Transient Ischemic Attacks: A Neurologic Emergency?
March 1, 2008 4 minutes read
Transient Ischemic Attacks: A Neurologic Emergency?
Abstract & Commentary
By Dana Leifer, MD, Associate Professor, Clinical Neurology, Weill Medical College, Cornell University. Dr. Leifer reports no financial relationship relevant to this field of study. This article originally appeared in the February 2008 issue of Neurology Alert. It was edited by Matthew Fink, MD, and peer reviewed by M. Flint Beal, MD. Dr. Fink is Vice Chairman, Professor of Critical Care Neurology, NewYork-Presbyterian Hospital, and Dr. Beal is Professor and Chairman, Department of Neurology, Cornell University Medical College. Drs. Fink and Beal report no financial relationship relevant to this field of study.
Synopsis: Two recent studies suggest that rapid TIA evaluation and treatment can reduce stroke risk.
Sources: Lavallée PC, et al. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): Feasibility and effects. Lancet Neurology 2007;6:953-960; Rothwell PM, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): A prospective population-based sequential comparison. Lancet 2007;370:1432-1442.
Recent evidence suggests that there is a significant risk of stroke after transient ischemic attack (TIA) and that TIAs precede as many as a quarter of strokes. The risk of recurrent stroke in the first week after a TIA or minor stroke is as high as 10%. Nevertheless, patients with a TIA often do not receive a rapid, comprehensive evaluation. Two recent studies provide evidence that rapid intervention after TIA actually does reduce the risk of stroke.
In the SOS-TIA trial, Lavallée and colleagues randomized patients between standard medical care and rapid evaluation at a specialized TIA clinic located in Paris, France. This clinic was available 24 hours/day, 7 days/week. The clinic was advertised in mailings to physicians and emergency departments throughout the Paris metropolitan area. Patients received evaluation within 4 hours of admission, including examination by a vascular neurologist, CT or MRI, carotid duplex ultrasound, transcranial Doppler, and ECG. Echocardiography was performed when cardiac embolism was suspected. Blood tests, including fasting lipid panel and glucose, hemoglobin A1c, C-reactive protein, creatinine, and CBC, were performed. Patients who were not fasting returned at a later time for lipid studies and glucose measurement. Antithrombotic therapy was started in almost all patients, and therapy to lower blood pressure and cholesterol were begun, when appropriate. Patients with atrial fibrillation were admitted for anti-coagulation, and patients with high-grade carotid stenoses were admitted for revascularization.
During the three years of the study, 1085 patients were evaluated, with the number increasing from 316 in the first year to 407 in the last year. As expected from prior studies, symptoms were short in duration, with a median length of 10 minutes in the 535 patients with definite clinical TIAs and no brain damage on imaging, and 15 minutes in the 108 patients with definite clinical TIAs and brain tissue damage. The main finding was that the 90-day risk of stroke was only 1.24%; the expected risk based on ABCD2 scoring1 was 5.96%. When the sample was limited to the 552 patients seen within 24 hours of their TIA, the 90-day stroke risk was 1.63% compared to an expected risk of 6.49%. These results suggest that rapid evaluation of TIA patients is effective in reducing stroke risk, although the lack of a control group is admittedly a shortcoming of the study. The results appear to reflect a variety of interventions. Of those with TIA or minor stroke, 98% were started on antithrombotic therapy. Thirty patients were started on oral anticoagulation for atrial fibrillation. Antihypertensive therapy was started or modified in 28% of the 701 patients with definite TIA or minor stroke, and lipid-lowering therapy was started or modified in 45%. Carotid revascularization was performed in 43 patients, with a median delay of 6 days.
Another recent study by Rothwell and co-workers provides additional evidence for the efficacy of rapid evaluation of TIA patients. In the initial baseline period, TIA patients were referred to a specialized clinic but received scheduled appointments, with a median delay of 3 days from referral. Subsequent tests were generally scheduled within a week of the initial clinic appointment, and treatment recommendations were made to the referring physician but not started by the TIA clinic. In the second phase of the study, referring physicians were instructed to send suspected TIA patients directly to the clinic on a walk-in basis. Antithrombotic treatment was begun in the clinic after brain imaging, which was performed on the day of evaluation in the clinic when appropriate. The main finding was that the 90-day risk of stroke fell from 10.3% in the first phase to 2.1% in the second phase (P = 0.0001). The findings appear to reflect several differences in treatment between the two phases. At 30-day follow-up, patients in the second phase were more likely to be receiving statin treatment, to be on antihypertensive therapy, and to be treated with aspirin and clopidogrel in combination. Mean blood pressures were lower at 30 days in phase 2. Similar numbers of patients underwent carotid surgery, but surgery was performed more quickly in phase 2.
In conclusion, these two papers both provide evidence that rapid evaluation and treatment (within 24 hours) of TIA patients are likely to reduce the risk of stroke. The results suggest that additional efforts to educate the general population and health care providers about the importance of dealing with TIAs as an emergency will reduce the incidence of stroke.
Reference
1. Johnston SC, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369:283-292.
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