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

Thrombolytic therapy in AMI restores infarct artery patency, preserves LV function, and decreases hospital mortality. Although hemorrhagic complications including stroke can occur, the incidence of stroke is not increased compared with control groups. Aspirin must be administered as soon as possible to inhibit platelet function, and an adjunctive role for early beta-blocker therapy may be important. Acute cardiac catheterization and coronary angioplasty need not be routinely performed in stable patients after tPA therapy, but should be considered in unstable patients. Two trials suggest that aggressive use of coronary angioplasty or bypass graft surgery before hospital discharge to preserve infarct artery patency and to prevent postinfarction ischemia is associated with an important improvement in long-term prognosis. Thrombolytic therapy should be considered standard care for patients whose ischemic chest pain lasts 20 min to at least 6 h in duration and who have an injury current on their ECG unless they are at increased risk for bleeding. The need for and timing of cardiac catheterization, coronary angioplasty, and surgical revascularization after AMI requires further evaluation.
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PMID:Thrombolytic therapy for acute myocardial infarction. 252 96

We compared combination therapy with low-dose aspirin plus ticlopidine to therapy with aspirin alone or ticlopidine alone in patients suffering transient ischemic attack or cerebral infarction. In 17, 24, and 23 patients, respectively, 300 mg/day aspirin, 200 mg/day ticlopidine, and 81 mg/day aspirin plus 100 mg/day ticlopidine were administered orally. Aspirin alone markedly inhibited platelet aggregation induced by arachidonic acid, partially inhibited platelet aggregation induced by adenosine diphosphate, and did not inhibit platelet aggregation induced by platelet activating factor. Ticlopidine alone inhibited platelet aggregation induced by adenosine diphosphate and platelet activating factor, but did not inhibit platelet aggregation induced by arachidonic acid. Combination therapy with aspirin plus ticlopidine markedly inhibited platelet aggregation induced by all three agonists. Plasma concentrations of beta-thromboglobulin and platelet factor 4 remained unchanged by aspirin alone, were slightly reduced by ticlopidine alone, and were markedly reduced by aspirin plus ticlopidine. Plasma concentration of thromboxane B2 was reduced by aspirin alone or with ticlopidine, but not by ticlopidine alone. The level of 6-ketoprostaglandin F1 alpha was reduced only by aspirin alone. Bleeding time was significantly prolonged by aspirin alone and by ticlopidine alone, although the greatest prolongation was produced by aspirin plus ticlopidine. Our results indicate that the combination of aspirin plus ticlopidine is a potent antiplatelet strategy, although the clinical importance of the changes observed need to be determined by a properly designed and controlled prospective study.
Stroke 1989 Dec
PMID:Combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia. 253 43

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

With a auto-balanced terbidimeter, the effects of ligustrazine, aspirin and betahistine on platelet aggregation were studied in 45 patients with acute ischemic stroke. The adopted parameters were: 1) the maximal aggregation (Amax), 2) the maximal aggregation velocity (Vmax), 3) the effective disaggregation rate in 5 minutes (DA 5), 4) the inhibition rate of aggregation given by drugs (IR), and 5) the concentration causing 50% inhibition of aggregation (IC 50). The results indicated that these three drugs could inhibit platelet aggregation both in vivo and in vitro. Aspirin could promote the aggregated platelets disaggregation in vivo and ligustrazine, in vitro. Regarding the effects on inhibiting platelet aggregation in vitro, ligustrazine was the most noticeable among the 3 drugs and aspirin was more effective than betahistine. The IC50 of ligustrazine, aspirin and betahistine were 0.568 mg/ml, 1,286 mg/ml and 1.722 mg/ml respectively. The authors considered that all three drugs possessed anti-platelet effects but they showed some differences among them.
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PMID:[The effects of ligustrazine, aspirin and beta-histine on platelet aggregation in patients with acute ischemic stroke]. 259 Dec 68

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 Ticlopidine Aspirin Stroke Study (TASS) and the Canadian-American Ticlopidine Study (CATS) were established by the Syntex Corporation to evaluate the potential efficacy of the antiplatelet agent ticlopidine. TASS was designed to address the use of the drug in the prevention of stroke in patients who had been diagnosed as having had one or more transient ischemic attacks (TIAs), using aspirin as a positive control. CATS was designed as a placebo-controlled trial to evaluate the drug's usefulness in prevention of a second stroke in patients after an initial stroke. Both studies were established in a "triple-blind" fashion where the patients, investigators, and Syntex were unaware of the patient assignments as to ticlopidine or control. In order to monitor the studies for potential toxicity/efficacy, Syntex established a "Safety Committee." The presentation describes, from the viewpoint of the Safety Committee, some of the issues raised by the results as they developed, by the investigators, the company, and the regulatory authorities involved. The decisions reached are discussed along with the rationale for those decisions and the outcomes.
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PMID:The "trials" of a long-term clinical trial: the Ticlopidine Aspirin Stroke Study and the Canadian-American Ticlopidine Study. 269 Dec 11

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

Platelet activating factor, a potent inducer of in vivo platelet activation and thrombosis, has been shown to be excessively active in acute ischemic stroke patients. Therefore, we studied the effect of aspirin/dipyridamole therapy in inhibiting platelet activating factor-induced platelet activation in acute ischemic stroke patients, 23 taking aspirin/dipyridamole and 21 untreated. Aspirin/dipyridamole-treated patients failed to show suppression of platelet activating factor-induced platelet aggregation even though collagen-induced activation was inhibited, suggesting that platelet activating factor acts by cyclooxygenase-independent mechanisms. Failure to suppress cyclooxygenase-independent mechanisms of platelet activation may explain the limited usefulness of current antiplatelet therapy, aspirin in particular, in stroke prevention. The role of selective platelet activating factor antagonists both in isolation and combined with aspirin needs to be investigated for their usefulness in the treatment and prevention of ischemic stroke.
Stroke 1989 May
PMID:Effect of therapy on platelet activating factor-induced aggregation in acute stroke. 271

We report the results of the Ticlopidine Aspirin Stroke Study, a blinded trial at 56 North American centers that compared the effects of ticlopidine hydrochloride (500 mg daily) with those of aspirin (1300 mg daily) on the risk of stroke or death. The medications were randomly assigned to 3069 patients with recent transient or mild persistent focal cerebral or retinal ischemia. Follow-up lasted for two to six years. The three-year event rate for nonfatal stroke or death from any cause was 17 percent for ticlopidine and 19 percent for aspirin--a 12 percent risk reduction (95 percent confidence interval, -2 to 26 percent) with ticlopidine (P = 0.048 for cumulative Kaplan-Meier estimates). The rates of fatal and nonfatal stroke at three years were 10 percent for ticlopidine and 13 percent for aspirin--a 21 percent risk reduction (95 percent confidence interval, 4 to 38 percent) with ticlopidine (P = 0.024 for cumulative Kaplan-Meier estimates). Ticlopidine was more effective than aspirin in both sexes. The adverse effects of aspirin included diarrhea (10 percent), rash (5.5 percent), peptic ulceration (3 percent), gastritis (2 percent), and gastrointestinal bleeding (1 percent). With ticlopidine, diarrhea (20 percent), skin rash (14 percent), and severe but reversible neutropenia (less than 1 percent) were noted. The mean increase in total cholesterol level was 9 percent with ticlopidine and 2 percent with aspirin (P less than 0.01). The ratios of high-density lipoprotein and low-density lipoprotein to total cholesterol were similar in both treatment groups. We conclude that ticlopidine was somewhat more effective than aspirin in preventing strokes in this population, although the risks of side effects were greater.
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PMID:A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group. 230 95


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