Sources of Embolism in Ischemic Stroke
Cardiac sources account for approximately 20-25% of all ischemic strokes, with atrial fibrillation being the single most common embolic source, followed by valvular heart disease, reduced ejection fraction, and aortic arch atheroma. 1
Major Cardiac Sources of Emboli
High-Risk Cardiac Sources
Atrial fibrillation is the leading cardiac cause of embolic stroke, responsible for the majority of cardioembolic events and conferring a fivefold increased stroke risk. 1, 2, 3 Thrombi form predominantly in the left atrial appendage due to blood stasis, and can develop within 48 hours of continuous atrial fibrillation. 1
Valvular heart disease represents a major embolic source, including: 4
- Rheumatic mitral stenosis (accounts for 10% of cardioembolic strokes) 3
- Mitral regurgitation 5
- Aortic stenosis and regurgitation 5
- Prosthetic cardiac valves (10% of cardioembolic strokes) 3
- Infective endocarditis 4
Reduced left ventricular ejection fraction is a critical embolic source, with stroke risk inversely proportional to ejection fraction—patients with EF <29% have 1.86 times the stroke risk compared to those with EF >35%, representing an 18% increase in stroke risk for every 5% decline in ejection fraction. 4
Dilated cardiomyopathy was identified as the most common high-risk cardiac source in one large TEE study (19.65% of cases). 5
Recent myocardial infarction serves as an embolic source through associated atrial fibrillation development and mural thrombus formation. 4
Moderate-Risk Cardiac Sources
Intracardiac structural abnormalities include: 4
- Patent foramen ovale (PFO)—particularly relevant in younger patients and cryptogenic stroke, accounting for up to 40% of cryptogenic strokes in younger populations 4
- Atrial septal defect 4
- Atrial septal aneurysm (embolic risk increases substantially when combined with PFO) 4, 2
Mitral annular calcification was found in 5.7% of ischemic stroke patients undergoing TEE evaluation. 5
Non-Cardiac Embolic Sources
Aortic Arch Atheroma
Complex atherosclerotic plaque in the ascending aorta or proximal arch (thickness >4 mm) was detected in 33% of stroke patients, with ulcerated plaques present in the majority of these cases and mobile components in some. 5, 6 The embolic mechanism involves plaque rupture during procedures or spontaneous embolization. 1
Artery-to-Artery Embolism
Large-artery atherosclerosis with ≥50% luminal narrowing of extracranial or intracranial carotid or vertebrobasilar arteries causes stroke through artery-to-artery embolism or hemodynamic insufficiency. 4, 1 This mechanism accounts for approximately 20% of ischemic strokes. 1
Uncommon Sources
Non-atherosclerotic vasculopathies include: 1
- Arterial dissection (especially important in patients <50 years)
- Vasculitis
- Fibromuscular dysplasia
- Moyamoya disease
Hypercoagulable states encompass inherited and acquired conditions such as antithrombin III deficiency, protein C/S deficiency, antiphospholipid antibodies, and lupus anticoagulant. 1
Carotid-web lesions are increasingly recognized, particularly in younger stroke patients. 1
Evaluation Strategy
Initial Cardiac Assessment
All patients require transthoracic echocardiography (TTE) to screen for structural heart disease, reduced ejection fraction, valvular abnormalities, and intracardiac thrombi. 7
Extended cardiac rhythm monitoring is mandatory to detect paroxysmal atrial fibrillation, which may be intermittent and missed on initial ECG. 7
Transesophageal Echocardiography Indications
TEE should be performed when: 7, 6
- Patient age <55 years with cryptogenic stroke
- TTE reveals abnormalities requiring further characterization
- Clinical history suggests cardioembolic source (palpitations, known valvular disease)
- No cause identified after initial workup
TEE identifies potential treatable cardioembolic sources in 61% of patients without recognized stroke cause. 6
Vascular Imaging
Carotid imaging (duplex ultrasound, CTA, or MRA) must be obtained within 48 hours to exclude ipsilateral large-artery stenosis >50%. 7
Urgent vascular imaging (CTA or MRA) is required even when lacunar stroke is suspected, because NIHSS scores correlate poorly with large vessel occlusion presence. 7
Laboratory Studies
Essential laboratory evaluation includes lipid profile and hemoglobin A1c to assess modifiable risk factors. 7
Critical Clinical Pitfalls
The most common diagnostic error is failing to exclude both cardioembolism and large-artery stenosis before labeling a stroke as lacunar—a patient with atrial fibrillation and a small subcortical infarct requires anticoagulation, not antiplatelet therapy alone. 7
In patients younger than 50 years, arterial dissection and other uncommon etiologies are frequently missed if not specifically sought. 1
Approximately one-third of all ischemic strokes remain cryptogenic despite comprehensive evaluation, often because two plausible mechanisms coexist or the workup is incomplete. 1
Cardioembolic strokes have the worst prognosis among stroke subtypes, with 22.6% mortality within 90 days compared to 3.3% for small-vessel disease, making accurate source identification critical for secondary prevention. 4