Chapter 4 Cardiac Embolism

Cardiac embolism represents one of the most common mechanisms of ischemic stroke. It is most common in the elderly as a consequence of the high incidence of atrial fibrillation, but it is also one of the most frequent causes of stroke in the young. Yet several factors often make the diagnosis of cardiac embolism complicated: (1) cardiac embolism can produce infarctions in any vascular distribution; (2) some of the potential sources of cardiac embolism are prevalent in the general population; (3) cardioembolic sources often coexist with atherosclerotic vascular lesions in the cerebral vasculature. Furthermore, even when the diagnosis of a cardioembolic stroke is typically followed by the initiation of anticoagulation for secondary prevention, this intervention has only been scientifically validated for atrial fibrillation and mechanical valve prosthesis. With these caveats in mind, Table 4-1 lists the potential causes of cardiac embolism divided according to the strength of the evidence supporting the pathophysiological association.

TABLE 4-1 Cardiac sources of embolism.

* Includes atrial flutter.

Brain infarctions caused by cardiac embolism tend to share similar radiological characteristics regardless of the type of cardiac disease responsible for the embolism. These general characteristics are listed in Table 4-2 and illustrated in Figure 4-1. The pattern of acute multiple bilateral infarctions on diffusion-weighted imaging (DWI), especially when involving the anterior and posterior circulation territories, is strongly associated with cardiac embolism.^1,2 Infarctions with embolic appearance and acute multiple brain infarctions on DWI^2–4 should raise suspicion of a cardiac source but may also be produced by artery-to-artery embolism. In fact, it is essentially impossible solely on the basis of brain imaging to distinguish cardioembolic infarctions from infarctions due to aortic embolism. It is important to keep in mind that cardioembolic strokes can have atypical presentations, such as relatively small subcortical infarctions.⁵ Thus the presence of radiological features highly suggestive of cardiac embolism should prompt comprehensive cardiac assessment, but their absence does not exclude the possibility of a cardioembolic mechanism.

TABLE 4-2 Radiological characteristics of cardioembolic strokes.

Figure 4-1 Patterns of ischemic infarction from cardiac embolism. (A) Computed tomography (CT) scan shows infarctions in two vascular territories (bilateral middle cerebral artery strokes). (B) CT scan reveals anterior and posterior circulation strokes. (C) CT scan displays a typical wedge-shaped infarction based on the cortex. (D) CT scan shows a wedge-shaped cortical infarction associated with a hyperdense vessel sign in an M2 branch of the right middle cerebral artery (arrow). (E) Axial diffusion-weighted imaging magnetic resonance imaging (DWI MRI) revealing scattered areas of restricted diffusion indicative of acute ischemia within the left middle cerebral artery territory. (F) DWI MRI showing multiple small ischemic infarction in a pattern consistent with “embolic shower.”

The advent of echocardiography, particularly transesophageal echocardiography (TEE), has provided a wealth of information on various cardiac abnormalities that may increase the risk of ischemic stroke. Transthoracic echocardiography (TTE) provides better visualization of the left ventricle and mitral valve, but it typically adds little to TEE in the evaluation of stroke patients. TEE offers better visualization of the left atrium, left atrial appendage, interatrial septum, aortic valve, and aortic arch. The superiority of TEE for the study of the cardiac structures more commonly associated with embolism makes it the preferred choice for the evaluation of cardiac embolism in combination with electrocardiography (to detect myocardial ischemia and arrhythmias) and Holter monitoring (to recognized paroxysmal arrhythmias not apparent on the electrocardiogram [ECG]).⁶ TTE is justified when myocardial ischemia, areas of ventricular hypokinesis/akinesis, or dilatated cardiomyopathy are suspected by the history or the initial ECG. Although we strongly advocate the use of TEE for the study of cardiac sources of embolism after a transient ischemic attack (TIA) or stroke, in this chapter we present several examples of diagnostic TTE, because it was the institutional practice at Jackson Memorial Hospital’University of Miami to perform a transthoracic study first.

This chapter summarizes information on the most commonly encountered sources of cardiac embolism. It presents various illustrations of the radiological pattern of the brain infarctions and echocardiographic appearance of the cardiac disorders. It concludes with a reference to aortic, embolism, which that is included here because its diagnosis hinges on the use of TEE and the neuroimaging features of strokes caused by aortic embolism are essentially indistinguishable from those due to cardiac embolism.

ATRIAL FIBRILLATION

Case Vignette

A 72-year-old man with history of hypertension, dyslipidemia, and coronary artery disease presented with sudden left-sided weakness. Examination revealed an irregularly irregular pulse, left visual field deficit, left hemiparesis, and left hemihypoesthesia with neglect. ECG confirmed the suspicion of atrial fibrillation, and brain imaging showed a right middle cerebral artery infarction (Figure 4-2). TEE was remarkable for left atrial enlargement but did not show any atrial thrombus or dense spontaneous echo contrast. The patient was initially treated with aspirin because of concerns about possible hemorrhagic transformation of the cerebral infarction. Beta-blockers were successful in maintaining the ventricular rate controlled. Warfarin was started 3 days after the stroke without complications. The patient evolved favorably and remained free of stroke recurrence 3 years later.

Figure 4-2 (A) Twelve-lead electrocardiogram showing irregular rhythm and absence of p waves, which characterize atrial fibrillation. Atrial activity is represented by fibrillatory or f waves, seen between QRS complexes. (B) Computed tomography scan of the brain shows two areas of infarction in the right hemisphere, an acute lesion in the right middle cerebral artery territory and a more chronic stroke in the border zone between the middle and posterior cerebral arteries. (C) Diffusion-weighted sequence of the brain magnetic resonance imaging confirms the area of acute ischemia in the right middle cerebral artery distribution.

♦ Stroke may be the presenting manifestation of atrial fibrillation.

♦ Paroxysmal atrial fibrillation carries a risk of thromboembolism similar to that associated with chronic atrial fibrillation.

♦ Atrial fibrillation is one of the most common causes of stroke in older patients. Moreover, the risk of thromboembolism from atrial fibrillation increases with age.

♦ Because of the high frequency of atrial fibrillation among elderly patients with ischemic strokes of embolic appearance, these patients must be exhaustively studied with serial electrocardiograms, Holter monitoring (24-48 hours), and probably prolonged ambulatory heart rhythm monitoring (several days to weeks).^7–9

♦ There are no distinctive radiological features to discriminate atrial fibrillation from other causes of cardiac embolism.

♦ Echocardiography is a useful tool to assess the risk of embolism in patients with atrial fibrillation. Embolic risk is increased when the following findings are present (Figure 4-3 and 4-4):

♦ Left atrial thrombus

♦ Left atrial dilatation^10,11

♦ Thrombus in left atrial appendage^12,13

♦ Dense spontaneous echo contrast^12,13

♦ Reduced left atrial appendage peak flow velocities (≤ 20 cm/sec)¹²

♦ Left ventricular systolic dysfunction¹¹

♦ Complex aortic arch plaque^12,13

♦ TEE should always be performed before cardioversion in patients with atrial fibrillation lasting longer than 48 hours or of unknown duration.¹⁴

♦ Anticoagulation is clearly indicated for primary and secondary stroke prevention in patients with atrial fibrillation.¹⁵ Aspirin should only be used in patients with low risk of thromboembolic complications (i.e., young age, no cardiovascular risk factors, absence of echocardiographic markers of increased embolic risk).¹⁵ When anticoagulation is contraindicated by concurrent conditions, aspirin is prescribed and radiofrequency ablation procedures to restore sinus rhythm permanently are an option. Percutaneous occlusion of the left atrial appendage is being investigated as another alternative for these cases.¹⁶

♦ Sick-sinus rhythm (or tachycardia-bradycardia syndrome) is frequently associated with atrial fibrillation in older patients and may therefore increase the risk of stroke (Figure 4-5). This disorder is best treated with insertion of a pacemaker.

Figure 4-3 A 64-year-old man with history of hypertension and paroxysmal atrial fibrillation who had elected not to be treated with oral anticoagulation was transferred to our hospital with diagnosis of acute stroke. (A) Computed tomography scan of the brain showed areas of wedge-shaped cortical infarction in multiple territories, including the posterior division of the left middle cerebral artery, the anterior division of the right middle cerebral artery, and the external border-zone region between the right middle and posterior cerebral arteries. (B) Transesophageal echo view at the level of the midesophagus showing the left atrial appendage obliterated by a thrombus (arrowhead). AV, aortic valve. (C) Closer view of the thrombus (solid arrow) within the left atrial appendage also allows identification of spontaneous echo contrast in the left atrium (open arrow). LA, left atrium; LAA, left atrial appendage. (D) Detail view of the round echodensity located at the entrance of the left atrial appendage, consistent with a thrombus (solid arrow).

Figure 4-4 Echocardiographic predictors of increased stroke risk in patients with atrial fibrillation. (A) Spontaneous echo contrast or “smoke” (arrow) seen in the left atrium on transesophageal view. (B) Doppler flow velocities measured at the left atrium appendage entrance. Low-amplitude signals (slow velocities) represent decreased left atrial appendage blood flow and indicate predisposition for thrombus formation. (C) Left atrial enlargement seen on apical transthoracic echocardiogram view; the left atrial size in this patient approached that of the left ventricle. (D) Apical four-chamber transthoracic echo view revealing the presence of a left atrial thrombus (arrow). LA, left atrium; LAA, left atrial appendage; LV, left ventricle.

Figure 4-5 Twenty-four-hour Holter monitor strip of a 63-year-old patient with recent ischemic stroke and sick-sinus syndrome. Note the presence of a fast supraventricular tachycardia (A) and sinus bradycardia (B), the diagnostic hallmark of the tachycardia-bradycardia syndrome.

DILATED CARDIOMYOPATHY

♦ Patients with dilated left ventricle and severely depressed left ventricular systolic function have considerably increased risk of stroke because of elevated incidence of ventricular thrombus formation (Figure 4-6) and higher risk of atrial fibrillation.

♦ The stroke risk is increased regardless of whether the cause of the dilated cardiomyopathy is ischemic or nonischemic.

♦ Peripartum cardiomyopathy should be considered in patients presenting with stroke during puerperium.

♦ Assessment of left ventricular function and evaluation for possible mural or apical clots are best accomplished using transthoracic echocardiography (see Figure 4-6).

♦ In patients with associated atrial fibrillation, it is also important to study the left atrial chamber and left atrial appendage (Figure 4-7).

♦ Anticoagulation is generally accepted as the optimal strategy for secondary prevention after a stroke attributed to dilated cardiomyopathy.¹⁷ For primary stroke prevention, anticoagulation is only indicated in patients with documented atrial fibrillation or left ventricular thrombus¹⁷ but might be useful in patients without these complicating conditions as well.¹⁸

Figure 4-6 Images illustrating a case of multiple embolic strokes secondary to left ventricular thrombus due to nonischemic dilatated cardiomyopathy. (A) Computed tomography scan of the brain showing bilateral infarctions. (B) Detail of a large left ventricular apical thrombus seen on transthoracic echocardiogram (arrow).

Figure 4-7 Another example of a patient with ischemic stroke secondary to dilatated cardiomyopathy, in this case associated with atrial fibrillation. (A) Parasternal long axis transthoracic echocardiogram view showing a dilated left ventricle filled with thrombus. Also note the presence of a thrombus attached to the left atrial wall (arrow). (B) Parasternal short axis transthoracic view at the level of the aorta. Two rounded echodensities are seen within the left atrium consistent with thrombi (arrows). AV, aortic valve; LA, left atrium; LV, left ventricle; MV, mitral valve.

MYOCARDIAL INFARCTION

♦ The risk of stroke is increased within the first 3 to 4 months after a myocardial infarction, with the highest embolic risk occurring during the first 2 weeks. The increased risk persists after this period in patients with depressed left ventricular function¹⁹ or atrial fibrillation.

♦ Thus it is important to exclude concurrent myocardial ischemia in all patients presenting with acute ischemic stroke.

♦ Transmural anterior wall infarctions carry higher risk, but stroke may complicate inferior wall infarctions as well.

♦ TTE should be performed to determine whether left ventricular thrombus formation has occurred over dyskinetic wall segments (Figure 4-8). Thrombi with mobile or pedunculated components are most dangerous.

♦ Patients with left ventricular apical aneurysms are at particularly high risk of embolism (Figure 4-9).

♦ Anticoagulation for at least 3 to 6 months is recommended for patients with stroke due to acute myocardial infarction with documented left ventricular mural thrombus.²⁰ In patients with transmural myocardial infarction but without documented mural thrombus, short-term anticoagulation may be justified if the stroke was attributed to concurrent myocardial ischemia.

Figure 4-8 A 58-year-old man with history of hypertension and smoking presented to the emergency department with angina and fluent aphasia. (A) Computed tomography scan showed low attenuation changes in the territory of the posterior division of the left middle cerebral artery. (B) Acute left middle cerebral artery branch infarction was confirmed by magnetic resonance imaging (diffusion-weighted sequence shown). (C) Electrocardiogram in the emergency department showed ST elevation in the anterior leads with reciprocal ST depression in the inferior leads in a pattern typical for myocardial infarction of the anterior wall. (D) Detail of the anterior precordial leads showing significant ST elevation in V1 to V3 (E) Apical two-chamber transthoracic echocardiogram view showing a thrombus in the LV apex (arrow).

Figure 4-9 Echocardiographic predictors of increased risk of stroke after a myocardial infarction. (A) Large thrombus (arrow) protruding into the left ventricular cavity from the apex seen on transthoracic echocardiogram. (B) Detailed view showing the large echodensity within the left ventricle consistent with thrombus. (C) Left ventricle apical aneurysm (arrow) following extensive anterior wall myocardial infarction visualized on this apical two-chamber transthoracic echocardiogram view. (D) Transthoracic echocardiogram view after injection of echo contrast. Note the swirling of blood flow in the area corresponding to the left ventricle apical aneurysm (arrow). LA, left atrium; LV, left ventricle.

INFECTIVE ENDOCARDITIS

Case Vignette

A 46-year-old man with recent community-acquired pneumonia and history of diabetes presented with worsening dyspnea. Examination revealed that the patient was confused and febrile, and careful cardiac auscultation denoted a new systolic murmur with characteristics suggestive of mitral regurgitation. Brain imaging showed scattered, small, acute ischemic infarctions in cortical locations. Echocardiography disclosed a vegetation attached to the mitral valve (Figure 4-10, F and G), and blood cultures grew Staphylococcus aureus. The patient was successfully treated with vancomycin and rifampin first and later switched to nafcillin with rifampin when susceptibilities proved that the organism was not methicillin-resistant. The patient did not have recurrent episodes of systemic or cerebral embolism, and repeat echocardiography 4 weeks later confirmed resolution of the vegetation.

Figure 4-10 Diffusion-weighted sequence of brain magnetic resonance imaging showing multiple small lesions (open arrows)

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