Preventing Stroke in Patients with Transient Ischemic Attacks

Author: Melody Ryan, Laroy P. Penix
Date: Nov 15, 1999

Stroke is the third most common overall cause of death and the leading cause of adult disability in the United States. New therapeutic interventions instituted in the period immediately after a stroke have revolutionized the approach to ischemic cerebrovascular disease. Recognition of a transient ischemic attack provides an opportunity to prevent a subsequent stroke. Specific stroke prevention treatment depends on the cause of the transient ischemic attack, its cerebrovascular localization and the presence of associated coexisting medical problems. Modification of stroke risk factors is the principal therapeutic approach. Antiplatelet agents and anticoagulants have been shown to be effective in reducing the occurrence of stroke in certain populations. Several well-designed studies have recently demonstrated the effectiveness of carotid endarterectomy in preventing strokes related to extracranial carotid artery disease. (Am Fam Physician 1999;60:2329- 41.)

Approximately 550,000 new strokes and 150,000 stroke-related deaths occur each year in the United States.(1) About 80 percent of strokes are due to ischemic cerebrovascular disease, and the rest are attributable to hemorrhagic causes such as subarachnoid or intracerebral hemorrhage.(1) Even though great strides have been made in the identification and treatment of risk factors for stroke and the development of new therapeutic interventions, ischemic stroke continues to be a significant public health problem.

A completed stroke is caused by irreversible brain injury secondary to the interruption of blood flow. In contrast, a transient ischemic attack (TIA) is a temporary focal neurologic deficit caused by the brief interruption of local cerebral blood flow. The prevalence of TIAs ranges from 1.6 to 4.1 percent, depending on gender and age. Stroke occurs in one third of patients who have a TIA.(2)

The duration of a focal neurologic deficit that leads to cerebral infarction has arbitrarily been determined to be 24 hours or greater. Any focal neurologic deficit that resolves completely within 24 hours is considered a TIA.(3) However, a TIA in the carotid territory typically lasts only seven to 10 minutes.(3) The diagnosis of a TIA indicates that no irreversible neurologic injury has occurred and provides an excellent opportunity to prevent permanent damage.

Differential Diagnosis and Symptoms

The first step in the evaluation of a patient with possible TIA is to determine if the event in question actually represents a TIA. Table 1 lists conditions that can present with focal neurologic deficit and are sometimes confused with TIAs. These conditions should be ruled out before the diagnosis of TIA is made. Excluding other diagnoses reduces the possibility of inappropriately labeling a patient with the diagnosis of cerebrovascular disease and launching into a course of costly and potentially dangerous diagnostic testing.

The symptoms of a TIA depend on the region of the brain that is supplied by the transiently occluded cerebral artery. Precise localization may be difficult because anatomic variations, especially in the arteries that form the circle of Willis, are the rule rather than the exception. The clinical findings most frequently associated with ischemia in various arterial distributions are listed in Table 2. However, other symptoms may occur, and many other clinical stroke syndromes have been described.

If a TIA is recognized, steps can be taken to prevent future ischemic stroke. All TIAs should be promptly investigated because the risk of ischemic stroke is highest soon after a TIA (i.e., 5 percent in the first month).(4)

Diagnostic Evaluation

INITIAL TESTS

The goals of diagnostic testing are to identify or exclude causes of TIAs that require specific therapy, to assess modifiable risk factors and to determine the prognosis.(4) The initial tests recommended for all patients with TIA are listed in Table 3.(4)

The complete blood count with differential rules out profound anemia, polycythemia, leukocytosis, thrombocytopenia and thrombocytosis as hematologic causes of stroke or as factors that may influence therapy. The chemistry profile demonstrates hypoglycemia that can present with focal neurologic deficits or hyperglycemia that can worsen the outcome after stroke.(5)

A prothrombin time and an activated partial thromboplastin time are needed to rule out coagulopathies. The erythrocyte sedimentation rate serves as a screening test for autoimmune disorders, and syphilis serology screens for neurosyphilis.

An electrocardiogram (ECG) should be obtained in all patients with TIA or stroke. The ECG is used to detect arrhythmias (e.g., atrial fibrillation) as the cause of ischemia. Computed tomographic (CT) scanning of the head is necessary to rule out intracranial bleeding or tumors. CT evidence of old infarcts, if present, may reveal the vascular distribution of previous ischemic events.

Cerebrovascular ultrasound studies are recommended in all patients with TIA symptoms. These tests are noninvasive but have some limitations. Carotid duplex studies (e.g., Doppler plus B-mode imaging) detect extracranial carotid disease well but may miss intracranial carotid artery disease, vertebral artery disease and complete occlusion.

ADDITIONAL TESTS

One or more of the tests listed in Table 4(4) may be performed in patients with TIA. Transthoracic and transesophageal echocardiographic examinations do not usually reveal a cause for TIA unless the patient has clinical heart disease. Nonetheless, transthoracic echocardiography is almost always employed in younger patients and in patients for whom no other cause of TIA can be found.(4) This examination may also be helpful in identifying atrial thrombus in patients with atrial fibrillation. Transesophageal echocardiography may be useful in confirming suspected atrial appendage thrombus, valvular defects, atrial septal defects, mitral valve vegetation and atrial septal aneurysms.

Transcranial Doppler ultrasonography can reveal intracranial stenosis of the trunks of the middle cerebral or posterior cerebral arteries. However, stenotic lesions in smaller branches may be missed.

More recently, magnetic resonance angiography has been used to detect stenosis in extracranial or intracranial cerebral arteries. Arteriography is usually reserved for special situations such as intracranial vasculitis or arterial dissection.(4) This study is also performed when cerebrovascular surgery is being considered.(4) Although arteriography is expensive and invasive, it is the gold standard for defining occlusive cerebrovascular disease.

Special testing for hypercoagulable states should be reserved for use in patients less than 50 years of age, patients with a history of thrombotic disease and patients in whom no other cause of TIA is found.(4) Holter monitoring is recommended for use in patients who had palpitations close in time to the TIA and patients who have an enlarged left atrium.

Lumbar puncture is not routinely recommended as part of the evaluation of patients with TIA. However, this study may be warranted if central nervous system infection is suspected or the presenting symptoms suggest subarachnoid hemorrhage but the CT scan is negative.

Treatment

REDUCTION OF RISK FACTORS

Current theories on the pathogenesis of TIA suggest that effective measures to prevent stroke should also prevent the recurrence of TIA. The initial approach is to modify risk factors that are amenable to treatment (Table 5).(6-31) In this section, emphasis is placed on risk factors that have a definite correlation with the incidence of stroke.

The Stroke Council of the American Heart Association has recommended aggressive treatment of chronic hypertension to maintain the systolic blood pressure below 140 mm Hg and the diastolic blood pressure below 90 mm Hg.(4) However, even modest reductions in blood pressure (i.e., 9 mm Hg systolic and 5 mm Hg diastolic) can reduce the relative risk of stroke by about one third.(32) Comprehensive recommendations for the treatment of hypertension have been made by the sixth Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.(7)

Cigarette smoking is associated with an increased risk of stroke. Hence, patients should be strongly encouraged to stop smoking.(4)

The association of alcohol intake with stroke risk is dose-dependent. Some investigators have described a J-shaped curve for stroke risk, with a slightly increased risk of stroke in patients who are abstinent compared with those who consume moderate amounts of alcohol. Conversely, the risk of stroke is doubled in patients who consume three or more alcohol drinks per day.(33) Although absolute statements on alcohol consumption cannot be made based on the available data, heavy drinking should be discouraged.

TABLE 5Summary of National Stroke Association Recommendationsfor the Prevention of a First StrokeCondition RecommendationHypertension Follow the recommendations on lifestyle modification, initiation of specific therapy and multidisciplinary management strategies as given in the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.(7)Myocardial Use acetylsalicylic acid (aspirin) therapy in infarction patients with previous myocardial infarction or warfarin (Coumadin) to an International Normalized Ratio of 2.0 to 3.0 in patients with atrial fibrillation, left ventricular thrombus or significant left ventricular dysfunction.(8-12) Use statin agents after myocardial infarction in patients with normal to high lipid levels.(13-17)Atrial fibrillation[*] Use warfarin therapy in patients [greater than] 75 years of age with or without risk factors for stroke. In patients 65 to 75 years of age, use warfarin therapy in those with risk factors for stroke, and use warfarin or aspirin therapy in those without such risk factors. In patients [less than] 65 years of age, use warfarin therapy in those with risk factors and aspirin therapy in those without risk factors.(18)Diabetes mellitus Follow the recommendations of the American Diabetes Association(19) on controlling diabetes to reduce microvascular complications.(20) (Further studies are needed to determine if aggressive glycemic control lowers the risk of stroke.)Lipid levels Use statin agents in patients with high cholesterol levels and coronary heart disease,(13-17) and follow the guidelines of the National Cholesterol Education Program for the dietary and pharmacologic management of patients with hyperlipidemia or atherosclerotic disease.(21)Asymptomatic Use carotid endarterectomy in patients with carotid artery asymptomatic carotid stenosis of 60 percent or disease[[dagger]] greater (but less than 100 percent); surgical morbidity and mortality rates for the surgeon and institution should be less than 3 percent.(9, 22-27)Lifestyle factors Use measures to modify patients' smoking, alcohol consumption, physical activity and diet according to published guidelines.(28-31)[*]--Risk factors include previous transient ischemic attack, systemicembolism or stroke, hypertension and left ventricular dysfunction. Effortsto improve patient and physician awareness of the benefits and risks ofwarfarin therapy serve as a first step toward increasing appropriate use.In warfarin treatment, the goal is to achieve an International NormalizedRatio of 2.0 to 3.0, with a target value of 2.5.18[[dagger]]--Asymptomatic carotid artery stenosis of at least 60 percentshould be replicated in other studies.Adapted with permission from Gorelick PB, Sacco RL, Smith DB, Alberts M,Mustone-Alexander L, Rader D, et al. Prevention of a first stroke: areview of guidelines and a multidisciplinary consensus statement from theNational Stroke Association. JAMA 1999;281:1115.

COPYRIGHT 1999 American Academy of Family PhysiciansCOPYRIGHT 2000 Gale Group

 
© 2006, DrPlace.com, All Rights Reserved.