Treatment program and comparison between anticoagulants and platelet aggregation inhibitors after transient ischemic attack.

Burén, A; Ygge, J

doi:10.1161/01.str.12.5.578

Cited by 46 publications

(14 citation statements)

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“…[28][29][30][31][32][33][34] Twelve studies (n = 6310 patients) met the inclusion criteria (Appendix). 13,[15][16][17][18][19][20][21][24][25][26][27] The mean age of patients was 63.1 (SD ± 3.57) years. The mean follow-up was 22 months ( Moderate intensity OAC versus APT Of eight studies in which OAC were compared with APT, seven studies (n = 4464) were classified as moderate intensity (INR 2.1-3.6) and one as high (INR 3-4.5).…”

Section: Resultsmentioning

confidence: 99%

Oral anticoagulants and non-cardioembolic stroke prevention

2008

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Section: Resultsmentioning

confidence: 99%

Oral anticoagulants and non-cardioembolic stroke prevention

2008

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“…Table 2 also summarizes outcome by type and stability of ischemic event: TIA; TIA or minor stroke (the minor stroke cases of Bradshaw and Brennan 16 cannot be separated from their TIA cases); embolism; stable stroke; and all strokes thrombotic 5 Baker et al, 6 Hill et al, 7 -8 National Cooperative Study, 910 Veterans Administration Cooperative Study," Enger and Boyesen, 14 Pearce et al, 15 Bradshaw and Brennan. 16 Studies begun in 1974 or later: Buren and Ygge, 17 Olsson et al, 18 Garde et al, 19 Cerebral Embolism Study, 20 Duke et al 21 ACT, anticoagulant therapy; C, control; <, worse than; >, better than; NS, difference not significant. or embolic, stable or evolving.…”

Section: Pooled Resultsmentioning

confidence: 99%

Anticoagulant therapy in cerebrovascular disease: review and meta-analysis.

Jonas

1988

Stroke

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Sixteen acceptably randomized studies of anticoagulant therapy after cerebral or retinal ischemia or infarction are reviewed and the results among 1,046 anticoagulated patients and 1,071 controls are analyzed. The following conclusions are derived. 1) Anticoagulant therapy has not been shown to be better than control management after transient ischemia or nonprogressing ischemic stroke; this is true whether the control management was deliberately ineffectual treatment (generally studies completed in 1974 or earlier) or platelet antiaggregant therapy (pooled results of three recent studies). 2) Although a study done 30 years ago demonstrated no benefit, a recent study showed benefit from anticoagulant therapy in patients who had had cerebral emboli of cardiac origin; additional controlled data are needed. 3) There is evidence that patients with thrombosis in evolution might benefit from anticoagulant therapy; additional controlled data are needed. (Table 1). Materials and MethodsStudies were found through computerized search, direct search of the cumulative Index Medicus, suggestions from colleagues, and review of references in articles already discovered. Being well aware that an analysis such as this, especially when the work of one person, can suffer from error, incompleteness, and bias, 22 I solicit references to studies I have missed and alternative interpretations of the data I have summarized. I will, on request, provide more extensive notes on my own interpretations, as well as the various calculations.Where possible, I have used the end points of stroke or death (S + D) occurring during observation. The overall expected S + D per patient-month of observation for a given (arm of a) study is the sum of S + D for the treated and control groups divided by the sum of the patient-months for the two groups. This overall expected S + D rate multiplied by the patient-months of observation for each group separately gives the expected S + D for each group. Significance is defined as /?<0.05. Where feasible, I have pooled the S + D results for meta-analysis. Certain studies present results in forms not suitable for S + D analysis and are therefore not amenable to meta-analytic pooling; the authors' end points are given for these studies and the authors' analyses of significance are recorded. Table 2 summarizes the S + D results from 10 studies in which patients with stroke and transient ischemic attacks (TIAs) were randomized to ACT or to deliberately ineffectual treatment (placebo, no treatment, or deliberately ineffectual doses of anticoagulants). Among 20 identifiable groups or subgroups from these 10 studies there is one (the Cerebral Embolism Study 20 ) in which the ACT outcome was significantly better than control. In three other instances (the completed stroke and embolism groups from the National Cooperative Study 910 and the male stroke group from the Veterans Administration Cooperative Study") the ACT results were significantly worse than control. In the other 16 groups or subgroups the difference between...

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“…7 It is also well known that the risk of perioperative stroke is increased in these patients. Two comparatively new developments, however, are re ported to affect operative risk.…”

Section: Concomitant Medical Diseasementioning

confidence: 99%

Section: Availability Of Nonsurgical Prophylactic Treatmentmentioning

confidence: 99%

“…One recent random ized study of anticoagulants and platelet aggregation inhibitors in TIA patients found only 3.3% of antico agulated patients to have sustained cerebral infarction during a two-year follow-up. 7 More interest in recent years has centered on the use of the antiplatelet-aggregating agents, such as aspirin, dipyridamole, and sulfinpyrazone, in ischemic cere brovascular disease. Four prospective controlled stud ies summarized by Dyken in 1979 8 reported decrease in transient ischemic attacks, cerebral infarction, and death in the groups treated with aspirin, and two more recent studies support these results.…”

Section: Availability Of Nonsurgical Prophylactic Treatmentmentioning

confidence: 99%

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Carotid lesions--to operate or not to operate?

Ziegler¹

1983

Stroke

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Ischemic cerebrovascular disease, a major public health problem, is accompanied, and possibly caused in a large percentage of cases, by extracranial arterial lesions. A rapidly expanding body of surgical litera ture records the success of procedures designed to re pair these lesions along with a decline in recent years in surgical mortality for such procedures. If an area of carotid abnormality is a constant threat to adequate cerebral blood flow, why not remove it? There is no fully documented analysis of replies to this important question, but the present view addresses five areas of study that may result in a postponement or rejection of the decision to operate. These areas are not mutually exclusive; rather, they are variables that interact and should be considered in conjunction. Availability of Nonsurgical Prophylactic TreatmentThere is little evidence that surgical or medical treat ment produces major reversals in deficits of cerebral function already caused by cerebral infarction. Treat ment is primarily directed toward prevention of future ischemic episodes. At the present time two medical treatments are available: anticoagulants and platelet aggregation inhibiting agents. No justice can be done here to the massive body of literature on prophylactic results with these agents; however, discussion of the surgical decision would be incomplete without a brief comment on the current status of medical treatment.Despite decades of study, the place of anticoagu lants in ischemic cerebrovascular disease remains un certain. Although several studies have reported the success of these agents in preventing further ischemic attacks, there are only four well-designed prospective controlled studies. One major problem, as in most studies of treatment of this condition, has been that of properly defining controls. All patients with transient ischemic attacks are not alike. The large number of variables that should be considered in stratifying pa tients has been thoughtfully discussed by Brust, 1 but no study has done this stratification completely. Uncer tainty persists as to the actual prognosis in various types of TIA patients. In one recent follow-up study of 314 patients with TIAs, there was an amazingly low 6 In summary, anticoagulation remains a viable alternative, particularly on a short-term basis, but there is still uncertainty about its role vis-a-vis surgery and the treatments discussed below. One recent random ized study of anticoagulants and platelet aggregation inhibitors in TIA patients found only 3.3% of antico agulated patients to have sustained cerebral infarction during a two-year follow-up. 7

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Treatment program and comparison between anticoagulants and platelet aggregation inhibitors after transient ischemic attack.

Abstract: TRANSIENT ischemic attacks (TIA) occur in 25-40 percent of patients who subsequently sustain a cerebral infarct. But not all of those afflicted consult a doctor before a stroke occurs.

Cited by 46 publications

References 5 publications

Oral anticoagulants and non-cardioembolic stroke prevention

Oral anticoagulants and non-cardioembolic stroke prevention

Anticoagulant therapy in cerebrovascular disease: review and meta-analysis.

Carotid lesions--to operate or not to operate?

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