Cardiovascular Anesthesiology: Echo Didactics & Rounds
A 69-yr-old woman was scheduled for mitral valve replacement and coronary artery bypass graft surgery. Her medical history included mitral stenosis and a single coronary artery disease. She was given anticoagulation therapy for paroxysmal atrial fibrillation. Preoperative transthoracic echocardiography demonstrated mitral stenosis and trivial aortic regurgitation but no abnormal intracardiac structures. After induction of general anesthesia, we placed a transesophageal multiplane probe (Philips Electronics, Eindhoven, Netherlands). Two dimensional transesophageal echocardiography (TEE) confirmed doming and calcification of the mitral valve. Color flow Doppler imaging in the midesophageal long- and short- axis views demonstrated a trivial eccentric jet of aortic regurgitation from the commissure between the right and left coronary cusp. The midesophageal long-axis view showed the presence of a filamentous structure on the aortic valve (AV), which was not noticed by the preoperative transthoracic echocardiography. The structure was very thin, approximately 10-mm long, and was flapping in the aortic root (Figs. 1A and B), (Video clip 1; please see video clip available at www.anesthesia-analgesia.org).
We first performed mitral valve replacement with a mechanical valve from the right atrium via the atrial septum. Second, we performed coronary artery bypass to the left anterior descending branch with the left internal thoracic artery. Third, we opened the ascending aorta to observe the flapping structure. The structure was attached to the free edge of the left coronary cusp. We decided to resect it to avoid systemic embolization and to confirm the diagnosis. The structure was a 12-mm fibrous tissue (Fig. 2). We presumed it was a flapping piece torn from the commissure between the right and left coronary cusp along the edge of the left coronary cusp. Because pathological examination revealed that the structure consisted of connective tissue covered by a single layer of endothelial cells, we diagnosed Lambl’s excrescence. After uneventful weaning from cardiopulmonary bypass, subsequent TEE confirmed that the filamentous structure on the AV was no longer present and the degree of aortic regurgitation remained trivial.
The differential diagnoses of the flapping structure in the AV included imaging artifact, vegetation, thrombus, redundant leaflet, flap due to aortic dissection, papillary fibroelastoma, and Lambl’s excrescence. The TEE imaging from multiple planes excluded a possibility of imaging artifact. We easily excluded the diagnosis of vegetation, because inflammatory findings and a history of infections endocarditis were absent. We also excluded thrombus because the structure was very thin and filamentous. We dismissed the possibility of a redundant leaflet or a flap due to aortic dissection, because three cusps of the AV were depicted clearly by TEE. The distinction between papillary fibroelastoma and Lambl’s excrescence was particularly difficult. Papillary fibroelastoma typically appears on echocardiography as a small pedunculated, homogenous, well-demonstrated mobile mass attached by a small stalk. Although these findings may be applied to Lambl’s excrescence, the stalk of papillary fibroelastoma has a broader base than Lambl’s excrescence. Papillary fibroelastoma has a jelly-like appearance, whereas Lambl’s excrescence consists of fibrous tissue.
Lambl’s excrescences are valve strands and have a small mobile density of connective tissue. They are thin (<1 mm), long (>10 mm) filiform projections from heart valves and show undulating independent motion.1 They are more commonly seen on the mitral valve than on the AV, typically near the closure line of the mitral valve. Although it was first reported that they were composed of fibrin, morphologic analysis revealed collagen.1,2 Valve strands were reported in 39% of elderly patients who had TEE for suspected cardiogenic embolic stroke, giving an odds ratio (95% confidence interval) of ischemic stroke in patients with mitral valve strands of 2.2 (1.4–3.6; P < 0.005).3 In other studies, however, no relation between brain infarction or clinical embolic events and valve strands was demonstrated.4 Cohen et al. have shown that strands on native mitral valves do not increase the risk of recurrent brain infarction.5 More recent reports suggest that no specific treatment is needed in patients with stroke who had native valve strands as a single abnormality.6,7 However, we decided to resect the flapping structure to confirm a precise diagnosis. Further study is necessary to determine how to treat Lambl’s excrescence.
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