Because transient ischemic attack (TIA) predisposes to stroke, its prevention (modification of lifestyle as outlined in Chapter 24 and therapy for hypertension, hyperlipidemia, and other cerebrovascular risk factors, cardiac disease, and carotid stenosis) and treatment (surgical, endovascular, medical, or lifestyle modification) reduce the risk for subsequent cerebrovascular events. Patients must be aware that it is important to get immediate medical consultation whenever the warning signs of acute ischemic cerebrovascular disease occur (see Appendix E-1 and Chapter 12). Warning signs include sudden weakness or numbness of the face, arm, and leg, especially on one side of the body; sudden darkening or loss of vision, particularly in one eye; loss of speech or trouble talking or understanding speech; and sudden unexplained dizziness, unsteadiness, double vision, or sudden fall, especially along with any of the other symptoms.

The evaluation and treatment of TIA are outlined in Chapters 12 and 16.

Because cardiac diseases (particularly arrhythmias, congestive heart failure, valvular disease, myocardial infarction, atrial septal defects) predispose to stroke, prevention and specialized treatment of these cardiovascular contributors can be anticipated to reduce the occurrence of stroke. (The specific treatment of patients with cardiac disorders that are already causing TIA or stroke is outlined in Chapter 16.) For primary prevention, smoking cessation, dietary adjustment and weight control, physical exercise, and control of hypertension and blood lipid abnormalities (in particular, reducing elevated levels of total and low-density lipoprotein cholesterol and increasing the high-density lipoprotein cholesterol fraction) are of benefit. Aspirin, 75 to 100 mg daily, may reduce the risk for ischemic heart disease in selected patients, particularly those with risk factors. Individual decisions are required regarding therapy for specific cardiac diseases (see also Chapter 16).

Among cardiac arrhythmias, atrial fibrillation (the estimated lifetime risk of developing atrial fibrillation/flutter is 25%) is the most powerful risk factor for embolic brain infarction by increasing its risk by fivefold. Therefore, every attempt should be made to restore sinus rhythm in appropriate cases, preferably with electric or pharmacologic cardioversion, especially if atrial fibrillation is of recent onset (<48 hours). Many issues must be considered before cardioversion is performed, such as the potential for maintaining sinus rhythm after the procedure, the benefit of cardioversion, and risk for adverse complications, including risk for systemic embolic events. The best candidates for long-term successful cardioversion are
patients who have short-term atrial fibrillation with no significant atrial enlargement and with minimal coronary artery disease. Conversion of atrial fibrillation to a normal rhythm is associated with risk for embolization, which often occurs within 48 hours after conversion. Therefore, anticoagulant therapy with heparin should usually precede cardioversion, especially in patients with associated mitral valve disease, cardiac enlargement, congestive heart failure, or previous embolization. People without previous heart disease and embolization may be exempted from such heparin therapy if transesophageal echocardiogram shows no thrombus in the heart. If acute cardioversion has failed, it is usually recommended to repeat cardioversion after 3 to 4 weeks of anticoagulation with warfarin. If sinus rhythm is not restored, long-term stroke prevention through anticoagulation with aspirin (for “low stroke risk” people) or vitamin K antagonists (such as warfarin) or nonvitamin K antagonists oral anticoagulants (such as apixaban, dabigatran, or rivaroxaban) for “high stroke risk” people should be considered.

Stroke risk is usually determined by the CHA₂DS₂-VASc scale with the scoring as shown in Table 28-1 (see for details regarding the CHA₂DS₂-VASc scale).
The stroke risk may be determined based on the total score. In general, a score of 0 for males and 1 for females indicate “low stroke risk,” 1 or more for males and 2 or more for females indicate “low to moderate stroke risk,” and higher scores indicate high risk. All nonvitamin K antagonists oral anticoagulants listed above were shown in large randomized controlled trials to be at least noninferior to warfarin in reducing the risk of ischemic stroke and have a lower risk of intracranial hemorrhage in patients with nonvalvular atrial fibrillation. In addition, unlike warfarin, they do not require laboratory tests to monitor their effect.