ISCHEMIC STROKE / CLASSIFICATION AND ETIOPATHOGENESIS
Cardioembolic stroke
Created 06/12/2021, last revision 24/09/2023
- 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
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Arrhythmias
Valvular disease
Intra-cardiac lesions
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Myocardial disorders
Septal defects and shunts (uncertain association)
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Overview of cardioembolic conditions by frequency of occurrence |
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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 |
rare
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patent ductus arteriosus (PDA)
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uncertain |
PFO and/or septal aneurysm
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Atrial fibrillation (AF, Afib)
→ see separate chapter
Valvular heart disease (VHD)
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
- 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)
- 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 |
warfarin (class 1) |
warfarin + aspirin (class 2a) |
warfarin (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 surgery complications
- occurs during coronary artery bypass grafting (CABG) and intracardiac procedures → Neurological complications during extracorporeal circulation