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The TTE showed:
Left Ventricular Apical Akinesis
Left Ventricular Enlargement
Apical Thrombus that is laminated, immobile and is mostly along the apical septal wall.
The central portion of the thrombus appears liquefied.
The TEE showed:
Apical Thrombus that was mobile along the anterior wall. The apical portion was laminated.
In the 2CV, the mid segment of the anterior wall had a mobile thrombus attached to the subendocardium.
In other views the thrombus was mobile and irregular in the mid-apical portion of the anterior wall.
Anterior and Anteroseptal Akinesis
The 3D TEE really showed the thrombus as with an irregular border.
Predisposing factors are:
Other disease states that predispose a patient to an apical thrombus are:
Apical thrombus is most likely to occur after an acute anterior myocardial infarction, especially if an apical aneurysm is present. The thrombus is more likely to occur during the first week after the myocardial infarction, before scare formation has occurred. Mortality rate is increased if the thrombus forms within 48 hours after the myocardial infarction. Up to 10% of apical thrombi may embolize. During cardiac surgery,
manipulation of the heart and/or placement of an apical LV vent may induce embolization of the thrombus.
In the absence of a myocardial infarction, apical thrombi are more likely to be found in patients with
cardiomyopathy - Dilated (DCM), Peripartum (PPCNM) Tako-Tsubo (TTCM) cardiomyopathies have all reported the presence of an apical thrombus. A study on apical thrombi who were cardioverted did not have any cases of embolization and suggested that cardioversion was safe. (You might want to reconsider that conclusion until more studies are done.)
TTE is more likely to visualize the apical thrombus because the apical thrombus is in the near field in the TTE apical windows whereas by TEE the apical thrombus is in the far field. Zoom, increased frequency, and adjustments in gain can help find apical thrombi but it may be missed by TEE.
Echocardiographic features of an apical thrombus are:
Contrast agents can improve the detection of thrombi by opacifying the left ventricular cavity.
High Frequency settings can improve endocardial border detection when thrombi are laminated.
B Color imaging may also help delineate between myocardium and thrombus formation.
Thrombi that are mobile, immature, filamentous, and have central liquefaction (different densities with a central zone of an echolucent area), or irregular borders are at highest risk of embolization. Thrombi that are
immobile, laminated or layered, homogeneous, and echo dense are the lowest risk for embolization.
Hypereosinophilic syndrome can have apical thrombi associated with the disease. The underlying subendocardium is fibrotic. Antiphospholipid antibody syndrome associated with Systemic Lupus Erythematosus (SLE) has reported DVTs and apical thrombi. Apical thrombi that have central liquefaction can simulate a hydatid cyst.
The presence of an apical thrombus can serve as a marker for myocardial nonviability. In patients where
an apical thrombus is present, the adjacent myocardium tended to be nonviable (0.7 viable segments) compared to patients without an apical thrombus (1.8 viable segments).
Apical thrombi have been diagnosed by 3D echocardiography. However, at this time, 2D echocardiography, especially TTE is the gold standard for diagnosis of apical thrombi. TEE can also diagnose apical thrombi, however, at this time TTE is the preferred method to diagnose an apical thrombi.
For this case, the theurapeutic options were to either leave to clot alone and anticoagulate the patient or resect it. Since the clot was irregular and mobile we decided to resect the clot. In patients with apical aneurysms a DOR procedure could be performed, but, that was not indicated in this case.
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