Common causes
- Left atrial appendage clots
- Left atrial clots
- LV mural thrombus (Post MI, DCM)
- Mitral aortic valve infective vegetations
Conditions that could be commoner than we think!
- Aortic valve calcific debri
- Aortic arch atheromas
- Paradoxical embolism through foramen ovale.*
If we consider incidence of patent foramen ovale in general population is up to 20% the problem of paradoxical embolism could be really significant.PFO is a potential right to left channel of more than 5 square cm .
Unusual causes
- Mitral annular and posterior leaflet calcification
- Tumor embolus (Myxoma etc)
- Prosthetic valve thrombus.
Cause never known and identified.
There are times a cardiac source can never be identiifed.This can very well happen , as a transient arrhytmia can trigger a thrombus formation and subsequent examination are totally normal .The incidence of such group can never be known !
A brief account on cardiac embolus
Cardiac embolus constitute an important cause for stroke or TIA. There are number of important conditions that can result in cardiac embolism. The embolus could be a thrombus(95% of times ) , Vegetation, tumor, calcific debri, cholesterol , atheromatic particles , rarely chordal and subchordal structures following it’s rupture.The size of the embolus could vary between <.5mm to 1-2cm in diameter.The average size is 1cm . The clinical presentation depends upon the size, content of the emboli(Thrombus vs non thrombus) ) site of trapping, freshness of thrombus, natural lytic process.
The common sites of trapping is middle cerebral artery.The average diameter of MCA is around 2 mm.So one can imagine almost most of the cardiac emboli can not traverse it, and hence a dense stroke .But , micro thromboemboli , can safely cross cerebral circulation.they usually present as TIA or a chronic lacunar infarcts and many times vascular dementias. Cardiac thrombus rarely gets struck within the carotids.This is especially common if there is associated critical carotid stenosis.The situation is a dire emergency.(Inspite of the fact there is circle of willis for
How do you investigate ?
A complete physical examination with well documented clinical history
A meticulous echocardiography with possibly a TEE (Transesophagel echo) may done .
Underlying disorder to be tackled.
When a emboli is released from the heart , what determines it’s entry into carotid ?
The aortic ejection force is such that whatever particle that exit from the heart , tend to hit on the carotid first.Only if it fails to accept it , it is pushed across the aortic arch into the descending aorta.This result in peripheral embolism .Some times a emboli gets struck within the carotid .This especially happens if there is associated with critical carotid obstruction .This can result in massive stroke and sudden neurological death( The threat is real inspite of the presence of circle of willis which supposed to come to rescue in cases of sudden unilateral carotid obstruction)
What is the relationship between atrial fibrillation and cardiac emboli ?
For long ,the two conditions were thought to closely linked entities.AF slows blood flow across the atria, predispose to left atrial clots and possibly increased stroke.So vigorous means to restore sinus rhythm were attempted. But to our surprise, the incidence of stroke was not greatly reduced between optimal anticoagualtion and sinus rhythn restoration. This indicated many of the cardiac source of embolism could be distal to left atrium aortic arch atheromas, carotid etc (AFFIRM study)
Restoration of AF into SR can possibly prevent thrombus formation only in one chamber , while systemic anticoagualtion can prevent thromboembolism virtually any where from the high risk zones across the LA, LV, Valves, Aorta, arch, carotids etc. So , it defies scientifc logic , to attempt AF restoration by all means (The exotic pulmonary vein isolation etc !) to eliminate one of the cause of stroke.
Dr.S.Venkatesan MD 