Carotid and vertebral‐basilar transient ischemic attacks: Effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence— A population study

Whisnant, Jack P.; Niall, E. F. Cartlidge; Elveback, Lila R.

doi:10.1002/ana.410030204

Cited by 182 publications

(62 citation statements)

References 6 publications

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“…3 In spite of the fact that the differences did not reach significant levels because of the low overall number of IBIs in the present series, IBIs were more than twice as common among the patients with either arterial hypertension, heart disease, or diabetes compared to those patients without these disorders. Recently Whisnant and others 19 have shown that TIA patients with high diastolic pressure had a significantly higher net probability of stroke than those with lower values and those under antihypertensive therapy.…”

Section: Discussionmentioning

confidence: 94%

Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

Harris¹,

Bayhan²,

Branston³

et al. 1982

Stroke

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The effect of indomethacin (3mg/kg IA) preloading on the pathophysiology of a model of acute cerebral ischaemia has been tested. Primates anaesthetised with alpha-chloralose were used. Indomethacin reduced basal blood flow by 39% and reduced CO2 reactivity by 71%. Water content changes of the cerebral cortex and relationships between blood flow and extracellular potassium (Ke), and calcium (Cae) activities have been measured. Indomethacin infusion did not effect the water content of the left side but there was more water in all regions of the right hemisphere which were rendered ischaemic. There water increases were significant for blood flows greater than 5ml/100g/min in exposed areas. There was a significant increase in the flow thresholds for change in Ke and Cae. Possible mechanisms for these changes have been discussed.

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Section: Discussionmentioning

confidence: 94%

Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

Harris¹,

Bayhan²,

Branston³

et al. 1982

Stroke

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“…The risk of ICH increases with the duration of anticoagulant therapy 28 ; one study reported that 70% of ICHs occurred <1 year after the start of anticoagulant therapy, but the authors did not mention the average duration of anticoagulant therapy for all patients. 2 It is not clear how anticoagulants induce ICH.…”

Section: Resultsmentioning

confidence: 99%

Intracerebral hematomas during anticoagulant treatment.

Franke

Jonge

Swieten

et al. 1990

Stroke

189

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We retrospectively studied 79 patients from three centers who suffered an intracerebral hemorrhage during treatment with anticoagulants and compared them with 84 patients from one center who suffered a spontaneous intracerebral hemorrhage without anticoagulant treatment Mortality after 30 days was slightly higher in patients with anticoagulant treatment (67%) than in those without (55%), and the proportion of patients who attained moderate or complete recovery was slightly smaller in the treated group (22% and 36%, respectively); neither difference was statistically significant. Volume of the supratentorial hematoma was measured from computed tomograms in 70% of the patients in both groups and was significantly greater in the 55 patients treated with anticoagulants than in the 59 patients not so treated. Volume was not related to the degree of anticoagulation. Based on the total number of patients treated with anticoagulants in the Heerlen region, we conclude that for patients older than 50 years of age the risk of intracerebral hemorrhage during anticoagulant treatment is increased approximately eightfold but is unrelated to the degree of anticoagulation. Our results suggest that intracerebral hemorrhage is more frequent and more extensive in patients treated with anticoagulants but that once it has occurred in such patients intracerebral hemorrhage is not significantly more serious than in untreated patients. (Stroke 1990;21:726-730) T he occurrence of intracerebral hemorrhage (ICH) in patients treated with anticoagulants is a serious complication, often fatal. The risk of ICH in patients >50 years of age who have been treated with anticoagulants is estimated to be 10 times that in untreated subjects of the same age.1 In that study, outcome in treated patients was not different from that in untreated patients, but ICH was diagnosed mainly on clinical grounds. Additionally, it is uncertain whether the risk of ICH is related to the duration and degree of anticoagulation. According to some studies the risk is greatest during the first 6 months, 2 whereas other workers have found that most ICHs occur after at least 1 year of anticoagulation.1 Though ICH in patients receiving anticoagulants often results from overtreatment, many authors have reported a therapeutic degree of anticoagulation at the moment of the bleeding. Received June 23, 1989; accepted January 9, 1990. has not yet been studied in relation to the use of anticoagulants.The purpose of our retrospective study, which we believe is the largest of its type, was to examine the influence of anticoagulation treatment on the risk of ICH, the volume of the hematoma, and the clinical course compared with patients suffering an ICH who were not treated with anticoagulants.

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“…Symptoms of VB insufficiency were defined as those typically referable to the posterior fossa circulation, such as bilateral motor or sensory symptoms, diplopia, dysarthria, gait ataxia, dysmetria, homonymous hemianopsia, and drop attacks. [17,27] Patient age ranged from 45 to 76 years (average 63 years). Four patients were men and two were women.…”

Section: Clinical Materials and Methodsmentioning

confidence: 99%

Stent placement for vertebral artery occlusive disease: preliminary clinical experience

Fessler¹,

Wakhloo²,

Lanzino³

et al. 1998

FOC

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Symptoms of vertebrobasilar insufficiency may precede neurological sequelae in up to 50% of patients. Although select patients may benefit from microsurgical revascularization, combined perioperative morbidity and mortality rates can be as high as 20%. The authors present their preliminary clinical experience using stent placement for symptomatic vertebral artery (VA) occlusive disease. Six patients with clinical symptoms of vertebrobasilar insufficiency in whom VA stents were placed from 1995 to 1998 were identified. Diagnostic four-vessel cerebral angiography identified causative stenotic, atherosclerotic lesions in all cases. A transfemoral or transradial artery approach after the patient had undergone full heparinization was chosen for endovascular stenting. Guidewire placement across the lesion followed by urokinase infusion preceded stenting. Prestent angioplasty was performed in two patients. Following the procedure, all patients were maintained on daily antiplatelet therapy. Patient age ranged from 45 to 76 years (average 63 years). Four patients were men and two were women. Angiography revealed greater than 95% stenosis in five patients and greater than 70% stenosis in one. Three patients had complete occlusion of the contralateral VA; in one other, the VA supplied only the posterior inferior cerebellar artery; and the remaining two patients had VAs with greater than 70% stenosis. Ten stents were placed in six patients for five VA origin lesions and one distal VA stenosis. A VA dissection occurring poststenting was treated by placement of three additional stents. One patient had transient double vision. All had resolution of their presenting symptoms. Follow up ranged from 1 to 24 months (average 8.4 months). Angiograms obtained in four patients at least 3 months postprocedure have revealed stent patency in all cases without evidence of restenosis. Vertebral artery stent placement can be safely performed and is a viable treatment option for carefully selected patients with vertebrobasilar insufficiency.

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Carotid and vertebral‐basilar transient ischemic attacks: Effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence— A population study

Cited by 182 publications

References 6 publications

Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

Intracerebral hematomas during anticoagulant treatment.

Stent placement for vertebral artery occlusive disease: preliminary clinical experience

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