Stroke affects more than 700,000 Americans each year, with approximately 85% of these being ischemic in nature.1 A substantial portion of these individuals suffered a prior stroke or TIA (200,000), thus creating the opportunity for secondary prevention and risk factor modification. Among ischemic strokes, 15% to 33% are thought to be embolic in origin with the highest rates of embolization seen among younger individuals (<45 years old).2 Embolic strokes are characteristically associated with increased rates of disability and mortality compared to other stroke mechanisms.3
Strokes from an embolic source often have sudden onset of the worst neurological symptoms, multifocal presentation, aphasia without hemiparesis, or co-occurrence of systemic emboli. Embolism should be suspected in individuals who demonstrate ischemic involvement in multiple vascular territories or lack a clearly identifiable etiology for stroke on brain and vascular imaging. The most common sources of cerebral emboli are nonvalvular atrial fibrillation, valvular heart disease, and left ventricular thrombi. The similarity of cardiovascular and cerebrovascular risk factors makes determination of a embolic etiology particularly challenging. Despite this, identification of the etiology of stroke as embolic has critical importance in selection of the most appropriate treatment.
The correlation of potential cardiac sources of emboli to stroke occurrence is variable. As a result, adequate evaluation of TIA and stroke patients should also include exploration of noncardiac causes. Vascular imaging with carotid duplex, transcranial Doppler, magnetic resonance (MR) or computed tomography (CT) arteriography are helpful in evaluating potential arterial sources of stroke. Small subcortical infarcts (lacunar strokes) are often associated with small vessel disease, particularly in patients with hypertension and diabetes mellitus. Younger patients may have vascular pathology other than atherosclerosis such as arterial dissection, fibromuscular dysplasia, dolichoectatic arteries, fusiform aneurysms, and primary central nervous system or systemic vasculitides. Brain imaging with MR or CT is valuable in identifying structural abnormalities that may present as stroke mimics.
Considering the importance of the heart and great vessels as sources of emboli, echocardiography has a fundamental role in the evaluation of the patient with suspected embolic infarction, particularly those with multiple vascular distribution stroke or those without a clear vascular etiology for the stroke. Both the Clinical Guidelines for the Use of Echocardiography4 and the Appropriate Use Criteria for Echocardiography5 support the role of echocardiography in the evaluation of selected patients with a suspected cardio-embolic event, especially younger patients and those with no obvious other etiology of their neurologic event. The use of echocardiography is a Class III indication4 and felt to be an inappropriate use of echo5 in patients in whom management decisions will not be altered by the echocardiographic findings.
While transesophageal echocardiography (TEE) is superior to transthoracic echocardiography (TTE) in detecting many potential cardio-embolic sources, evidence for the superiority of warfarin over antiplatelet therapy in treating most of these sources is lacking, as will be discussed.