Pathogenesis and Pathophysiology. There are three major types of embolism--cardiogenic, intra-arterial, and paradoxical (.Fig, 45.-7.). Emboli from any source tend to be arrested in a recipient artery, depending on the location of branch points and the size of the embolic material. Once lodged, embolic matter often migrates distally within 48 hours, allowing reperfusion of the previously ischemic zone. This reperfusion frequently causes extravasation of blood through the disintegrated endothelial linings and hemorrhagic conversion of the ischemic lesions, so-called hemorrhagic infarction.
Recent advances in technology have improved the identification of previously unrecognized potential cardiogenic embolic sources and have documented the fact that a higher proportion of ischemic strokes than previously suspected are embolic in origin. Arrhythmias, especially atrial fibrillation and sick sinus syndrome, are important causes of brain embolism. Valvular disease--rheumatic, congenital, calcific, and bacterial and nonbacterial vegetations--is another very important donor source for embolism. Thrombi also form within the heart in patients with myocardial infarcts, myocardiopathies, ventricular aneurysms, and other diseases that cause endocardial and myocardial damage.
Atherosclerotic stenosis of the ICA or VA causes intraarterial thromboembolism when the thrombus formed on the ulcerative plaque dislodges and travels up to a distal intracranial cerebral artery. Usually emboli are composed of clot, platelet clumps, or fragments of plaques. Embolism is especially apt to occur just after a clot is formed, before it becomes organized and adheres to the arterial wall. Cholesterol crystals, fat, tumor, and foreign body material, particularly talc and cornstarch injected by drug abusers,
are less frequent intra-arterial embolic materials. Another important source of intra-arterial embolism is atheromatous aortic plaques. Transesophageal echocardiographic studies have shown that protruding, often mobile and pedunculated, atheromas and clots can be found in the thoracic aorta and are a relatively common source of embolism.y Angiography and cardiac surgery with clamping of the aorta promote embolism from aortic lesions.
A less common form of embolism, paradoxical embolism, occurs when the heart serves as a conduit for emboli arising from blood clots in the peripheral veins; these clots pass through septal defects, a patent foramen ovale (PFO), or pulmonary arteriovenous (AV) fistulas to reach the brain and systemic circulation ( . Fig...45-8 ). Because PFOs usually open during exertion, stroke frequently occurs during Valsalva maneuvers, exertion, and sexual intercourse.
Epidemiology and Risk Factors. At least 30 percent of ischemic strokes are caused by cardiogenic embolism. The lesions with the highest risk are probably atrial fibrillation, acute myocardial infarction with mural thrombosis,
Figure 45-7 Examples of potential sources of embolism: (a) cardiac mural thrombus; (b) vegetation on heart valve; (c) emboli from carotid plaque. Also shown: (d) infarcted cortex in area supplied by terminal anterior cerebral artery due to e(Adaptedfrom Jones EF, Kalman JM, Calafiore P, et al: Proximal aortic atheroma. An independent risk factor for cerebral ischemia. Stroke 1995;26:218-224; with permission.)
Figure 45-8 Common routes of paradoxical embolisn(A) Cross-section through the thorax showing patent foramen ovale (asterisfB) Right-to-left shunts; atrial septal defect (ASD), ventricular septal defect (VSD), and fistula between the pulmonary artery and pulmonary vein. Clot from the leg vein ascends via the inferior vena cava. RA = right atrium; LA = left atrium; LV = left ventricle; PA = pulmonary artery; PV = pulmonaryAdapted from Jones EF, Kalman JM, Calafiore P, et al: Proximal aortic atheroma. An independent risk factor for cerebral ischemia. Stroke 1995;26:218-224; with permission.)
ventricular aneurysms, prosthetic heart valves, rheumatic heart disease with atrial enlargement, myocardiopathies, and bacterial and marantic endocarditis. Cardiac surgery now also poses an important risk of embolism from the heart and aorta.
Clinical Features and Associated Disorders. Brain embolism usually presents abruptly with clinical abnormalities. Fluctuations or worsening symptoms and sudden improvements are common during the first 24 to 48 hours, probably because of emboli passing distally. Usually embolic infarcts are large, and deficits are more severe in patients with emboli than with in situ occlusions. Single or infrequent but longer lasting TIAs may precede embolic infarctions. Embolic events often occur during activity or sudden straining, coughing, or sneezing. Infarcts may involve multiple vascular territories and are mixed in age. Early angiographic or TCD studies may show the presence of distal intra-arterial emboli. Hemorrhagic conversion of infarcted areas is commonly noted on CT and MRI scans. Infarcts are often wedge-shaped and involve the cerebral cortical surface.
Intra-arterial sources of cerebral embolism are usually atheromatous plaques at the carotid bifurcation, but occasionally responsible proximal vascular lesions are detected
at the originating sites of the common carotid arteries or vertebral arteries from the subclavian arteries or aorta. Cardiac sources of emboli are listed in Iable.45-2 .
Differential Diagnosis and Evaluation. Embolic strokes are often difficult to separate from in situ thrombosis engrafted on stenotic lesions and intracerebral hemorrhage. Patients with brain hematomas more often develop signs gradually, whereas embolic strokes often begin instantly and in about 80 percent of patients reach their maximum intensity at or near onset. Decreased consciousness, headache, and vomiting are more common acutely in patients with hematomas than in those with embolic infarction. Still, CT is most often needed to differentiate hematomas from ischemia.
In patients with pre-existing arterial stenotic lesions and superimposed acute thrombosis, preceding TIAs are common and may occur several times over a period of weeks
_TABLE 45-2 -- COMMON CARDIAC SOURCES OF EMBOLI_
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