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Left atrial appendage : CT-based classification in stroke patients and healthy controls

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DISSERTATIONS | MIIKA KORHONEN | LEFT ATRIAL APPENDAGE - CT-BASED CLASSIFICATION... | No 435

uef.fi

PUBLICATIONS OF

THE UNIVERSITY OF EASTERN FINLAND Dissertations in Health Sciences

ISBN 978-952-61-2626-5 ISSN 1798-5706

Dissertations in Health Sciences

THE UNIVERSITY OF EASTERN FINLAND

MIIKA KORHONEN

LEFT ATRIAL APPENDAGE

CT-based Classification in Stroke Patients and Healthy Controls Stroke is a major global health risk causing

mortality and long-term disability. A cardiogenic etiology accounts for one out of every five ischemic strokes and the left atrial

appendage (LAA) is considered to be the most important source of cardiac emboli. This

thesis attempts to reveal the morphological features of the LAA that might predispose

to cardioembolic stroke and to evaluate the impact of background factors on LAA morphology and blood flow in non-stroke patients by utilizing computed tomography.

MIIKA KORHONEN

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(27)

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\Table 1. Sources for cardioembolic events according to the SSS-TOAST classification (adapted from Ay et al.) (43)

High-risk primary sources Low or uncertain primary risk sources

Mechanical or bioprosthetic heart valve Mitral annulus calcification Rheumatoid mitral or aortic valve disease Left ventricular aneurysm without thrombus AF or paroxysmal AF Atrial septal aneurysm

Sustained atrial flutter Patent foramen ovale Thrombus in the left atrium or

in the left ventriculum

Isolated left atrial turbulence (“smoke”) without mitral stenosis or AF

Sick sinus syndrome

Recent myocardial infarction (within 4 weeks) Chronic myocardial infarction with ejection fraction less than 30%

Symptomatic congestive heart failure with ejection fraction less than 30%

Dilated cardiomyopathy

Nonbacterial thrombotic endocarditis Infective endocarditis a

Papillary fibroelastoma a Left atrial myxoma a

a Not predominantly of thrombotic origin

(28)

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(29)

Figure 1. Illustration of the overlap between terms. (1) For example, carotid artery stenosis not detected due to lack of proper evaluation (2) Cardiac source present but not detected (3) e.g.

atrial thrombosis without recognized AF (4) e.g. carotid artery stenosis which is not detected despite proper evaluation (5) Clinical and imaging profile findings support the diagnosis without large-artery stenosis (6) Cardiac source present but not detected due to lack of proper

evaluation (7) e.g. undiagnosed paroxysmal AF that lasts for only short periods each day.

Adapted from Kamel et al. (51)

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(30)

Table 2. Possible risk factors for cardioembolic stroke and their effect on forming thrombus \

according to Virchow’s triad.

Risk factor Description

Atrial fibrillation Disorganised atrial electrical activity and fast irregular atrial contraction results in abnormal blood flow and inflammatory reaction (56).

Systolic heart failure Abnormal blood flow because of low cardiac output, dilated chambers and poor contractility. In addition, dysfunction of heart endothelium, and abnormalities in hemostatis and platelets have been demonstrated. (61)

Recent myocardial infarction Causes ventricular akinesia/dyskinesia which results in abnormal blood flow and endothelial denudation with consequent platelet activation (62).

Patent foramen ovale A common (~25%) congenital feature in the heart where an embryologic passage from right to left atrium still exists and, thus, may serve as a pathway for venous thrombi to enter the major circulation. Patient with PFO may suffer more often from cryptogenic strokes. (51,63-65)

Prostethic heart valves Prostethic valves (mechanical or bioprosthetic) form a foreign surface in contact with the bloodstream and, therefore, form an elevated risk for thrombus formation. Bioprosthetic valves associate with lower risk for stroke but equal long-term mortality with mechanical valves. (66,67)

Infective endocarditis Endocarditis predisposes to the formation of vegetation (i.e. amorphous mass of platelets, fibrin, microorganisms and inflammatory cells), which may detach as an embolic particle. Risk for stroke is elevated months after endocarditis. (68)

Other risks Several other, but more rare, etiologies for

cardioembolic strokes exist, e.g. mitral calcification and intracardiac tumors (for example, papillary fibroelastoma, myxoma and metastases).

Inflammatory mechanism is also associated with progression of atherosclerosis and plaque rupture.

(34,51,69)

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(31)

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(32)

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Figure 2. Upper images: MRI scans of a patient suffering from cardioembolic infarctions (white lesions) in different arterial territories. Lower image: CT scan of the brain with multiple cardioembolic infarctions in a single arterial territory and petechial hemorrhagic transformation.

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(33)

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-\)(\."\'#&\"#-.),3L\*"3-#&\2'#(.#)(\(\(/,)0-/&,\#'!#(!\ #(#(!-L\

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1#."\ ",.Z-*# #\ &),.),3\ ',%,-\ (\ -((\ 1#."\ .,(-."),#\ "),#)!,*"3\

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PQ\),\,#\Y \'3\\)(-#,\PA@QK

\

(34)

Table 3. Diagnostic work-up procedures with suspected cardioembolic stroke (adapted from Yang et al.) (98)

2.2 ATRIAL FIBRILLATION .6.6->"(#">">$!# #,>

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Procedures Aim

12-lead ECG, telemetry and/or 24-hour Holter monitoring

To recognize persistent/paroxysmal AF, atrial flutter and recent myocardial infarctions.

TTE To identify left ventricular thrombus, intracardiac masses, vegetations, valve stenosis/thrombus, PFO, septal aneurysm and hemodynamic abnormalities

TEE To confirm or to evaluate the diagnosis for example with infective endocarditis or prosthetic valve thrombosis if TTE is non-diagnostic

To evaluate PFO is passage closure is considered

To help clinical decision-making if the TTE finding is non- diagnostic

Contrast-enhanced

TTE/TEE To evaluate PFO is passage closure is considered

Cardiac CT To confirm the presence and size of thrombus in prosthetic valve thrombosis and to evaluate the valve motion

To help clinical decision-making if the TTE finding is non- diagnostic

Cardiac MRI To help clinical decision-making if TTE, TEE or cardiac CT finding is non-diagnostic

Cinefluoroscopy To confirm the presence and size of the thrombus in the prosthetic valve thrombosis and to evaluate valve motion Prolonged rhythm

monitoring with implantable or wearable devices

To recognize silent AF

(35)

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Figure 3. Illustration of the electrical activity during cardiac cycle in sinus rhythm and in atrial fibrillation. Adapted from Mayo Clinic’s Patient Care & Health Information (114).

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(36)

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Figure 4. Typical progression of AF and its therapeutically suitable actions. Actions in the top yellow bars protect from serious outcomes, e.g. stroke, whereas the blueish bars indicate actions for symptom relief or AF-related complications in the future. Rate control is used both in symptom relief and to improve the cardiovascular outcome. Red bars present the nature of AF with time and the change of AF driver type. The bottom bar displays the transition of AF typical locations. Adapted from European Society of Cardiology’s Guidelines for the management of AF and Iwasaki et al. (99,109)

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