You are on page 1of 1

Cardiogenic Embolism

Embolism of cardiac origin accounts for approximately 15% to 20% of all ischemic
strokes. These cardiac emboli may be composed of platelet, fibrin, platelet-fibrin,
calcium, microorganisms, or neoplastic fragments. The most common substrate for
cerebral embolism in older individuals is atrial fibrillation, accounting for half to twothirds of emboli of cardiac origin.
Other cardiac conditions with high embolic potential include acute MI, infective
endocarditis, rheumatic mitral stenosis, mechanical prosthetic heart valves, dilated
cardiomyopathy, and cardiac tumors.
Congenital heart disease is probably the most common cardiac disorder causing
ischemic stroke in children. With the increased survival of many children with
congenital heart disease, strokes are being seen with increased frequency. Children
with congenital heart disease and a low hemoglobin concentration are at special
risk for arterial strokes; those with a high hematocrit are more likely to experience
cerebral venous thrombosis (Perloff, 1998). Emboli from cardiac sources may be
silent or cause severe neurological deficit or death.
Nonrheumatic atrial fibrillation is the most common cause of cerebral embolism
overall. The presumed stroke mechanism is thrombus formation in the fibrillating
atrium or atrial appendage, with subsequent embolization. Patients with atrial
fibrillation have an average annual risk of stroke of ~5%. The risk of stroke can be
estimated by calculating the CHADS2 score.
Cardioembolic cerebral infarcts are often large, multiple, bilateral, and wedge
shaped. Any vascular territory may be affected. Ischemic strokes with a potential
cardiac source are more often associated with Wernicke aphasia, homonymous
hemianopia without hemiparesis or hemisensory disturbances, and ideomotor
apraxia. Other features suggestive of a potential cardiac source of embolism include
posterior division of the MCA, ACA, or cerebellar compromise; involvement of
multiple vascular territories; or a hemorrhagic component of the infarction.
An embolic stroke occurs in approximately 1% of hospitalized patients with acute
MI. Left ventricular thrombi are commonly associated with recent anterior wall
transmural MI. Almost all episodes of embolism occur within 3 months following
acute MI, with 85% of emboli developing in the first 4 weeks. A decreased ejection
fraction is an independent predictor of an increased risk for stroke following MI (Loh
et al., 1997).
Most cases of mitral stenosis are due to rheumatic heart disease. Systemic emboli
occur in 9% to 14% of patients with mitral stenosis, with 60% to 75% having
cardioembolic cerebral ischemia. Systemic embolism may be the first symptom of
mitral stenosis, particularly if it is associated with atrial fibrillation.