1. Dr. Parag Moon
Senior Resident
Dept. of Neurology
GMC, Kota.
2. Stroke and ischemic heart disease are among
the most common causes of death and
disability in the world.
A cardioembolic stroke occurs when the heart
pumps unwanted materials into the brain
circulation, resulting in the occlusion of a
brain blood vessel and damage to the brain
tissue.
3. MECHANISMS OF STROKE
5%
20%
LARGE ARTERY
ATHEROSCLEROSIS
25%
20%
30%
CARDIOEMBOLISM
CRYPTOGENIC
LACUNES
OTHERS
Albers GW et al. Antithrombotic and Thrombolytic Therapy for Ischemic Stroke; Chest 2001.
4. Divided into three groups –
(1) Cardiac wall and chamber abnormalities -
cardiomyopathies, hypokinetic and akinetic
ventricular regions after myocardial
infarction, atrial septal aneurysms, ventricular
aneurysms, atrial myxomas, papillary
fibroelastomas and other tumors, septal
defects and patent foramen ovale;
5. (2) Valve disorders -rheumatic mitral and
aortic valve disease, prosthetic valves,
bacterial endocarditis, fibrous and fibrinous
endocardial lesions, mitral valve prolapse and
mitral annulus calcification; and
(3) Arrhythmias, -particularly atrial fibrillation
and "sick-sinus" syndrome.
6. CARDIOEMBOLIC SOURCES
Acute MI
50%
10%
5%
15%
10% 10%
Nonvalvular
Atrial Fibrillation
LV thrombus
Valvular heart
disease
Prosthetic
valves
Other less
common sources
(PFO, ASA,
aortic debris, etc.)
8. Most embolic events occur during typical
activities of daily living
Some start during rest or sleep.
Sudden coughing, sneezing or rising at night to
urinate are known to precipitate embolism
Deficit from a cardioembolic stroke is typically
maximal at outset.
11% of these patients had a stuttering or
stepwise course,10% had fluctuations or
progressive deficits.
When progression occurs, it is usually due to
distal passage of emboli.
9. 4.7-12% of cases, cardioembolic infarctions
show a rapid regression of symptoms (the
spectacular shrinking deficit syndrome)
When progression occurs, it is usually due to
distal passage of emboli.
Hemorrhagic transformation occurs in up to
71% of cardioembolic strokes.
Two types-petechial or multifocal, which is
normally asymptomatic and secondary
hematoma, which has mass effects and
clinical deterioration
10. Predictors of hemorrhagic transformation
1. Decreased alertness
2. Total circulation infarcts
3. Severe strokes (NIHSS >14)
4. Proximal middle cerebral artery occlusion,
5. Hypodensity in more than one third of the
middle cerebral artery territory
6. Delayed recanalization (> 6 hours after
stroke onset) with absence of collateral
11. Presence of embolism is suggested on CT or
MRI
1. Location and shape of the lesion
2. Presence of superficial wedge-shaped
infarcts in multiple different vascular
territories
3. Hemorrhagic infarction
4. Visualization of thrombi within arteries
Typically, hemorrhage occurs into proximal
reperfused regions of brain infarcts
12.
13.
14. Transesophageal echocardiography (TEE)-
better visualization of the atria, cardiac
valves, septal regions and aorta.
Diagnostic yield is 2-10 times that of TTE.
An echo-enhancing agent (such as agitated
saline) can also help reveal an intracardiac
shunt.
15. Transcranial Doppler (TCD)
Embolic particles passing under TCD probes
produce transient, short-duration, high-intensity
signals referred to as HITS (high-intensity
transient signals).
Monitoring of emboli with TCD may guide
treatment decisions (e.g., performing TCD
pre- and postinitiation of anticoagulation to
assess whether HITS cease).
16. Can be hypertensive, ischaemic, valvular or
lone
16% of all ischemic strokes are associated
with AF
AF increases the relative risk of ischemic
stroke about five-fold
18. Echo parameters predicting stroke-
Moderate to severe left ventricular
dysfunction
Decreased left atrial flow velocity
(<15cm/sec)
Ventricular dilatation
Decreased left atrial ejection
Atrial enlargement
Spontaneous echo contrast
19. Guidelines recommend anticoagulation in
patients with more than 1 moderate risk
factors (age 75 years or older, hypertension,
heart failure, ejection fraction below 35% or
fractional shortening less than 25% and
diabetes mellitus) (evidence A).
Aspirin, 81–325 mg daily, is recommended as
an alternative to vitamin K antagonists in
low-risk patients or with contraindications to
oral anticoagulation (evidence A).
20. Anticoagulants (unfractionated heparin or
LMWH ) started in the first 48 hours vs other
treatments in acute cardioembolic stroke
Didn’t show a significant reduction in
recurrent stroke within 7 to 14 days with
anticoagulation
Symptomatic intracranial bleeding were
increased with early anticoagulation therapy
21. Current guidelines->
1) Anticoagulation should be started as soon
as possible in patients with AF after brain
imaging for a TIA
2) Should be delayed in ischemic stroke,
according to ischemic lesion extension,
clinical severity and cardiologic comorbidity,
stroke in favour of anti-platelet therapy
22. Non pharmacologic-
“Maze” procedure -complex lesioning of the
left atrium and the pulmonary veins isolation
Surgical excision of the left atrium appendage
23. Warfarin vs. placebo found a relative risk
reduction of 2.5% to 4.7% per year for
ischemic stroke and absolute stroke rate
reduction of 33% to 86%
Warfarin is more efficacious than aspirin in
stroke risk reduction.
Combination of warfarin plus antiplatelet
versus warfarin alone didn’t show an additive
beneficial effect; risk of bleeding was
increased in patients receiving combination
24. Absolute risk of hemorrhage in patients with
AF on warfarin 2% per year, 0.3% to 0.6% were
intracranial haemorrhage
25. Predictors of LA clot and embolism
1. Severity of mitral stenosis
2. Presence of MR
3. LA enlargement
4. Atrial fibrillation
5. Spontaneous echo contrast
6. Pulmonary hypertension
7. Rt ventricular systolic pressure
27. Factors predicting stroke in PFO
1. Younger age
2. Association with atrial septal aneurysm(ASA)
3. Presence of a right-to-left shunt at rest,
4. Size of the PFO
5. Association with thrombophilic conditions
28. Diagnosis
Transcranial Doppler ultrasound with the
microbubble technique, more accurate
Transesophageal echocardiography
Treatment
1. Antiplatelets drugs
2. Anticoagulants,
3. Closure of PFO by transcatheterization
4. Closure of PFO by surgery.
29. Thromboembolic-7 to 34% per year without
anticoagulant therapy and 1 to 5% per year with
oral anticoagulation
Risk factors tor thromboembolism
1. Site of valve replacement, mitral >aortic valve
2. Kind of mechanical valve used,
bileaflet<monoleaflet and caged ball
3. AF
4. Left ventricular dysfunction
5. Spontaneous echocardiographic contrast
6. Increasing age
30. Major embolism rate without antithrombotic
therapy was 4.0% per year, 2.2% year with
antiplatelets and 1.0% per year with
anticoagulants
INR range of 2 to 3 for bileaflet mechanical
aortic valves, 2.5 to 3.5 for mechanical mitral
valves and for monoleaflet valves
Additional antiplatelet-stroke during
anticoagulation or concomitant vascular risk
factors
31. Most stroke within two to four weeks of acute MI.
Anterior AMI, in whom the risk of ischemic stroke
is 12%
Predictors of stroke -
1. AF
2. ST segment elevation
3. Left ventricular thrombus
4. LV aneurysm
5. Systolic dysfunction
6. Older patients with large transmural Infarcts
7. Congestive heart failure,
32. Heparin followed by low-intensity oral
anticoagulation (INR 1.6 to 2.5) reduced
stroke by about 70% in the weeks following
AMI
Long-term anticoagulation beyond three
months is not justified unless other major
cardiac embolic risk factors, such as mural
thrombosis, are present.
33. Sick sinus syndrome -secondary prevention
in patients with well established SSS,
anticoagulation should be considered
Mitral annulus calcification
Mitral valve prolapse
35. Prevention Strategies for Cardioembolic
Stroke: Present and Future Perspectives; The
Open Neurology Journal, 2010, 4, 56-63
Cardioembolic Stroke: Clinical Features,
Specific Cardiac Disorders and Prognosis;Curr
cardiology review ;april 2010; 6(1) ;pg 150-
161
Cardioembolic stroke: An update on etiology,
diagnosis and management :Annals of indian
academy of neurology : 2008: Volume :
11 Issue : 5 Page : 52-63
