but only 1/4 of these patients die of cerebral complications, death in half of the cases being of coronary origin. Very rapid treatment with anticoagulants after TIA slightly diminishes the number of established cerebral ischemic accidents, but increases the risk of cerebral hemorrhage. Among the anti-aggregant agents, only Aspirin at high dosage (1 to 1.3 g/24 h) appears to be effective in preventing relapses of TIA and/or of CVA and/or on mortality which results from it. Carotid endarterectomy after TIA does not alter long-term survival, dependent on the increased cardiac mortality, but appears to reduce markedly the long-term recurrence rate of TIA and/or CVA. Globally, however, benefits of surgical treatment can be obtained only if post-operative cerebral mortality and morbidity are extremely low, conditions obtained in highly specialized centers only. Spontaneous course of angiographically detected asymptomatic stenosis shows, for a mean 4-year survival, a relatively low level of TIA (3,3 to 19%) and of CVA (0 to 12%) whatever the anatomic type of the stenosis. Prophylactic endarterectomy in practised hands has a low operative mortality (0 to 2%), a limited perioperative cerebral morbidity (1.3 to 4.5%) and a satisfactory later relapse rate of CVA (less than 5% at 4 years). These findings indicate comparable courses for spontaneous and treated cases globally, as well as with respect to cardiac mortality. In the absence of randomized trials it is a controversial point as to whether carotid surgery is superior to a spontaneous course in cases of asymptomatic stenosis.
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PMID:[The fate of patients with carotid stenosis. Comparative study, based on the literature, of their natural history and evolution under medical treatment or following endarterectomy]. 389 29

The effects of halothane anesthesia on cardiopulmonary (low pressure) baroreflex control of peripheral resistance were studied in 10 ASA class I young men. Graded (-5, -7.5, -10, -12.5 mmHg) lower body negative pressure (LBNP) was used to produce progressive decreases in thoracic blood volume and central venous pressure. These stimuli activate reflexes from cardiopulmonary baroreceptors. Volunteers were studied while awake and during 1 MAC (0.75%) and 1.25 MAC (0.93%) halothane anesthesia. Hetastarch (6%) in 0.9% normal saline was infused into patients before baseline recordings were initiated. Blood pressure, stroke volume, cardiac output, and systemic and forearm vascular resistance decreased and forearm blood flow increased during halothane anesthesia. In awake subjects, LBNP did not alter heart rate or blood pressure, but stroke volume and cardiac output decreased. Blood pressure was maintained by cardiopulmonary baroreflex-mediated increases in peripheral resistance. In anesthetized subjects, decreases in stroke volume and cardiac output during LBNP were similar to awake responses, however, hypotension occurred because reflex resistance increases were markedly attenuated. The authors conclude that halothane anesthesia blunts cardiopulmonary baroreflex resistance responses provoked by mild decreases in thoracic blood volume in humans.
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PMID:Halothane anesthesia attenuates cardiopulmonary baroreflex control of peripheral resistance in humans. 406 21


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