Cardioembolic stroke

1. Cardioembolic stroke 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% 25% 20% 30% CARDIOEMBOLISM CRYPTOGENIC LACUNES LARGE ARTERY ATHEROSCLEROSIS OTHERS Albers GW et al. Antithrombotic and Thrombolytic Therapy for Ischemic Stroke; Chest 2001.

4. Causes of cardioembolic strokes 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. 50% 15% 10% 5% 10% 10% CARDIOEMBOLIC SOURCES Nonvalvular Atrial Fibrillation Acute MI LV thrombus Valvular heart disease Prosthetic valves Other less common sources (PFO, ASA, aortic debris, etc.)

7. Stoke data bank classification   Strong Sources  (prosthetic valves, atrial fibrillation, sick-sinus syndrome, ventricular aneurysm, akinetic segments, mural thrombi, cardiomyopathy and diffuse ventricular hypokinesia ) Weak Sources (aortic and mitral stenosis , aortic and mitral regurgitation, congestive heart failure, mitral valve prolapse , mitral annulus calcification and hypokinetic ventricular segments).

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. Clinical features

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 Decreased alertness Total circulation infarcts Severe strokes (NIHSS >14) Proximal middle cerebral artery occlusion, Hypodensity in more than one third of the middle cerebral artery territory Delayed recanalization (> 6 hours after stroke onset) with absence of collateral

11. Presence of embolism is suggested on CT or MRI Location and shape of the lesion Presence of superficial wedge-shaped infarcts in multiple different vascular territories Hemorrhagic infarction Visualization of thrombi within arteries  Typically, hemorrhage occurs into proximal reperfused regions of brain infarcts Imaging

12. 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.

13. 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).

14. 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 Atrial fibrillation

15. Risk stratification-CHADS2 score

16. 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

17. 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). Treatment

18. 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

19. Current guidelines-> Anticoagulation should be started as soon as possible in patients with AF after brain imaging for a TIA Should be delayed in ischemic stroke, according to ischemic lesion extension, clinical severity and cardiologic comorbidity , stroke in favour of anti-platelet therapy

20. Non pharmacologic- “Maze” procedure - complex lesioning of the left atrium and the pulmonary veins isolation Surgical excision of the left atrium appendage

21. 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 Secondary prevention

22. Absolute risk of hemorrhage in patients with AF on warfarin 2% per year, 0.3% to 0.6% were intracranial haemorrhage

23. Predictors of LA clot and embolism Severity of mitral stenosis Presence of MR LA enlargement Atrial fibrillation Spontaneous echo contrast Pulmonary hypertension Rt ventricular systolic pressure Rheumatic heart disease

24. Anticoagulation- secondary prevention Surgical-open valvotomy Mitral valve replacement Treatment

25. Factors predicting stroke in PFO Younger age Association with atrial septal aneurysm(ASA) Presence of a right-to-left shunt at rest, Size of the PFO Association with thrombophilic conditions PATENT FORAMEN OVALE (PFO)

26. Diagnosis Transcranial Doppler ultrasound with the microbubble technique, more accurate Transesophageal echocardiography Treatment Antiplatelets drugs Anticoagulants, Closure of PFO by transcatheterization Closure of PFO by surgery.

27. Thromboembolic-7 to 34% per year without anticoagulant therapy and 1 to 5% per year with oral anticoagulation Risk factors tor thromboembolism Site of valve replacement, mitral >aortic valve Kind of mechanical valve used, bileaflet < monoleaflet and caged ball AF Left ventricular dysfunction Spontaneous echocardiographic contrast Increasing age Prosthetic valve

28. 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

29. Most stroke within two to four weeks of acute MI. Anterior AMI, in whom the risk of ischemic stroke is 12% Predictors of stroke - AF ST segment elevation Left ventricular thrombus LV aneurysm Systolic dysfunction Older patients with large transmural Infarcts Congestive heart failure, Myocardial infarction

30. 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.

31. Sick sinus syndrome -secondary prevention in patients with well established SSS, anticoagulation should be considered Mitral annulus calcification Mitral valve prolapse Others

32. Thanks

33. 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 References