Sharyl R. Martini, MD, PhD and Thomas A. Kent, MD

1. What is stroke? How common is stroke? How common is it in the setting of cardiac disease?

    Stroke is a focal disturbance of blood flow to the brain. Stroke is not a single disease but the end result of many different pathophysiologies leading to cerebrovascular occlusion or rupture. It can be classified as either primarily ischemic (80%) or hemorrhagic (20%). Ischemic strokes can develop a hemorrhagic component, termed hemorrhagic conversion, especially if the stroke is large. There are approximately 700,000 strokes per year in the United States, and it is the leading cause of disability. The biggest risk factor for stroke is prior stroke, and the second biggest risk factor is age. Risk factors common to both stroke and atherosclerotic cardiac disease include hypertension, diabetes, and smoking. In addition, cardiac diseases such as atrial fibrillation and valvular disease are risk factors for stroke. Strokes occur after cardiac procedures at a rate of 0.7% to 7%, depending on the procedure, and may be due to intrinsic disease or emboli or microemboli from the procedure itself.

2. What is a transient ischemic attack, and why is the clinical recognition of it important?

    Transient ischemic attack (TIA) is a neurologic deficit that, by definition, resolves within 24 hours, although most resolve within 5 to 15 minutes. It is important to identify TIAs because they represent an opportunity to intervene with appropriate strategies to prevent future strokes and permanent disability. Ninety-day stroke rates for patients with TIA are in excess of 10% in some series, with the greatest risk within the 48 hours to first week after the TIA. Longer duration, a lesion on diffusion-weighted magnetic resonance imaging (MRI), and the presence of large cerebral artery stenosis (seen on carotid duplex, computed tomographic [CT], or magnetic resonance [MR] angiography) are all associated with a higher risk of stroke following TIA.

3. What are the major causes of stroke and TIA?

    The major etiologies of ischemic stroke are cardioembolism, small vessel vasculopathy leading to lacunar stroke, and large vessel atherosclerosis (including intracranial atherosclerotic plaque rupture, as well as embolization from large arteries, such as the carotid, vertebral, and basilar arteries, to cerebral arteries [Fig. 59-1 and Table 59-1]). Hemorrhagic strokes include subarachnoid hemorrhage (usually due to aneurysm rupture) and intraparenchymal hemorrhage. Intraparenchymal hemorrhages are classified by their location: subcortical (associated with uncontrolled hypertension in 60% of cases) versus cortical (more concerning for underlying mass, arteriovenous malformation, or cerebral amyloid angiopathy; see Fig. 59-1). Figure 59-2 summarizes the major causes of stroke and their relative frequency.

    Among the other potential causes of stroke, dissection of the blood vessels needs to be considered, especially if there is face or neck pain or a history of trauma. Illicit drug use is a possible cause of either ischemic stroke (cocaine-, stimulants-, or “bath salts”–induced spasm) or hemorrhagic stroke (as a result of vascular injury or sudden massive increase in blood pressure). Patent foramen ovale (PFO) remains a controversial cause of stroke (see Question 18). Other, rarer, causes of stroke include hypercoagulable states (e.g., lupus and antiphospholipid antibody syndrome) and genetic disorders, such as homocystinuria and fibromuscular dysplasia.

4. How are stroke and TIA diagnosed?

    Stroke and TIA are diagnosed clinically, and no imaging correlation is usually required for the diagnosis, although imaging procedures are performed to rule out other causes, such as tumor. Focal neurologic deficits with sudden onset should be considered as a vascular event until proven otherwise because of the possibility of recurrence or progression of the deficit. Focal weakness, numbness, facial asymmetry, or speech difficulties are classic presentations. Altered level of consciousness, vertigo, and cranial nerve deficits are often seen with vertebrobasilar-brainstem strokes. See Table 59-1 for lists of the clinical signs and symptoms of the major subtypes of stroke: large vessel atherosclerosis and thrombosis, cardioembolic stroke, and small vessel stroke.

5. What should be done in cases of suspected stroke or TIA?

    A head CT must be performed immediately to distinguish ischemic from hemorrhagic strokes (see Fig. 59-1) because these are managed very differently. The CT itself does not diagnose stroke; it is primarily used to rule out causes other than ischemic stroke, including hemorrhagic infarction, tumor, subdural hematoma, and other causes. Figure 59-1 demonstrates the CT findings of strokes and stroke mimics.

    In cases of suspected stroke, one should page the stroke team (when one exists) or the service responsible to rapidly address stroke—every minute counts. Immediately check blood glucose because hypoglycemia or hyperglycemia can cause focal neurologic deficits mimicking stroke. Also obtain an electrocardiogram (ECG) and basic blood analysis (complete blood cell count, coagulation studies, and renal/electrolyte panel). The ECG and cardiac workup initially can reveal atrial fibrillation or the surprisingly common coexistence of various kinds of acute cardiac syndromes with stroke.

6. How are ischemic acute strokes treated?

    Three possible treatments are now suggested to improve outcomes after acute ischemic stroke: (1) intravenous tissue plasminogen activator (tPA); (2) aspirin; and, in the case of large strokes, (3) hemicraniectomy performed before clinical herniation.

tPA

The only medication approved by the U.S. Food and Drug Administration (FDA) for acute ischemic strokes is intravenous (IV) tPA, administered within 3 hours of symptom onset. Based on the European Cooperative Acute Stroke Study III (ECASS III), American Heart Association (AHA) guidelines recommend treatment with IV tPA in selected patients out to 4.5 hours after symptom onset, but this is not yet approved by the FDA. Note, however, that the earlier tPA is given, the better the clinical outcome. The greatest benefit of tPA occurs at earlier time points. It is critical to give tPA as soon as possible if head CT does not reveal signs of hemorrhage or hypodensity. Only tPA is approved for acute stroke thrombolysis. Only eight stroke patients need to be treated with IV tPA to result in one patient with complete or near-complete recovery, and this number needed to treat (NNT) takes into account the increased risk of hemorrhage after tPA administration. Patients of any age benefit from tPA. Contraindications to IV tPA for the treatment of stroke are given in Box 59-1. Although tPA administration is not contraindicated in the setting of moderately elevated international normalized ratios (INR of 1.3-1.7), recent studies suggest an increased risk of brain hemorrhage compared to tPA administraton with a normal INR. Importantly, patients who have their strokes after cardiac catheterization and who meet these criteria may still benefit from tPA, despite the recent administration of heparin and glycoprotein IIb/IIIa inhibitors, although this is outside the usual protocols and should be done only with expert help. In this situation, various treatments have been reported, including intraarterial therapy or IV abciximab, but these uses remain investigational.