Transesopnageal echocardiographic anatomical and functional assessment of right atrial appendage: comparison with left atrial appendage and implications for local thrombus formation in patients with mitral stenosis

ABSTRACT

Right atrial appendage [RAA] thrombi and dysfunction have been reported in patients with atrial fibrillation [AF]. Although pulmonary embolism was a life-threatening complication of AF, there are little data about RAA and its thrombi in AF. Furthermore, to date there have been no prospective studies designed to examine RAA in patients with rheumatic mitral stenosis [MS]. To define RAA anatomical and functional parameters and to compare them with left atrial appendage [LAA] parameters in patients with moderate MS both in AF and in sinus rhythm [SR] and to study the implications for local thrombus formation. Transthoracic [TTE] and multiplane transesophageal echo [TEE] were performed in 31 patients with moderate MS [16 in SR. Group I and 15 in AF, Group II]. We measured mitral valve area [MVA], mean pulmonary artery pressure [MPAP], left atrial diameter [LAD], LV EDD and ESD, EF%, RAA and LAA neck width, length, area, ratio of neck to area, and emptying velocity. We assessed also the incidence of RA-RAA and LALAA SEC and thrombi. Adequate visualization of RAA was highly feasible by TEE in 31/34 [91%] of patients. RAA anatomic and functional parameters were independent of imaging plane. Patients in AF had significantly increased LAD [p=0.004] and MPAP [p<0.0001] than those in SR. The RAA area was proportional to the LAA area [r=0.87, p<0.0001] only in patients with SR. On the other hand, RAA neck width and ratio of neck width to area were greater than those of LAA while LAA length and area were greater than those of RAA regardless the presence of AF. AF caused more enlargement in LAA [10.21 +/- 4.15 Vs 5.41 +/- 1.78, p<0.0001] compared to RAA [5.37 +/- 2.08 Vs 4.40 +/- 1.44, p=NS] while more dysfunction in RAA / [reduced emptying velocities [0.45 +/- 0.11]-[0.28 +/- 0.08], [40%] p<0.0001] compared to that of the LAA [0.43 +/- 0.08] - [0.32 +/- 0.14], [25.6%] p<0.01/ ]. AF caused higher prevalence of RAA spontaneous echo contrast [SEC] [66.7%] than in SR [37.5%], [p<0.0001]. Also it caused higher RAA thrombosis [46.7%] than in SR [25%], [p=0.001]; and finally RAA SEC was the only independent predictor of RAA thrombosis in SR [p=0.04] while the reduced ejection velocity was the only independent predictor of RAA thrombosis in MS patients with AF [p=0.04]. RAA imaging was highly feasible. RAA anatomic and functional parameters were independent of imaging plane. AF was associated with RAA minimal remodeling, maximal dysfunction and subsequently thrombosis. RAA dysfunction and SEC were independent predictors for RAA thrombosis. RAA SEC and thrombosis were directly proportional to LAA remodeling and dysfunction. Therefore, assessment of not only LAA but also RAA may be important during TEE examination of patients with MS