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

This is a review of extant concepts of transient ischemic attacks (TIAs), their definitions, prognostic significance, pathogenesis, physiology, and management. The natural history of TIAs depends upon the risk factors of the population group studied, so that therapeutic trials should be controlled and randomized and not dependent upon published natural history data. A strong association between TIAs and coronary artery disease has now been established. It may be difficult to establish the cause or pathogenesis of TIAs in any given patient in view of the relatively poor correlation between the patient's symptoms and location of arterial plaques. Recent studies have suggested mechanisms aside from impaired perfusion or embolization from carotid plaques or vertebral basilar disease. There are no proven indications for carotid endarterectomy, a procedure which has been excessively used in the United States, but presently ongoing prospective, randomized, controlled multi-center studies will likely resolve this important issue. Neither is there scientific validation for the use of long-term anticoagulants, but data support the efficacy of ASA in reducing the incidence of stroke and myocardial infarction in patients with TIAs.
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PMID:Transient ischemic attacks: an update. 203 99

Thromboxane B2 (TXB2) levels in bleeding time blood and in serum were measured in 13 elderly patients with cardiovascular disease, seven of whom were receiving continuous treatment with low dose acetylsalicylic acid (ASA, 125 mg every second day--250 mg daily) for prevention of stroke. Blood sampling was performed openly, but assays of TXB2 were performed by a blinded investigator. In patients treated with ASA, median serum TXB2-levels were 4% and TXB2-levels in bleeding-time blood were less than 16% of the corresponding levels in patients without ASA (P less than 0.01). The results show that in elderly atherosclerotic patients very low doses of ASA substantially suppress TXB2 formation, not only in serum but also at the site of local haemostasis. The extent of suppression is comparable to that previously reported from young healthy subjects.
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PMID:Low dose acetylsalicylic acid and thromboxane release at the site of plug formation in vivo in elderly patients with cardiovascular disease. 231 26

Three hundred and thirty one carotid endarterectomies were performed on 279 patients during a period of twenty years from 1965 to 1984. The indication for surgery was transient ischemic attack in 67.4%, stroke in 22.7% and asymptomatic carotid stenosis in 10.0% of the operations. The overall major cerebral complication rate attending the operation was 9.6%. During the last four years' period from 1981 to 1984 the procedure morbidity was 3.6% and there was no mortality. Postoperative complications comprised 31 ipsilateral strokes and one contralateral stroke; the complications occurred during the first 24 hours in 28 cases and on the fourth or fifth day in four cases. Of these patients 11 succumbed to internal carotid thrombosis, one to cerebral infarction without thrombosis and one to intracerebral hemorrhage. The associated factors for major complications were analyzed retrospectively in the light of 32 parameters. Patients of advanced age, patients with type II diabetes mellitus, elevated serum triglycerides, high-grade stenosis or occlusion of the contralateral carotid artery, negative smoking history and those undergoing a second operation proved to be at high risk of early postoperative cerebral complications. These complications can be reduced by intraoperative use of heparin, preoperative ASA treatment and a short clamping time. Also peroperative use of shunt is obviously of benefit.
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PMID:Early cerebral complications in carotid endarterectomy: risk factors. 234 71

Anesthesia was induced in 20 patients, ASA physical status I and II, with either propofol (2.5 mg.kg-1), vecuronium (100 micrograms.kg-1), and 100% oxygen (Group A), or with equal doses of propofol and vecuronium but with 70% nitrous oxide in oxygen (Group B). All patients were premedicated with lorazepam 2 mg orally. In both groups systolic arterial pressure decreased after 3 minutes (P less than 0.05) due to decreases in cardiac output and stroke volume (P less than 0.05). Systemic vascular resistance in both groups did not change immediately after administration of propofol but increased (P less than 0.05) following intubation. Addition of nitrous oxide did not alter hemodynamic parameters associated with propofol induction.
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PMID:Does nitrous oxide affect the hemodynamic effects of anesthesia induction with propofol? 256 83

Out of 235 patients with recent cerebral transient ischaemic attacks, 208 subjects were available for final evaluation after 6 months' randomised treatment with either pentoxifylline (PTX 1200 mg/day) or a combination (ASAD) of acetylsalicylic acid (ASA, 1050 mg/day) and dipyridamole (D, 150 mg/day). Prevention of TIA, stroke or death attributable to previous events were endpoint criteria. The pentoxifylline group (n = 100) exhibited no recurrent episodes in 86 patients (86%). TIA occurred in 9 patients, stroke in 5 patients and there was 1 death. In the ASAD group (n = 108) no recurrence of ischaemic episodes was recorded in 82 cases (75.9%). TIA occurred in 20 patients, stroke in 6 patients and there were 3 deaths of vascular origin. Side effects were recorded in 4 ASAD and 1 PTX patients. The total rate of recurrence was 14% with PTX as compared to 24.1% with ASAD treatment.
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PMID:Comparative study of pentoxifylline vs antiaggregants in patients with transient ischaemic attacks. 263 19

The morphological and functional aspects of the left ventricle (LV) were assessed by echocardiography and cardiac catheterization performed simultaneously in 41 patients. Eleven were normal (N), 14 had aortic stenosis (AS) and 16 had aortic regurgitation (AR). Of the 14 patients with AS, eight were in New York Heart Association (NYHA) functional class I and II (ASA group) and six were in NYHA functional class III and IV (ASB group). Of the 16 patients with AR, seven were in NYHA functional class I and II (ARA group) and nine in functional class III and IV (ARB group). In the ASA group normal values of the LV function were obtained because of the development of an adequate hypertrophy that in normalizing the systolic stroke was able to keep a suitable function. In the ASB group there was a reduction of the LV function due to an increase of the systolic stroke and to the reduction of the contractile muscle state. Thus, in the whole AS group we found an inversed relation between the ejection fraction and the systolic stroke. In the ARA group we found a normal cardiac function as consequence of an adequate development of the LV dilation and hypertrophy. Despite the find of reduction of the contractile state, the systolic stroke normalizing was capable to keep the cardiac function at normal values. The ARB group presented an important depression of the cardiac function due the increase of the systolic stroke and to the decrease of the contractile state of the cardiac muscle.
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PMID:[Analysis of the mechanical properties of the left ventricle in patients with aortic valve disease]. 263 9

The effectiveness of labetalol (a combination nonselective beta and alpha-1-adrenergic receptor antagonist) in modifying hemodynamic responses associated with rapid sequence induction and tracheal intubation was evaluated. In a double-blind study, 24 ASA physical status I or II male patients scheduled for elective surgery were given either IV labetalol, 0.25 mg/kg (n = 8) or 0.75 mg/kg (n = 8), or a saline placebo (n = 8). Five minutes later, patients were given oxygen by mask and IV vecuronium, 0.01 mg/kg. Ten minutes after giving labetalol or placebo, cricoid pressure was applied and anesthesia was induced with IV sodium thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) 1 minute prior to intubation. The mean duration of laryngoscopy was 17 +/- 3 seconds. Prior to induction, the 0.25 mg/kg and 0.75 mg/kg doses of labetalol significantly (p less than 0.05) reduced mean arterial pressure by 4.4 +/- 1.9 and by 8.6 +/- 2.0 mmHg, respectively, but did not significantly alter heart rate or cardiac output. The 0.75 mg/kg dose of labetalol also significantly (p less than 0.05) decreased total peripheral resistance by 10.1 +/- 3.0%. Within 30 seconds after intubation, patients in all three groups exhibited increases in heart rate, mean arterial pressure, total peripheral resistance, and rate pressure product and a decrease in stroke volume. However, patients in the 0.25 and 0.75 mg/kg labetalol groups, compared to those in the placebo group, had significantly lower increases in peak heart rate (33 +/- 2 and 27 +/- 3 vs. 44 +/- 7 beats/minute), peak mean arterial pressure (38 +/- 6 and 38 +/- 7 vs. 58 +/- 7 mmHg), and peak rate pressure product (7,726 +/- 260 and 7,215 +/- 300 vs. 14,023 +/- 250 units). The results show that these doses of labetalol significantly blunt, but do not completely block, autonomic responses to rapid sequence induction and intubation.
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PMID:Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol. 269 7

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

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


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