Key points
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Intracardiac thrombi constitute an important clinical condition because of their potential complications.
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Detection of ventricular thrombi is generally performed by transthoracic echocardiography, while atrial thrombi are generally evaluated by transesophageal echocardiography.
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Contrast-enhanced computerized tomography is more sensitive for detecting ventricular and atrial thrombi than transthoracic echocardiography, but the technique has been demonstrated to be inferior to transesophageal echocardiography for displaying atrial thrombi.
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Cardiac magnetic resonance imaging provides superior specificity for the evaluation of tissue characteristics and helps differentiate thrombi from other masses ( Table 6.1 ).
Table 6.1
Differentiating intracardiac thrombi from cardiac tumors .
Differentiating intracardiac thrombi from cardiac tumors
Imaging feature
Intracardiac thrombus
Intracardiac mass
Location
Left heart is more common
Right heart is more common
Morphology
Intrachamber masses
Rarely sessile
Infiltrative masses
Multiple masses
Appearance
Usually homogeneous
Usually heterogeneous
MRI
T2 hypointense when chronic
T2 hyperintense
Enhancement
No internal enhancement
Rarely peripheral pseudoenhancement when chronic
Often enhancing
Gadolinium-enhanced MRI
Progressively hypointense on contrast-enhanced inversion time scout sequence
Avid first-pass perfusion
Late gadolinium enhancement
Other discriminators
Pericardial disease is not directly associated
Left atrial enlargement or left ventricular infarction
Pericardial effusion is most common
Extracardiac cancer
Cystic masses of the left ventricle are rare. The differential diagnosis includes epithelial-lined cystic tumors, intracardiac teratomas, benign blood cysts, pericardial cysts, bronchogenic cysts, hydatid cysts, and thrombi. Echocardiography is a widely applied technique for the estimation of left ventricular masses; however, CMR has evolved to confer the capability for imaging cardiac masses and in some cases may offer additive information to echocardiography because of its high spatial accuracy and expanded possibilities for tissue characterization. Spontaneous clot dissolution can begin soon after its formation, and clot lysis is an integral part of this process. Be that as it may, a more rapid resolution has rarely been reported.
Intramyocardial dissecting hematomas constitute a rare complication of myocardial infarction, chest trauma, and percutaneous interventions. They can develop in the left ventricular free wall, the right ventricle, or the interventricular septum. Intramyocardial dissecting hematomas consist of a cavity filled with blood. The outer wall of the cavity is the myocardium and pericardium, and the inner wall, facing the ventricular cavity, is part of the myocardium and the endocardium.
Differential diagnosis includes pseudoaneurysms, intracavitary thrombi, and prominent ventricular trabeculations. Establishing the integrity of epicardium differentiates intramyocardial dissecting hematomas from pseudoaneurysms, as pseudoaneurysms comprise a complete rupture of the myocardial wall contained by the pericardium. The distinction from intracavitary thrombi relies on the clear identification of the endocardial layer surrounding the neoformation and its systolic expansion ( Table 6.2 , Algorithm 6.1 , Supplementary Videos 6.1 and 6.2 ).
| Predisposing conditions for left ventricular thrombi | |
|---|---|
| Left ventricular thrombi with impaired left ventricular function (more common) | Left ventricular thrombi with preserved left ventricular function (extremely rare) |
| Left ventricular apical aneurysms Following myocardial infarction with apical akinesia Following myocardial infarction in segments other than the left anterior descending territory Left ventricular pseudoaneurysms Dilated cardiomyopathy Apical ballooning (Takotsubo) syndrome | Hypercoagulable states Antiphospholipid antibodies Protein C deficiency Myeloproliferative disorders Essential thrombocythemia Myelofibrosis Salmonella septicemia Cardiac trauma Eosinophilic endocarditis Connective tissue disease Systemic lupus erythematosus Behçet disease On the surface of left ventricular tumors On device leads that inadvertently migrate to the left ventricle Administration of large doses of erythropoietin |
In more than 90% of cases, rupture occurs after the first myocardial infarction, and it has a strong correlation with single-vessel disease, reflecting a lack of collateral circulation. Risk factors include anterior wall infarct, large transmural infarction, age over 60 years, hypertension, female sex, single-vessel disease, and the absence of previous cardiac events.
Echocardiographic features of intramyocardial dissecting hematomas include the formation of 1 or more neocavitations within the tissue with an echolucent center, a thinned and mobile endomyocardial border surrounding the cavitary defect, ventricular myocardium identified in the regions outside of the cystic areas, and changes in the echogenicity of the neocavitation, suggesting blood content.
The management of intramyocardial dissecting hematomas depends on multiple factors, including the patient’s age, hemodynamic stability, the size of the hematoma, the presence of ventricular septal defects, left ventricular function, and pericardial effusion. Intramyocardial dissecting hematomas limited to the apex have a high probability of spontaneous reabsorption, and an initial conservative approach may be reasonable. Patients with the expansion of dissection on serial echocardiography, ventricular septal defects, compromised hemodynamics, and low ejection fractions in the anterior wall myocardial infarction should undergo surgery .
Cardiac thromboemboli may be implicated in more than 15% of ischemic strokes, and the left atrial appendage may be the site of more than 90% of thrombi originating in the left atrium. Fifty percent of left atrial thrombi occur in patients with rheumatic valvular disease, and nearly 90% of left atrial thrombi in patients with nonvalvular atrial fibrillation are limited to the left atrial appendage. TEE findings associated with the increased risk of thromboembolism include left atrial and left atrial appendage smoke, decreased left atrial appendage emptying velocity, left atrial enlargement, increased severity of mitral stenosis, and multiple left atrial appendage lobes. A left atrial appendage emptying velocity of less than 40 cm/s is associated with the increased risk of spontaneous echo contrast. As this velocity decreases below 20 cm/s, there is an even greater risk of visual left atrial appendage and thromboembolism. Patients with mitral stenosis in sinus rhythm should be treated with anticoagulation therapy if they have a history of paroxysmal atrial fibrillation, left atrial appendage thrombi, previous embolism, spontaneous echo contrast seen on TEE, or a left atrial diameter of greater than 50 mm .
The terms “left atrial diverticulum” and “accessory left atrial appendage” have both been used to describe structures protruding from the left atrium that have normal myocytes and are clearly different from a left atrial aneurysm. The incidence rate of left atrial diverticulum/accessory appendage is between 10% and 23%. This condition is thought to be associated with ectopic foci that initiate atrial fibrillation, incomplete ablation lines on the left atrial roof, and potential complications such as thrombus formation and cardiac tamponade during atrial fibrillation ablation ( Supplementary Video 6.3 ).
Left atrial ball thrombi appear to be an unusual occurrence in mitral stenosis. Symptoms are dyspnea, syncope, peripheral arterial embolism, and sudden cardiac death. The physical examination is the same as that for mitral stenosis. TEE has been recommended as the best choice for identifying the presence of left atrial thrombi and for guiding further therapy designed to reduce the thromboembolic risk. The presence of free-floating thrombi may be expected to indicate a higher embolic potential. Anticoagulation and thrombolytic therapies do not appear to have a role in the acute management of left atrial ball thrombi, although the importance of anticoagulation in the prevention of recurrence is obvious. Surgical removal of the thrombus with the simultaneous treatment of the underlying cause is the first choice treatment with good results in most cases ( Tables 6.13 and 6.14 ).
