Prognosis in patients with transient cerebral ischemic attacks

SUMMARY A total of 462 patients (mean age 52 years) affected by reversible focal ischemic attacks (RIAs) were followed prospectively in 8 neurologic institutions in Italy for 4 years. All cases were evaluated with a cerebral angiography and 21 % of angiograms were normal. At the end of the follow-up period the cumulated probability for death, stroke, cardiac event and new RIA was respectively 7%, 8%, 3% and 36%.The predictive value of the baseline characteristics of this series was evaluated by a mul tifactorial analysis which showed that RIA and stroke (specific cerebrovascular risk) were more likely to develop In patients with a history of more than one RIA and in those in whom multiple vascular territories were involved. Moreover, previous myocardial infarction, Intermittent claudkation, angina pectoris, time elapsed since the first attack, and duration and severity of the attack Itself were independently associated with general cardiovascular risk (death, stroke and myocardial infarction). We conclude that predictive factors, and thus also pathogenetic mechanisms, may be different for general cardiovascular risk and specific cerebrovascular risk in RIA patients.

Section: Discussionsupporting

confidence: 92%

“…Published stroke and death rates vary from less than !%,'• 2 to almost 25%. 3 Surgeons tend to report lower figures, 4 " 8 while higher rates emerge from citywide 39 or multi-centre experience, 10 usually reported by neurologists.…”

mentioning

confidence: 98%

Italian multicenter study on reversible cerebral ischemic attacks: VI--Prognostic factors and follow-up results.

Candelise¹,

Vigotti²,

Fieschi³

et al. 1986

“…5 Patients with TIA within the vertebrobasilar system have a good prognosis, 14 whereas patients with carotid symptoms have a poor prognosis. 10 However, the prognosis of patients with hemiparesis manifested from the vertebrobasilar territory is as bad as that of those with carotid symptoms, 18 while on the contrary, patients with vertebrobasilar symptoms have more TIAs without having completed strokes. 6 Patients with TIA can be treated medically with anticoagulants, 21 or sulfinpyrazone (which has recently been suggested).…”

Section: Discussionmentioning

confidence: 99%

Long-term anticoagulant therapy for TIAs and minor strokes with minimum residuum.

Olsson¹,

Müller²,

Berneli³

1976

One hundred seventy-eight patients with transient ischemic attacks (TIAs) or small strokes with slight symptoms persisting for more than 24 hours (incomplete recovery = IR) (TIA-IR) from both the carotid and the vertebrobasilar systems were treated with anticoagulants. Ten patients stopped the treatment because of severe side effects. Only one patient had a lethal cerebral infarction when the thrombotest values were above the therapeutic level; no other infarction happened during the treatment period. Moreover, the frequency of TIA decreased during the treatment, compared with descriptions of the natural course of TIA. One hundred four patients were observed for a mean of 21 months after the anticoagulant treatment ended. During the observation period, six patients had cerebral infarctions. This was a sixfold increase compared with the stroke incidence during treatment, and was almost identical with the incidence of strokes seen during the natural course of TIA. All the cerebral infarctions were in patients who had their initial TIA/TIA-IR from the carotid territory (within the same carotid artery which earlier had given symptoms). The investigation shows that long-term anticoagulant treatment is useful, especially in patients with carotid TIA/TIA-IR, and that this treatment should continue as long as the patients can manage it. In patients with vertebrobasilar symptoms of malignant character, it seems feasible to terminate the treatment after about one year. The mechanism of the anticoagulant treatment is obscure, but it does not appear to influence the progress of the atherosclerotic process.

“…There is no uniformity of opinion on the incidence of complications when anticoagulant is used to treat TIA. In the study of focal transient cerebral ischemic attacks reported by Baker and colleagues, 6 there were no serious complications of anticoagulant therapy. In 5-year follow up studies at Mayo Clinic 1 5% of treated patients developed intracerebral hemorrhage; however, 4% of patients not receiving anticoagulant also died of an intracerebral bleed.…”

Section: Treatment Related To Blood Constituentsmentioning

confidence: 86%

“…To evaluate how well the objectives of therapy for transient focal cerebral ischemic attacks have been accomplished, it is first necessary to understand fully the variable natural history of the disorder and realize the necessity to compare the results of any form of treatment with the observations of a similar group of patients not undergoing therapy. The natural history Pearce, et al 4 Baker, et al 6 Baker, et al 6 Friedman, et al 7 Marshall 8 Ziegler and Hassanein 9 Goldner,* et al 10 Whisnant, et al 11 Marshall 12 Olsson et al 13 Number •Goldner, Whisnant and Taylor reported on 140 TIA patients followed 15'years. Table 1 gives occurrence of stroke in 111 patients' of these attacks is so variable that no significant judgment can be made about the efficacy of a therapy from simple observations of an occasional patient.…”

Section: Principles Of Therapymentioning

confidence: 99%

Treatment of transient ischemic attacks.

Millikan¹,

McDowell²

1978

SUMMARY Transient ischemic attacks are the most important warning symptoms of impending stroke. They occur in up to one-half of all patients who develop stroke but, unfortunately, less than half of the patients who have them seek help from their physicians before stroke occurs. Physicians should regularly question patients about the possibility of such symptoms and patients with them should seek prompt help. When transient ischemic attack is diagnosed, patients should be evaluated for elevated blood pressure, hyperlipidemia, cardiac dysrhythmia, cardiac disease, anemia, polycythemia and thrombocytosis. When these conditions are found they should be treated. Patients with carotid system TIAs should be evaluated clinically and radiologically for evidence of vascular disease. The neck should be auscultated for bruit and absent pulses and the peripheral vessels palpated. Patients with carotid system TIAs should have angiography of all 4 cerebral vessels and the angiogram should be evaluated for the presence and number of arterial stenoses and the presence of ulcerated plaques. When patients with carotid system TIAs are found to have localized extracranial atherosclerotic obstruction or ulcerated plaques in a vessel appropriate to the side of their symptoms of cerebral ischemia, they should be considered for prompt surgical correction of the lesion. For patients with carotid system TIAs, who have multiple sites of extracranial vascular disease, medical treatment is advisable with either anticoagulants or platelet antiaggregating agents. In view of the recently reported favorable results using aspirin in the prevention of TIA and stroke, this agent may be preferable to anticoagulants in instances where hypertension, patient compliance and laboratory facilities are a problem.