Cardiac Sources of Brain Emboli

THE RECIPIENT ARTERIES

The recipient artery is the main determinant of the clinical symptoms and signs. When a recipient neck or intracranial artery is blocked, blood flow to the area of brain supplied by the blocked artery suddenly becomes insufficient and normal function stops. The neurologic symptoms that result from the arterial blockage depend on the area of brain that is underperfused. If an embolus blocks a posterior cerebral artery supplying the visual cortex, loss of vision in the opposite visual field might result. If an embolus blocks the left middle cerebral artery, the right limbs might become weak and numb, and the patient might become aphasic. An embolus to an intracranial vertebral artery might cause loss of cerebellar function and ataxia. The symptoms do not depend on the nature of the embolic material. The recipient artery cannot tell what is blocking it or where the material came from.

Whether the symptoms are transient or persist depends on the size and fate of the embolus. Emboli very often move through recipient arteries so quickly that no or very transient obstruction occurs. These passing emboli can be identified as so-called HITS (high-intensity transient signals) that pass quickly under an ultrasound probe monitoring an intracranial artery. Emboli can cause no symptoms, TIAs, or persistent infarction.

Most emboli that go into an internal carotid artery from the heart or aorta, or arise from the carotid artery, travel into the ipsilateral middle cerebral artery. The embolus might rest first within the carotid artery in the neck or head and then pass into the proximal middle cerebral artery or its superior or inferior divisions, or into one of the smaller cortical branches. Occasionally, the embolus might go into other branches of the intracranial carotid artery, the anterior cerebral artery, or the anterior choroidal artery.

If an embolus goes into a vertebral artery in the neck or arises from an extracranial vertebral artery most often it will travel rostrally into the ipsilateral intracranial vertebral artery or go even further to reach the basilar artery bifurcation or into one or both posterior cerebral arteries or the superior cerebellar arteries located at the top-of-the basilar artery. If the embolus is large enough it could obstruct the basilar artery itself, leading to severe brainstem ischemia or infarction. A shower of emboli can block multiple arteries simultaneously or sequentially.

DONOR SOURCES AND THEIR EMBOLIC MATERIALS

The nature of the embolic material determines the most likely prophylaxis and treatment.

Cardiac Sources. Emboli that arise from the heart often consist of red erythrocyte-fibrin thrombi that form in the atria or on the surface of myocardial infarcts or within ventricular aneurysms. The most common sources of embolism from the heart are arrhythmias, especially atrial fibrillation. Red thrombi form in the inefficiently contracting, dilated left atrium and left atrial appendage; valvular diseases are also common sources. White platelet-fibrin thrombi form along irregular valvular surfaces and prosthetic valves. Many times, white thrombi form the nidus for a superimposed red thrombus so that both are involved in the thromboembolism. In patients with systemic lupus erythematosus, antiphospholipid antibody syndrome, and cancer, a nonthrombotic fibrinoid valvulitis develops and serves as a nidus for white clots. Calcium present in calcific aortic valves and in mitral annulus calcifications can break loose and embolize to the brain. Bacteria and fungi engrafted upon valves in patients with infective endocarditis can travel into the bloodstream and into the cranium, causing meningitis, brain abscesses, and infarcts as well as infecting arteries, causing mycotic aneurysms. Tumor tissue present in cardiac myxomas and fibroelastomas can form the matter of emboli.