• cardioembolism occurs in 20-30% of stroke patients (some recent data suggest up to 50%)
    • approximately 50%  of cardioembolic strokes are due to atrial fibrillation (Afib or AF)  [Jabaudon, 2004]
    • the most common source is the left atrium or ventricle
    • paradoxical embolization via PFO is typical in younger patients
  • emboli structure:
    • fresh thrombus formed by fibrin and platelets (good response to tPA)
    • older organized thrombus
    • calcified plaque
    • valvular vegetations in endocarditis
    • myxoma fragment
  • an overview of cardiac conditions associated with cerebral embolization is given in the table below
  • embolization most commonly occurs in:
    • non-valvular atrial fibrillation (NVAF) – the risk of stroke is 5x increased, depending on the CHA2DS2VASc score
    • non-rheumatic and rheumatic valvular defects
  • in most cases, cardioembolic stroke or its recurrence can be prevented with anticoagulants  ⇒ early detection of a possible source of cardioembolism is essential for early initiation of optimal stroke prevention

diagnostic evaluation of cardioembolic stroke see here

The most common cardiac conditions associated with cerebral embolism


  • atrial fibrillation
  • sick-sinus syndrome (SSS)
Valvular disease
  • valvular rheumatic lesions
  • calcification of the Ao and Mi valves
  • valve replacement
  • bacterial and nonbacterial endocarditis
  • myxomatous valve degeneration
Intra-cardiac lesions
  • tumors (myxoma, rhabdomyoma, papillary fibroelastoma)
  • LAA thrombi, spontaneous echo contrast enhancement
Myocardial disorders
  • myocardial infarction
  • local hypo- or akinesis
  • heart failure
  • aneurysm
  • dilated cardiomyopathy (DCM)
Septal defects and shunts (uncertain association)
Overview of cardioembolic conditions by frequency of occurrence
very frequent
atrial fibrillation/flutter (12-18% of all strokes)
thrombus in the left atrium or ventricle
less frequent
valvular heart disease
spontaneous echo contrast in the left atrium
atherosclerotic plaques and thrombi in the ascending aorta
intracardiac tumors (myxoma, papillary fibroelastoma)
pulmonary AV malformations and shunts
patent ductus arteriosus (PDA)
PFO and/or septal aneurysm

Atrial fibrillation (AF, Afib)

see separate chapter

Valvular heart disease (VHD)

Mechanical Valve
  • mechanical valves are prone to thrombus formation and infectious complications (especially endocarditis)
  • risk of thromboembolism ~ 4%/year
  • WARFARIN  with a target INR 3 (2.5-3.5)  AHA/ASA 2021 2a/C-EO
  • ASA 75-100 mg may be added in patients at low risk of bleeding, especially before elective valve replacement (AHA/ASA 2021 I/C-LD)
  • for recurrent stroke, the ASA dose may be increased to 325 mg, or the target INR may be raised
  • dabigatran is inappropriate for patients with mechanical valve replacement
Tissue valve
  • in the absence of another indication for anticoagulation (severe LV dysfunction, history of embolism), switch to ASA 75-100 mg/d after 3-6 months of anticoagulant therapy  (AHA/ASA 2021 I/C-EO)
  • if antiplatelet therapy fails, add warfarin with a target INR of 2.5
Aortic valve disease
  • antiplatelet therapy – in patients with normal left atrial size and sinus rhythm (AHA/ASA 2021 I/C-EO)
    • moderate risk of cardioembolism
  • WARFARIN (target INR 2.5-3.5) – only in the presence of Afib or left atrial enlargement
  • more severe conditions often require surgery
Rheumatic mitral valve disease
  • WARFARIN (target INR  2.5-3.5)
    • DOAC has not yet been approved in this indication
    • rheumatic mitral valve disease + Afib   (AHA/ASA 2021 1/C-EO)
    • isolated rheumatic mitral valve disease   (AHA/ASA 2021 1/C-EO)
  • the routine addition of ASA to warfarin is not recommended (AHA/ASA 2014 III/C)
    • if embolization occurs despite adequate anticoagulation, aspirin 75-100 mg daily may be added (AHA/ASA 2014 IIb/C)
  • surgery is required for more severe disease
Mitral valve regurgitation
  • rarely symptomatic
  • prolapse alone is not an indication for anticoagulation therapy; antiplatelet agents are commonly used  (AHA/ASA 2014 I/C)
Atrial fibrillation
mechanical valve, moderate-severe mitral stenosis warfarin
other forms of valvular heart disease DOAC
Sinus rhythm
mechanical aortal/mitral valve warfarin
rheumatic mitral valve disease warfarin
non-rheumatic mitral valve disease antiplatelet therapy
aortic valve disease antiplatelet therapy
tissue aortal/mitral valve antiplatelet therapy


  • endocarditis occurs spontaneously or as a consequence of valvular disease
  • clinical presentaion:
    • TIA/stroke
    • multiple microembolizations causing an encephalopathy
    • bleeding (from mycotic microaneurysms or as a result of rupture of an inflamed artery)
  • source of septic (infective endocarditis) or aseptic emboli (NBTE, LSE)
  • diagnosis is based on:
    • positive blood cultures + elevated inflammatory markers
    • evidence of valvular vegetations on echocardiography

→ infective endocarditis

Nonbacterial thrombotic endocarditis (NBTE)

  • formerly known as marantic endocarditis
  • characterized by the formation of small sterile thrombotic vegetations on the valve leaflets (most commonly the mitral valve), resembling infective endocarditis, but without signs of inflammation (edema, cellular infiltration, possibly fibrinoid necrosis)
  • usually present:
    • in malignant tumors as a paraneoplastic syndrome (most commonly in gastric, pancreatic, biliary, and ovarian adenocarcinomas)
    • may accompany chronic thromboembolic diseases, chronic nephropathy with uremia,  etc.
  • may present with embolism of dislodged vegetation

Libman-Sacks endocarditis (LSE)

  • LSE is a form of nonbacterial endocarditis, also known as atypical verrucous endocarditis,  associated with systemic lupus erythematosus (SLE), antiphospholipid syndrome, and malignancy
    • one of the most common cardiac manifestations of lupus (after pericarditis)
  • a hypercoagulable state leads to endothelial injury and subsequent deposition of thrombi and inflammatory molecules in affected valves. The vegetations are formed by immune complexes, platelet thrombi, fibrin, and mononuclear cells
  • in addition to an asymptomatic course, LSE may present with embolization of dislodged vegetation
    • cerebral or retinal emboli (presenting as stroke or transient ischemic attack)
    • mesenteric ischemia (presenting as severe abdominal pain)
    • peripheral arterial embolism

Rheumatic endocarditis

  • valvular defects are the most serious complication of rheumatic fever (inflammation affecting children after tonsillitis or pharyngitis due to infection with group A β-hemolytic streptococcus)
  • caused by cross-reactive antibodies that attack certain tissues – heart (pancarditis), joints (arthritis), brain (chorea minor), skin, and subcutaneous tissue   (Cunningham, 2014)

Chronic heart failure (CHF)

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Acute myocardial infarction (MI)

  • in the acute and subacute phases, mural thrombus formation may develop in the ischemic and akinetic wall areas
  • in about 10% of patients with acute stroke, troponin elevation is present without concomitant MI; on the other hand, only borderline elevation of high-sensitivity troponin T may be found in some patients with acute MI
  • diagnostic evaluation:
    • TTE (higher sensitivity than TEE is reported for detection of thrombi in the LV), sensitivity is further increased by the use of an ultrasound contrast agent
    • cardiac MRI (high sensitivity) [Weinsaft, 2011]
  • management:
    • thrombus is demonstrated in LV:   WARFARIN (INR 2.0-3.0) for 3-12 months (usually 3 months)  (AHA/ASA 2021 I/B-NR)
    • patients with TIA/stroke and acute anterior wall MI with reduced EF (< 50%) without evidence of left ventricular thrombus:  consider warfarin for three months (AHA/ASA 2021 2b/C-EO)
    • DOAC safety is uncertain in this setting  (AHA/ASA 2021 2b/C-LD)
    • LMWH may be used instead of warfarin or as bridging therapy (AHA/ASA 2014 IIb/C)
    • in concomitant severe CAD with unstable AP, anticoagulant therapy may be combined with antiplatelet therapy

Patent foramen ovale (PFO)

Atrial septal defect

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Intracardiac tumors

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Cardiomyopathy (CMP)

  • stroke/TIA + cardiomyopathy (ischemic, nonischemic, restrictive) or left ventricular dysfunction with evidence of thrombi in the left atrium or ostium ⇒ anticoagulation for at least 3 months (AHA/ASA 2021 1/C-EO)
  • stroke/TIA + mechanical support ⇒ warfarin + ASA (AHA/ASA 2021 2a/C-LD)
    • do not use dabigatran  (AHA/ASA 2021 3/B-R)
  • in patients with low ejection fraction (EF) and sinus rhythm without evidence of intracardiac thrombus, the efficacy of anticoagulation is unclear; apply individualized approach  (AHA/ASA 2021 2b/B-R)
  • stroke/TIA + noncompaction cardiomyopathy ⇒ consider warfarin  (AHA/ASA 2021 2a/C-EO)
  • insufficient data to recommend DOACs for intracardiac thrombi ⇒ prefer warfarin
cardiomyopathy + stroke/TIA + sinus rhythm
thrombus in LV or LAA LVAD noncompaction cardiomyopathy other
(class 1)
warfarin + aspirin
(class 2a)
(class 2a)
an individual approach
(class 2b)

according to AHA/ASA 2021

Cardiac catheterization complications

  • diagnostic coronary angiography and interventional procedures may result in thromboembolism or atheroembolism from the aorta or its branches
    • peripheral embolization
    • stroke or ischemic retinopathy
  • periprocedural stroke is a rare complication with the use of low-profile catheters (< 0.5%); the risk is increased in:
    • patients with extensive aortic atherosclerotic plaque
    • procedures requiring multiple catheter exchanges or excessive catheter manipulation
    • the need for large-bore catheters and stiff wires
  • standard acute stroke therapy (thrombolysis, thrombectomy) and secondary prevention
  • rarely, contrast-induced encephalopathy (CIE) may occur

→ Cardiac Catheterization Risks and Complications

Cardiac surgery complications

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Cardioembolic stroke
link: https://www.stroke-manual.com/cardioembolic-stroke/