A 27-year-old female was referred to our advanced echocardiography department for Three-dimensional (3D) echocardiography for a better evaluation of a particle on the anterior mitral leaflet. The patient had a history of a stroke 9 months previously, which led to hemiparesis in her left limbs. She had no cardiovascular risk factors.
On initial transthoracic echocardiography in another general hospital, a particle was detected on the atrial side of the anterior mitral leaflet with moderate mitral regurgitation. The other echocardiographic findings were normal. Extensive molecular and serological investigations demonstrated wild-type factor V Leiden. Consequently, the particle on the anterior mitral leaflet was considered to be a source of embolism, for which she was treated with rivaroxaban. On follow-up transthoracic echocardiography after 8 months of treatment, the lesion on the anterior mitral leaflet was persistent [Video 1]. Accordingly, 2D transesophageal echocardiography was performed, which revealed a large patent foramen ovale (2 mm) and a particle on the atrial side of the anterior mitral leaflet with a tail [Video 2]. Next, 3D transesophageal echocardiography demonstrated accessory atrial mitral chordae tendineae, which were attached to the A2 scallop (near to the A1 scallop) of the anterior mitral leaflet on one side and to the anterior left atrial wall behind the ascending aorta wall on the other side [Figure 1]. The result was the prolapse of the A2 scallop, accompanied by a moderate eccentric mitral regurgitation jet toward the lateral left atrial wall. According to existing evidence, the patent foramen ovale in the context of a hereditary hypercoagulable state was the most probable etiology for the patient's stroke. Rivaroxaban was, therefore, continued.
Figure 1.
Three-dimensional mode (zoom) of transesophageal echocardiography shows the attachment of accessory atrial mitral chordae tendineae to the A2 scallop of the anterior mitral leaflet in proximity to the A1 scallop
Accessory left atrial mitral chordae tendineae constitute a congenital anomaly, the clinical implications of which have hitherto remained unknown. Nonetheless, the A2 scallop could be the most common site for the attachment of such chordae.[1] This congenital anomaly may lead to significant mitral regurgitation, which might even necessitate surgery.[2,3] The simulation of vegetation by left atrial mitral chordae in a patient has been previously reported.[4] Awareness of the possibility of this congenital anomaly can help prevent unnecessary treatments or diagnostic tests.[4]
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The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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