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

The Persantine Aspirin Trial focused on the question of whether the administration of the combination of aspirin and dipyridamole (Persantine) would result in a lower incidence of cerebral or retinal infarction or death than the administration of aspirin alone for persons with a history of recent carotid territory transient ischemic attacks (TIAs). Fifteen centers in the United States and Canada participated and 890 individuals were admitted and randomly allocated to either aspirin (325 mg) plus placebo or aspirin (325 mg) plus Persantine (75 mg) four times daily. Ninety eight percent of the subjects were followed for at least one year; many were followed for four to five years. The results of life table analysis indicate that the overall endpoint rates for the "aspirin only" and "aspirin plus Persantine" groups are identical. Thus, for TIA patients taking aspirin, the addition of Persantine contributes nothing. There was a clustering of stroke endpoints during the first month after randomization. Deaths from all causes were essentially equally divided between the two treatment groups.
Stroke
PMID:Persantine Aspirin Trial in cerebral ischemia. Part II: Endpoint results. The American-Canadian Co-Operative Study group. 286 Jul 40

This third paper from the Persantine Aspirin Trial examines the data to identify risk factors for stroke in persons with a history of carotid territory transient ischemic attacks (TIAs) Fifteen centers in the United States and Canada participated, and 890 subjects were admitted and randomly allocated to either aspirin plus placebo or aspirin plus dipyridamole (Persantine). Persons with the following characteristics were in greater jeopardy for stroke, retinal infarction, or death: older age, history of heart disease, history of peripheral vascular disease, and persisting neurologic deficit from a recent event. Elevated diastolic blood pressure, diabetes, use of estrogen, and smoking were not found to be risk factors. Elevated systolic blood pressure was a risk factor primarily in subjects with a history of heart disease. Estrogen use may actually have had a protective effect for women. This cannot be considered as a report of the natural history of TIA patients; it does identify risk factors in a specific cohort of subjects under treatment.
Stroke
PMID:Persantine aspirin trial in cerebral ischemia--Part III: Risk factors for stroke. The American-Canadian Co-Operative Study Group. 286 49

In a multicentre double-blind trial, 2500 patients with a clinical diagnosis of a recent cerebrovascular event of atherothrombotic origin (transient ischaemic attack, reversible ischaemic neurological deficit, or stroke) were randomised to receive either dipyridamole 75 mg plus acetylsalicylic acid 325 mg (DP-ASA, 1250 patients) or placebo (1250 patients) thrice daily. Follow-up was twenty-four months. On intention-to-treat analysis, 473 patients reached an end-point (stroke or death from any cause), 190 on DP-ASA and 283 on placebo. Survival curves for end-points showed 33% benefit in favour of the DP-ASA group (p less than 0.001). 108 patients died in the DP-ASA group and 156 in the placebo group (p less than 0.01). Results of an explanatory analysis were similar.
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PMID:The European Stroke Prevention Study (ESPS). Principal end-points. The ESPS Group. 289 Sep 51

Propofol, in both its new oil-in-water emulsion and the former cremophor-EL solution, is known to produce significant decreases in arterial blood pressure. The aim of this study was to obtain a precise hemodynamic profile of anesthesia induction with propofol under conditions of daily routine (additional 70% nitrous oxide) and to evaluate the influence of (1) premedication with lormetazepam and (2) additional i.v. injection of fentanyl. Forty patients (ASA classes I and II) were randomly assigned to one of four groups (A, B, C, and D). Anesthesia was induced with a sleep dose of propofol (mean: 2.4 mg/kg) and the patient was ventilated with 30% O2 and 70% N2O via a face mask. In groups B and D, 3 micrograms/kg fentanyl were injected immediately prior to propofol injection. Patients in groups A and B received no premedication. Patients in groups C and D received 2 mg lormetazepam on the evening prior to the anesthetic and 1 mg 2 h prior to the anesthetic orally. The following parameters were determined immediately prior to induction of anesthesia and 1, 3, 5, 8, and 10 min after the start of the propofol injection: heart rate (HR), mean arterial blood pressure (MAP), mean pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary occlusion pressure (POP), cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR). In all four groups a slight decrease in HR and SVR occurred while a marked decrease in arterial blood pressure (SAP, MAP, DAP) and cardiac output was seen. PAP and preload pressures showed no significant changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics under propofol-nitrous oxide anesthesia: effects of premedication with lormetazepam and of additional fentanyl]. 289 30

17,187 patients entering 417 hospitals up to 24 hours (median 5 hours) after the onset of suspected acute myocardial infarction were randomised, with placebo control, between: (i) a 1-hour intravenous infusion of 1.5 MU of streptokinase; (ii) one month of 160 mg/day enteric-coated aspirin; (iii) both active treatments; or (iv) neither. Streptokinase alone and aspirin alone each produced a highly significant reduction in 5-week vascular mortality: 791/8592 (9.2%) among patients allocated streptokinase infusion vs 1029/8595 (12.0%) among those allocated placebo infusion (odds reduction: 25% SD 4; 2p less than 0.00001); 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets vs 1016/8600 (11.8%) among those allocated placebo tablets (odds reduction: 23% SD 4; 2p less than 0.00001). The combination of streptokinase and aspirin was significantly (2p less than 0.0001) better than either agent alone. Their separate effects on vascular deaths appeared to be additive: 343/4292 (8.0%) among patients allocated both active agents vs 568/4300 (13.2%) among those allocated neither (odds reduction: 42% SD 5; 95% confidence limits 34-50%). There was evidence of benefit from each agent even for patients treated late after pain onset (odds reductions at 0-4, 5-12, and 13-24 hours: 35% SD 6, 16% SD 7, and 21% SD 12 for streptokinase alone; 25% SD 7, 21% SD 7, and 21% SD 12 for aspirin alone; and 53% SD 8, 32% SD 9, and 38% SD 15 for the combination of streptokinase and aspirin). Streptokinase was associated with an excess of bleeds requiring transfusion (0.5% vs 0.2%) and of confirmed cerebral haemorrhage (0.1% vs 0.0%), but with fewer other strokes (0.6% vs 0.8%). These "other" strokes may have included a few undiagnosed cerebral haemorrhages, but still there was no increase in total strokes (0.7% streptokinase vs 0.8% placebo infusion). Aspirin significantly reduced non-fatal reinfarction (1.0% vs 2.0%) and non-fatal stroke (0.3% vs 0.6%), and was not associated with any significant increase in cerebral haemorrhage or in bleeds requiring transfusion. An excess of non-fatal reinfarction was reported when streptokinase was used alone, but this appeared to be entirely avoided by the addition of aspirin. Those allocated the combination of streptokinase and aspirin had significantly fewer reinfarctions (1.8% vs 2.9%), strokes (0.6% vs 1.1%), and deaths (8.0% vs 13.2%) than those allocated neither. The differences in vascular and in all-cause mortality produced by streptokinase and by aspirin remain highly significant (2p less than 0.001 for each) after the median of 15 months of follow-up thus far available.
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PMID:Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. 916 79

17,187 patients entering 417 hospitals up to 24 h (median 5 h) after the onset of suspected acute myocardial infarction were randomized, with placebo control, between i) a 1 h intravenous infusion of 1.5 million units of streptokinase; ii) 1 month of 160 mg/day enteric-coated aspirin; iii) both active treatments; or iv) neither. Streptokinase alone and aspirin alone each produced a highly significant reduction in 5 week vascular mortality: 791/8592 (9.2%) vascular deaths among patients allocated streptokinase infusion versus 1029/8595 (12.0%) among those allocated placebo infusion (odds reduction: 25% +/- 4; 2p less than 0.00001); 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets versus 1016/8600 (11.8%) among those allocated placebo tablets (odds reduction: 23% +/- 4; 2p less than 0.00001). The combination of streptokinase and aspirin was significantly (2p less than 0.0001) better than either agent alone. Their separate effects on vascular death appeared to be additive: 343/4292 (8.0%) among patients allocated both active agents versus 568/4300 (13.2%) among those allocated neither (odds reduction: 42% +/- 5; 95% confidence limits 34% to 50%). There was evidence of benefit rom each agent even for patients treated late after pain onset (odds reduction at 0-4, 5-12, and 13-24 h: 35% +/- 6, 16% +/- 7 and 21% +/- 12 for streptokinase alone; 25% +/- 7,21% +/- 7 and 21% +/- 12 for aspirin alone; and 53% +/- 8,32% +/- 9 and 38% +/- 15 for the combination of streptokinase and aspirin). Streptokinase was associated with an excess of bleeds requiring transfusion (0.5% versus 0.2%) and of confirmed cerebral hemorrhage (0.1% versus 0.0%), but with fewer other strokes (0.6% versus 0.8%). These "other" strokes may have included a few undiagnosed cerebral hemorrhages, but still there was no increase in total strokes (0.7% streptokinase versus 0.8% placebo infusion). Aspirin significantly reduced nonfatal reinfarction (1.0% versus 2.0%) and nonfatal stroke (0.3% versus 0.6%), and was not associated with any significant increase in cerebral hemorrhage or in bleeds requiring transfusion. An excess of nonfatal reinfarction was reported when streptokinase was used alone, but this appeared to be entirely avoided by the addition of aspirin. Those allocated the combination of streptokinase and aspirin had significantly fewer reinfarctions (1.8% versus 2.9%), strokes (0.6% versus 1.1%), and deaths (8.0% versus 13.2%) than those allocated neither.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2.ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. 290 74

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.
Stroke
PMID:Enhanced in vivo platelet activation in subtypes of ischemic stroke. 316 Dec 20

We measured cytoplasmic ionized calcium concentrations [( Cai2+]) in aequorin-loaded gel-filtered platelets from 38 patients with acute occlusive stroke (12 treated with aspirin, 26 untreated) and 25 healthy controls. Compared with controls, baseline [Cai2+] was higher in untreated patients (p less than 0.002), maximal 36-72 hours after the onset of neurologic dysfunction (p less than 0.0001), in those patients with as well as those without major stroke risk factors. The increase in [Cai2+] after stimulation with 0.5 and 1.0 unit/ml thrombin (p less than 0.05), 2 and 4 micrograms/ml collagen (p less than 0.02), and 0.5 and 1.0 mM platelet activating factor (p less than 0.05) were also greater in untreated patients, but the profiles of these changes were parallel to those in controls. Even though the platelets of stroke patients are more sensitive to activation, they are functionally similar to those of controls. Aspirin treatment reduced baseline [Cai2+] as well as thrombin- and collagen-induced [Cai2+] changes. Platelet activating factor-induced increase in [Cai2+] was not altered by aspirin treatment. Our results suggest that the usefulness of aspirin in stroke is limited because aspirin does not suppress platelet responsiveness to all in vivo thrombogenic stimuli. Specific platelet activating factor antagonists may prove to be useful therapeutic agents in stroke.
Stroke 1988 Oct
PMID:Baseline and activated platelet cytoplasmic ionized calcium in acute ischemic stroke. Effect of aspirin. 317 82

Using gated radionuclide ventriculography and invasive cardiac monitoring, the effects of propofol alone and in combination with fentanyl on left ventricular (LV) volumes and function were investigated in 10 ASA III, unpremedicated patients (51-75 years) with coronary artery disease (NYHA II-III). Anesthesia was induced with propofol (2 mg/kg) followed by an infusion (100 micrograms.kg-1.min-1). Vecuronium (0.05 mg/kg) was administered and ventilation (FIO2, 1.0) was manually controlled via a face mask (FECO2, 4-5%). Data acquisitions were serially obtained over 15 minutes after the bolus IV injection of propofol and 5 minutes after the injection of fentanyl (5 micrograms/kg). Propofol induced a rapid decrease (15%) in mean arterial pressure (MAP) exclusively related to a decrease in cardiac index (CI), without reduction in indexed systemic vascular resistances (SVRI). Despite the decrease in MAP, heart rate did not change. The decrease in CI was associated with a lower preload. After the addition of fentanyl, MAP decreased significantly (35%) below the last set of propofol measurements. The decrease in MAP was associated with a reduction in CI and SVRI. Fentanyl was also associated with a significant decrease in heart rate (16%) resulting in a decrease in CI, whereas stroke index and end diastolic volume did not change. Neither global ejection fraction (EF) nor end systolic volume changed significantly at any time, nor were there changes in the ECG or in regional ejection fractions (REF). The absence of changes in REF was consistent with lack of wall motion abnormalities of the left ventricle. Propofol alone and in combination with fentanyl does not alter LV performance in patients with good LV function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular function during propofol and fentanyl anesthesia in patients with coronary artery disease: assessment with a radionuclide approach. 326 23

Although other mechanisms may be contributory, the antithrombotic properties of aspirin derive predominantly from its platelet-inhibitory effects. These are mediated via irreversible acetylation of platelet cyclo-oxygenase with subsequent blockade of platelet thromboxane synthesis. Long term administration of doses of aspirin as low as 20mg daily depresses platelet thromboxane formation by more than 90%; however, higher doses appear to be necessary to prevent thromboxane-dependent platelet activation in vivo. While there is evidence of biochemical selectivity with low doses of aspirin, significant reduction of the platelet-inhibitory eicosenoid, prostacyclin, occurs even at dosages ranging from 20 to 40mg daily. The ability of aspirin to prevent the occurrence or recurrence of vaso-occlusion has been extensively investigated. In the secondary prevention of myocardial infarction 7 placebo-controlled trials involving more than 15,000 patients have been completed. The dose of aspirin varied from 300 to 1500mg daily. Although none of the individual trials produced statistically significant reductions in total or coronary mortality, taken together the results are highly suggestive of a beneficial effect of aspirin. Similarly, 2 recent studies in patients with unstable angina demonstrated a protective effect of aspirin against acute myocardial infarction and death. While each study employed widely different doses of aspirin (324mg and 1250mg daily) similar reductions in mortality were reported. The effects of aspirin on the prevention of coronary artery bypass graft occlusion have been evaluated in 9 trials. Aspirin in doses of 100 to 975mg daily was shown to be of benefit in preventing early (less than 6 months) graft occlusion, particularly when therapy was started within 24 hours of operation. In patients with prosthetic vascular grafts of the lower limbs, aspirin has been shown to reduce platelet deposition, however further controlled trials will be required to establish the patient population most likely to benefit and, as in all these studies, the optimum dose of aspirin to employ. In patients with prosthetic heart valves it is clear that aspirin alone is insufficient to prevent thromboembolic complications and when administered as an adjunct to anticoagulant therapy it is associated with a high incidence of bleeding. In contrast, there is convincing evidence from several studies for the efficacy of aspirin in doses of 990 to 1300mg daily in the prevention of stroke and death in patients with transient ischaemic attacks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aspirin in cardiovascular disease. 328 22


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