Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study

Background The precise contribution of left atrial appendage (LAA) endocard ial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibri llation (AF), has not as yet been clearly described. This may be important because the LAA is the usual site for thrombus formation. Methods The purpose of this study was to describe endocardial surface chang es, through the use of scanning electron microscopy, in the left and right atrial appendages of patients with MV disease and the differences, if any, between patients with mitral stenosis and mitral regurgitation as well as b etween those with AF and sinus rhythm. Our second objective was to relate e ndocardial changes to plasma levels of von Willebrand factor (vWf), an esta blished marker for endothelial damage. LAA specimens were obtained immediat ely after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacem ent. Right atrial appendage (RAA) specimens were similarly obtained as cont rols for individual patients. The specimens were fixed in 2.5% glutaraldehy de solution overnight, stored in Sorensen's phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documen ted the most advanced lesion in each specimen as follows: (1) "minimal" cha nges, with minimal disruption of the endocardium; (2) "intermediate" change s or prethrombotic lesions; and (3) "advanced" changes, with endocardial di sruption and thrombotic lesions. Plasma levels of vWf were also measured (e nzyme-linked immunosorbent assay) in all patients, and results were compare d with those of age- and sex-matched healthy control patients. Results Advanced changes were more frequently seen in the endocardium of th e LAA when compared with the RAA (31% vs 6%), whereas minimal changes were more frequently seen in the RAA compared with the LAA (23% vs 6%) (P = .001 67). Similarly, the LAA from patients with mitral stenosis had a higher pro portion of "advanced" endocardial changes when compared with patients with mitral regurgitation (67% vs 24%; P=.0066). The LAA in patients with AF had more "advanced" changes (39% vs 27%), but this was not statistically signi ficant. Plasma vWf levels were significantly higher in patients with MV dis ease compared with healthy control patients (132 +/- 33 IU/dL vs 99 +/- 37 IU/dl; P=.0004) and in patients with advanced LAA changes compared with ear lier changes (149 +/- 34 IU/dL vs 121 +/- 31 IU/dL P = .042). Conclusions Endocardial damage occurs in the atrial appendages of patients with MV disease. Potentially thrombogenic changes are more commonly seen in the LAA compared with the RAA and in patients with mitral stenosis compare d with mitral regurgitation. These anatomic appearances may contribute to t he risk of intra-atrial thrombus formation in patients with mitral valve di sease, especially if AF is present.