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

The effectiveness of a single preinduction intravenous (IV) bolus of esmolol in blunting hemodynamic responses to rapid sequence induction and tracheal intubation was evaluated. In a randomized double-blind study, 32 ASA I and II healthy patients scheduled for surgery were monitored with electrocardiography (EKG) lead V5, arterial cannulation, and impedance cardiography. After preoxygenation and a priming dose of vecuronium (0.01 mg/kg), patients received either saline (n = 12), esmolol 100 mg (n = 10), or esmolol 200 mg (n = 10) as an IV bolus (20 ml volume). This procedure was immediately followed by a 5 ml IV saline flush, cricoid pressure, thiopental sodium 5 mg/kg, and succinylcholine 1.5 mg/kg. Patients receiving 200 mg of esmolol had a 50% reduction in the usual tachycardia associated with induction and a greater decline in systolic blood pressure (SP) (by 50%) prior to intubation as compared with the placebo group (p less than 0.05). The increase in diastolic blood pressure (DP) and the reduction in stroke volume (SV) produced by induction and intubation were similar in all the groups. Plasma norepinephrine levels at 1.5 minutes after intubation increased in the esmolol groups about 130% above that measured in the placebo group. This finding was associated with a more gradual return of peripheral resistance to baseline following tracheal intubation. However, both doses of esmolol effectively attenuated heart rate (HR), SP, and rate pressure product (RPP) increases (p less than 0.05 vs placebo) produced by laryngoscopy and tracheal intubation.
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PMID:Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol. 197 86

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

Thrombolytic therapy has been shown to limit infarct size, improve ventricular function, and decrease mortality in suspected evolving myocardial infarction (MI). Aspirin therapy also decreases mortality as well as stroke and reinfarction in suspected evolving MI. The combined ability of both agents to lyse as well as to prevent clots yields a greater benefit than either alone. The use of aspirin with thrombolysis also protects against the increase in reinfarction observed when thrombolytic therapy is given alone. While ongoing research is evaluating the optimal thrombolytic agent as well as the possible role of heparin, it is already clear that the use of aspirin with thrombolytic therapy will significantly decrease reinfarction, stroke, and vascular mortality in suspected evolving MI.
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PMID:Role of aspirin with thrombolytic therapy in acute myocardial infarction. 210 52

Neither low- nor very-low-dose Aspirin suppresses thromboxane A2 biosynthesis without inhibiting the formation of its functional antagonist prostacyclin. Although thromboxane synthase inhibitors selectively inhibit thromboxane A2 biosynthesis and increase prostacyclin formation in vivo, thromboxane synthase inhibitors can lead to an accumulation of prostaglandin H2 that substitutes for thromboxane A2 at their common receptors in platelets and smooth muscle. In contrast to those inhibitors of thromboxane A2 biosynthesis, thromboxane A2/prostaglandin H2 receptor antagonists do not affect the synthesis of prostacyclin and other prostaglandins but prevent thromboxane A2 and prostaglandin H2 from activating platelets and inducing vasoconstriction. The available thromboxane A2/prostaglandin H2 receptor antagonists are competitive antagonists. However, some of them, such as daltroban, S-145, GR 32.191, and Bay U 3405, produce a noncompetitive antagonism in human platelets due to their low dissociation rate. As a consequence, agonists equilibrate with the antagonist-occupied receptor pool so slowly that they fail to induce platelet activation. This property of some antagonists strongly increases their potency and the duration of their inhibitory effect. Therefore, a low dissociation rate is an important measure of the effectiveness of a thromboxane A2/prostaglandin H2 receptor antagonist in addition to its receptor affinity. Another approach in thromboxane A2 pharmacology is a combination of thromboxane synthase inhibition with thromboxane receptor antagonism in one drug, such as ridogrel. Such dual inhibitors present a very high inhibitory potential and prolong the skin bleeding time to a greater extent than Aspirin, thromboxane synthase inhibitors, or thromboxane A2/prostaglandin H2 receptor antagonists.
Stroke 1990 Dec
PMID:Thromboxane A2/prostaglandin H2 receptor antagonists. A new therapeutic principle. 214 33

Aspirin inhibits thromboxane A2 and prostaglandin formation in platelets and prostaglandin I2 (prostacyclin) in vascular cells. It prevents platelet aggregation by irreversible acetylation of cyclooxygenase, a key enzyme in the arachidonic acid metabolism. Oral aspirin can be extensively hydrolyzed to inactive salicylate in the stomach and the liver (first-pass) before it enters the systemic circulation. Presystemic acetylation of platelets thus occurs during aspirin absorption, with a concomitant sparing of peripheral vascular cyclo-oxygenase, mainly exposed to salicylate. On the basis of its antiplatelet effect, aspirin has been assessed during the past two decades in patients with a history of myocardial infarction, stroke, transient ischemic attack or unstable angina. A meta-analysis of randomized controlled trials of long term aspirin treatment for secondary prevention of vascular disease indicated that aspirin (300-1500 mg daily) significantly reduced fatal and non-fatal vascular events. More recently aspirin (160 mg daily) produced a significant reduction in hospital vascular mortality and in non-fatal events in patients with suspected acute myocardial infarction. Combination of aspirin with streptokinase was significantly better than either drug alone. On the other hand two primary prevention trials of aspirin in healthy doctors did not show any modification of vascular mortality despite an overall reduction of non-fatal myocardial infarction. Resolution of some problems related to the mechanism of action of aspirin and to selection of trial populations will possibly increase the benefit/risk ratio of aspirin treatment for prevention of vascular disease.
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PMID:Aspirin as an antithrombotic drug: from the aggregometer to clinical trials. 215 Jul 36

Many nonsteroidal anti-inflammatory drugs exert their effects by inhibiting the synthesis of prostanoids. More specifically, these agents block the synthesis of prostaglandin endoperoxide G2 from arachidonic acid by competing with arachidonate for binding to the cyclooxygenase active site of prostaglandin endoperoxide synthase. Studies of the molecular biology of prostaglandin endoperoxide synthase indicate that there is a single gene for the enzyme. Thus, tissue-specific effects of nonsteroidal anti-inflammatory drugs probably result from differences in drug distribution and/or metabolism and not from the existence of tissue-specific prostaglandin endoperoxide synthase isozymes. Aspirin causes inactivation of prostaglandin endoperoxide synthase by first binding to the cyclooxygenase active site and then acetylating the protein at Ser530. Although the cyclooxygenase activity is inactivated, the hydroperoxidase activity of prostaglandin endoperoxide synthase is unaltered by Aspirin or other nonsteroidal anti-inflammatory drugs. Replacement of Ser530 of the native enzyme with an alanine residue by site-directed mutagenesis yields a prostaglandin endoperoxide synthase with unaltered catalytic and substrate binding activities. Thus, the hydroxyl group of Ser530 is not essential for enzyme activity. Instead, it appears likely that acetylation of prostaglandin endoperoxide synthase by Aspirin simply places a bulky acetyl group at or near the cyclooxygenase active site, thereby interfering with arachidonic acid binding.
Stroke 1990 Dec
PMID:Molecular basis for the inhibition of prostanoid biosynthesis by nonsteroidal anti-inflammatory agents. 217 60

The ability of low-dose aspirin to irreversibly inhibit platelet-dependent cyclooxygenase provides a biologic mechanism to explain why this drug may decrease the risk of thrombotic cardiovascular events. Observational epidemiologic studies, both case-control and cohort, have suggested that aspirin might reduce the risk of cardiovascular disease by approximately 20 to 30%. An overview of 25 randomized trials of aspirin among individuals with a history of prior cardiovascular disease demonstrated that those receiving aspirin experienced a significant 25% reduction in the occurrence of "important vascular events," an endpoint that combines nonfatal myocardial infarction (MI), nonfatal stroke, and cardiovascular death. There were also significant 32% reductions in subsequent nonfatal MI, 27% reductions in nonfatal stroke, and 15% reductions in vascular mortality. Thus, individuals with a history of MI, stroke, transient ischemic attack, or unstable angina clearly benefit from aspirin. The Second International Study of Infarct Survival (ISIS-2) sought to determine if benefits would accrue if aspirin was given within the first 24 hours of suspected evolving MI. The aspirin group experienced a significant 23% reduction in 5-week vascular mortality compared with those receiving placebo. Aspirin was also associated with significantly fewer reinfarctions and strokes. Thus, among those with suspected evolving MI, aspirin significantly reduces the risk of reinfarction, stroke, and vascular mortality. These analyses indicate that aspirin is of proven value in the therapy of most patients who have survived MI, stroke, or unstable angina, as well as those evolving a suspected MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aspirin in chronic cardiovascular disease and acute myocardial infarction. 218 44

In terms of percentage of total deaths, stroke is second and fourth for women and men, respectively, but in terms of potential years of life lost, it is seventh and sixth, respectively. In both women and men, stroke rates have declined. Acetylsalicylic acid has been shown to reduce significantly stroke, death and stroke-related death in men, with no detectable benefit for women. A major hormonal effect appears unlikely to explain the lack of female responsiveness. The risk factors associated with stroke are generally not different in the two sexes. There is evidence that high dose estrogen, hypertension and smoking are important cumulative factors for premenopausal women. The risk of vascular disease is reduced by post menopausal hormone replacement. Pregnancy increases the risk of thrombotic cerebrovascular events, particularly during the second and third trimesters of pregnancy. Heavy drinkers have a fourfold increase and light drinkers a decrease to one-half of relative risk of stroke compared to nondrinkers. Cigarette smoking increases the risk of stroke. Lifestyle may also play a role.
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PMID:Stroke in women. 218 14

Two hundred and sixty-four patients were included in an open, randomized, multicenter trial, with the aim of determining whether nicardipine can be useful in the prevention of cerebral infarction. The patients had experienced one or more transient ischemic attacks, reversible ischemic neurologic defect, or stroke with minor permanent neurological deficit in the 12 months before enrolling in the study. Each patient was randomly assigned to received 250 mg of aspirin once daily plus 20 mg of nicardipine thrice daily (n = 170) or 250 mg of aspirin once daily (n = 94) for 12 months. During the 12-month treatment period, 12% of the aspirin-plus-nicardipine group and 19% of the aspirin-only group experienced an ischemic cerebrovascular event; at six months, the cumulative incidence of events was significantly lower in the aspirin-plus-nicardipine group than in the aspirin-only group. One patient in each group died of a recurrent stroke. Aspirin-related side effects were dyspepsia (reported by four patients), heartburn (by seven), nausea and vomiting (by four), and melena (by five); nicardipine-related side effects were transient hypotension (by two), headache (by four), ankle edema (by three), and constipation (by four). Results indicate that the addition of nicardipine to antiplatelet treatment may safely prevent the recurrence of ischemic cerebrovascular events.
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PMID:Nicardipine in the prevention of cerebral infarction. 222 48

Aspirin has been tested for its benefit in preventing cardiovascular disease in randomized trials in three categories of patients. In secondary prevention among those with a history of myocardial infarction (MI), stroke or transient cerebral ischemia, or unstable angina pectoris, 25 randomized trials demonstrated significant reductions from aspirin of 25% for the occurrence of an "important vascular event" (nonfatal MI, nonfatal stroke, or vascular death), 32% for nonfatal MI, 27% for nonfatal stroke, and 15% for vascular mortality. Among those evolving an MI, the Second International Study of Infarct Survival (ISIS-2) showed a significant reduction of 23% in five-week vascular mortality among those started on a one-month regimen of daily aspirin within 24 hours of the onset of symptoms of suspected MI. Aspirin also significantly reduced reinfarction, nonfatal stroke, and important vascular events. Finally, in primary prevention, the US Physicians' Health Study (PHS) showed a significant 44% reduction in the occurrence of a first MI among apparently healthy male physicians; numbers of strokes and vascular deaths were insufficient to permit conclusions for these endpoints. Thus, aspirin is of clear benefit in reducing MI, stroke, and vascular death in secondary prevention and among those evolving an MI. It is also beneficial in the primary prevention of MI among men over 40, but data concerning its effects on stroke and vascular death remain inconclusive.
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PMID:Prevention of cardiovascular disease: risks and benefits of aspirin. 223 Oct 66


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