Cardioembolic Stroke
One-third of strokes represent intracerebral or subarachnoid hemorrhage while two-thirds represent cerebral ischaemia (1)
Ischaemic stroke can result from a variety of causes such as atherosclerosis of the cerebral circulation, occlusion of cerebral small vessels, and cardiac embolism (1)
- one-third of ischaemic strokes are of unclear cause, it is increasingly accepted that many of these cryptogenic strokes arise from a distant embolism rather than in-situ cerebrovascular disease, leading to the recent formulation of "embolic stroke of undetermined source" (ESUS) as a distinct target for investigation
- ESUS working group investigators further proposed that the minimal stroke work-up should include brain neuroimaging with CT or MRI, 12-lead ECG, transthoracic echocardiography (TTE), 24 h Holter-ECG and imaging of both extracranial and intracranial vessels with any available imaging modality (DSA, MRA, CTA, or US)
Risk Factors for Cardioembolic Stroke
Atrial Fibrillation
- AF is associated with a 3-5 fold increased risk of stroke
- AF prevalence increases sharply from 0.1% among adults <55 years of age to almost 10% among those >80 years of age (4)
Systolic Heart Failure
- regional stasis, a hypercoagulable state, and likely undiagnosed AF appear to predispose heart failure patients to cardiac thrombus (5)
- these patients face at least a 3-fold higher risk of stroke than the general population (5)
Recent Myocardial Infarction
- a long-established risk factor for ischaemic stroke - association appears causal because thrombi are often seen overlying areas of ventricular dyskinesis which may predispose to a thrombogenic stroke
Patent Foramen Ovale
- affects approximately 25% of the general population
- may serve as a passageway for paradoxical embolism from the venous to arterial circulation
Aortic Arch Atheroma
- approximately 45% of individuals >= 45 years of age harbor atherosclerotic plaque in their aorta
- been associated with stroke risk (7)
- particulaly linked with stroke risk are large, ulcerated, non-calcified, or mobile atheromas (occur in approximately 8% of the population)
Prosthetic Heart Valves
- meta-analysis of studies published between 1985 and 1992 found that patients with a mechanical valve faced a 4.0% annual risk of stroke, which decreased with the use of oral anticoagulation to 0.8% for aortic valves and 1.3% for mitral valve (8)
Other possible causes of thromboembolic stroke include:
- infective endocarditis, dilated cardiomyopathy, papillary fibroelastoma, myxoma, and mitral calcification
Clinical Presentation
- classically the presentaton is with the sudden onset of neurological deficits that are maximal at onset - this compares to strokes due to small-vessel occlusion (also known as lacunar strokes) or large-artery atherosclerosis may have a more stuttering course
- cardiac embolism may lodge in distal arteries supplying the cerebral cortex while small-vessel occlusion affects subcortical tissue
- cardioembolic stroke can be differentiated from lacunar stroke by cortical signs such as aphasia or visual field deficits
- note though that clinical characteristics alone cannot reliably classify the underlying cause of ischaemic stroke
Investigation:
- neuroimaging
- majority of cardioembolic strokes involve lesions in a cortical territory
- about half of cardioembolic strokes involve multiple cerebral arterial territories (i.e., both internal cerebral arteries or one internal cerebral artery as well as the basilar artery)
- this distinguishes cardiac embolism from artery-to-artery embolism due to large-artery atherosclerosis in the cerebral circulation
- in cardioembolic stroke vascular imaging of the intracranial circulation in the acute phase, such as with computed tomographic or magnetic resonance angiography, often reveals an abrupt vessel cut-off without significant atherosclerotic narrowing of the upstream vessel
- ESUS working group investigators further proposed that the minimal stroke work-up should include brain neuroimaging with CT or MRI, 12-lead ECG, transthoracic echocardiography (TTE), 24 h Holter-ECG and imaging of both extracranial and intracranial vessels with any available imaging modality (DSA, MRA, CTA, or US) (3)
- possible aetiologies of ESUS:
- evidence has indicated that ESUS may often stem from subclinical atrial fibrillation (AF) which can be diagnosed with prolonged heart-rhythm monitoring (5)
- emerging evidence indicates that a thrombogenic atrial substrate can lead to atrial thromboembolism even in the absence of AF
- such an atrial cardiopathy may explain many cases of ESUS, and oral anticoagulant drugs may prove to reduce stroke risk from atrial cardiopathy given its parallels to AF
- improved imaging of ventricular thrombus plus the availability of NOAC drugs may lead to better prevention of stroke from acute myocardial infarction and heart failure
Reference:
- Krishnamurthi RV et al. Global Burden of Diseases IRFS and Group GBDSE. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health. 2013; 1:e259-281.
- Adams HP Jr et al Classification of subtype of acute ischaemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke. 1993; 24:35-41.
- Hart RG et al. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014 Apr; 13(4):429-38
- Wolf PA, Abbott RD and Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991; 22: 983-988
- Lovett JK, Coull AJ and Rothwell PM. Early risk of recurrence by subtype of ischemic stroke in population-based incidence studies. Neurology 2004; 62: 569-573
- Kronzon I, Tunick PA. Aortic Atherosclerotic Disease and Stroke. Circulation. 2006; 114:63-75.
- Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. 1994; 89:635-641
- Ringelstein EB et al. Computed tomographic patterns of proven embolic brain infarctions. Ann Neurol. 1989; 26:759-765