• cardioembolism is present in 20-30% of stroke patients (some recent data suggest up to 50%)
    • around 50%  of cardioembolic strokes are due to atrial fibrillation (Afib or AF)  [Jabaudon, 2004]
    • most commonly, the source is in the left atrium or ventricle
    • paradoxical embolization via PFO is typical in younger age
  • emboli structure:
    • fresh thrombus formed by fibrin and platelets (good effect of tPA)
    • older organized thrombus
    • calcified plaque
    • valvular vegetations in endocarditis
    • myxoma fragment
  • an overview of cardiac disorders 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 increased 5x – depending on the CHA2DS2VASc score
    • non-rheumatic and rheumatic valve defects
  • in most cases, cardioembolic stroke or its recurrence can be prevented by oral 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

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Atrial fibrillation (Afib, AF)

see separate chapter

Valvular Heart Disease (VHD)

Mechanical Valve
  • mechanical valves predispose to thrombus formation and infectious complications (especially endocarditis)
  • risk of thromboembolism ~ 4%/year
  • WARFARIN  with 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, ASA dose may be increased to 325 mg, or target INR may be increased
  • 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 atrium size and sinus rhythm (AHA/ASA 2021 I/C-EO)
    • moderate cardioembolism risk
  • WARFARIN (target INR 2.5-3.5) – only in concomitant Afib or enlarged left atrium
  • more severe disorders 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)
  • for more severe disorders, surgery is required
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
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 hemocultures + elevation of inflammatory markers
    • detection 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 often mitral valve), resembles infective endocarditis, but there are no signs of inflammation (edema, cellular infiltration, vascularization of the valve, possibly fibrinoid necrosis)
  • tends to be present:
    • in malignant tumors as a paraneoplastic syndrome (most often in adenocarcinomas of the stomach, pancreas, biliary tract, and ovary)
    • may accompany chronic thromboembolic diseases, chronic nephropathy with uremia,  etc.
  • may present with embolism of dislodged vegetations

Libman-Sacks endocarditis (LSE)

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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 crossreactive antibodies attacking 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

  • in the acute and subacute phases, mural thrombus formation may develop in the ischemic and akinetic wall area
  • in about 10% of patients with acute stroke, troponin elevation is present without concomitant MI; on the other hand, only borderline elevation of hs troponin T can be found in some acute MI patients
  • 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 proven in the left ventricle:   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 condition  (AHA/ASA 2021 2b/C-LD)
    • LMWH may be administered instead of warfarin or used 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)

see separate chapter

Atrial septal defect

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Intracardiac tumors

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  • 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; proceed individually  (AHA/ASA 2021 2b/B-R)
  • stroke/TIA + noncompaction cardiomyopathy ⇒ consider warfarin  (AHA/ASA 2021 2a/C-EO)
  • there are insufficient data to recommend DOAC 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 can lead to 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 higher in:
    • patients with extensive aortic atherosclerotic plaques
    • procedures requiring multiple catheter exchanges or excessive catheter manipulation
    • the need for large-bore catheters and stiff wires
  • standard acute therapy (thrombolysis, thrombectomy) and secondary prevention
  • as a rare complication, contrast-induced encephalopathy (CIE) may also develop

→ Cardiac Catheterization Risks and Complications

Cardiac surgery complications

  • occurs during coronary artery bypass grafting (CABG) as well as during intracardial procedures  → see separate chapter
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