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Echocardiography for Prediction of Cardioembolic Risk
Spectrum of Cardioembolism
The heart and the aorta are the sources of cardioembolism to any organ. Major clinical presentations involve either acute neurologic dysfunction—transient ischemic attack (TIA) or stroke—or peripheral vascular disease (e.g., acute limb ischemia, splenic or renal infarcts). All cardioembolic causes of TIA or stroke may also cause acute limb ischemia or organ infarcts, with additional thromboembolic sources being thrombus and atheroma in the descending thoracic and abdominal aorta. In 2016, the American Society of Echocardiography (ASE) issued comprehensive guidelines on the use of echocardiography for the evaluation of a cardiac source of emboli.
Stroke
Stroke is the third leading cause of death in developed countries. , The most common type of stroke is ischemic, which accounts for approximately 85% of all strokes. The TOAST criteria are a useful epidemiologic tool to classify stroke. , Cardioembolic strokes by the TOAST criteria fall into either category 2 (proven cardioembolic strokes) or category 4 (cryptogenic strokes) ( Table 115.1 ). ASGOD is an alternative stroke classification that expands on the TOAST concept by including the likelihood of a potential cardiac or aortic source to cause a stroke ( Table 115.2 ). For instance, a patient with mitral valve endocarditis presenting with stroke would be classified as an ASCOD category C1 (probably cardioembolic cause).
TABLE 115.1
Classification of Ischemic Strokes by the TOAST Criteria
Adapted from Adams HP Jr, et al: Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment, Stroke 24:35–41, 1993; and Petty GW, et al: Ischemic stroke subtypes: a population-based study of incidence and risk factors, Stroke 30:2513–2516, 1999.
| TOAST Subtype | Description | Relative Prevalence (%) |
|---|---|---|
|
Significant stenosis or occlusion of a large cervical or cerebral artery presumably caused by atherosclerosis | 16 |
|
Cerebral vessel occlusion caused by embolus arising in the heart (and thoracic aorta) | 29 |
|
Lacunar brain infarcts | 16 |
|
Stroke of unknown cause | 36 |
|
Vasculopathies, hypercoagulable states, and so on | 3 |
TABLE 115.2
ASCOD Classification of Ischemic Strokes
Adapted from Amarenco P, et al: The ASCOD phenotyping of ischemic stroke (Updated ASCO Phenotyping), Cerebrovasc Dis 36:1–5, 2013.
| Stoke Type | Causality Likelihood Grade | ||
|---|---|---|---|
| A | Atherosclerosis | 1 | Potential |
| S | Small-vessel disease | 2 | Possible but uncertain |
| C | Cardioembolic | 3 | Unlikely |
| O | Other | 0 | Absent |
| D | Dissection | 9 | Nondiagnostic workup |
Cardioembolic strokes account for 15% to 30% of ischemic strokes. The outcome of cardioembolic stroke is poor, with a 3-year mortality rate of almost 50% in some instances. Cardiac and aortic sources have different embolic potential ( Table 115.3 ). Intracardiac thrombi, vegetations, and tumors as well as aortic atheroma have high embolic potential. In contrast, some valvular pathologies (e.g., calcific aortic stenosis, mitral annular calcifications, and Lambl excrescences), abnormalities of the interatrial septum (e.g., atrial septal aneurysm or patent foramen ovale [PFO]), and conditions of blood stasis (e.g., “smoke” and sludge) have a moderate embolic risk.
TABLE 115.3
Cardiac Sources of Emboli and Their Embolic Potential a
| High Risk Potential | Moderate Risk Potential |
|---|---|
|
|
Echocardiography is essential for the evaluation, diagnosis, and management of stroke and systemic embolism. The 2016 guidelines on the use of echocardiography in the evaluation of a cardiac source of emboli provide comprehensive recommendations for both transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE). They provide three levels of recommendations for each category of potential causes of cardioembolism: echocardiography recommended, echocardiography potentially useful, and echocardiography not recommended.
The diagnostic yield of echocardiography in elucidating a cause of stroke depends on the clinical likelihood and findings on brain imaging ( Box 115.1 ). Cardioembolism is a very likely cause of systemic embolism when one or more of the following is observed: (1) multiple organs are affected (e.g., brain, kidney, spleen), (2) multiple vascular territories are involved (infarcts in the territories of the right renal artery; left middle cerebral artery, right posterior cerebral artery), and (3) ischemic strokes and organ infarcts occurring at multiple time points (a combination of acute, subacute and chronic lesions).
BOX 115.1
Brain Imaging Clues to Possible Cardioembolism
-
Presence of older previous infarcts
-
Multiple infarcts, especially in different arterial territories
-
Hemorrhagic infarcts
-
Infarct showing cortical extension
-
Large lenticulostriate infarct
-
Classic embolic sites
-
Stem occlusion of the middle cerebral artery
-
Bilateral sylvian fissure infarcts
Cardioembolic Stroke: Clinical and Neuroimaging Context
A complete medical history provides important clues to the possibility of cardioembolism. The abrupt onset of neurologic dysfunction with maximum deficit at the onset and absence of a stuttering course and a severe headache are important clues that suggest cardioembolism. Seizures that accompany such a presentation also may suggest cardioembolism. These clinical features are not always diagnostic because emboli fragment and reocclusion may present in a nonabrupt manner in some instances.
Brain imaging, either computed tomography or magnetic resonance imaging, provides useful clues to the presence of a possible embolic presentation (see Box 115.1 ). Additional clues include a history of palpitations or documented atrial fibrillation (AF) or other signs of systemic embolism involving other organs. Some studies have suggested that the most specific features for cardioembolism are infarcts in multiple territories and concurrent systemic embolism. , In the absence of other competing mechanisms of stroke, clinical and brain imaging data must be combined to identify the potential cardioembolic pathology. Thus, finding concomitant low-risk pathology, such as fibrin strands or uncomplicated mitral valve prolapse, cannot be used to infer causality. An important part of the evaluation is to identify the presence of increased intracranial pressure because this may be a relative contraindication against the use of early TEE in low-risk patients or patients with a normal TTE. Inappropriate agitation or straining during the procedure may worsen increased intracranial pressure.
Cryptogenic Stroke
Stroke presumed to be cryptogenic may have an embolic component that may not be considered based on clinical assessment but may become more obvious after TTE. The link with PFO is well established in this population, especially in those 55 years of age and younger. However, causality is more difficult to prove, and the outcome of intervention (closure of PFO) in the absence of recurrent neurologic events is questionable.
Echocardiographic Evaluation
TTE is the first-line imaging modality for evaluating cardioembolism because it is widely available, portable, cost effective, and, with the use of harmonic imaging and contrast, enables most predisposing factors to cardioembolism to be evaluated. TTE should be geared toward identifying three major pathophysiological predispositions. First, a careful, systematic, anatomical evaluation should occur to identify masses, such as thrombus, tumors, and vegetations within the heart, and atheroma and its complications within the aorta. Conditions that predispose to thrombus formation, such as old myocardial infarcts, severe left ventricular (LV) dysfunction, and valvular disease (e.g., mitral stenosis), should be explored. Last, a systematic evaluation to exclude conditions that serve as conduits for possible paradoxical embolism, such as PFO and atrial septal defect, should be performed.
TEE is superior to TTE in identifying thrombus within the left atrial appendage (LAA) and smaller vegetations and in the evaluation of prosthetic valves for thrombus or endocarditis. Contrast or agitated saline contrast to identify shunts may be used to enhance clinical decision making. TEE also may be required to evaluate patients for shunts that may predispose to paradoxical embolism, such as PFO and small atrial septal defects, and is useful in identifying thoracic aortic problems, such as thrombus, atherosclerotic plaques, and aortic dissection. A normal TTE may warrant further investigation by TEE if the suspicion or clinical presentation of cardioembolism is high because many of the aforementioned pathologies may be better identified using this latter technique.
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