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

BACKGROUND: The precise contribution of left atrial appendage (LAA) endocardial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibrillation (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 changes, 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 between those with AF and sinus rhythm. Our second objective was to relate endocardial changes to plasma levels of von Willebrand factor (vWf), an established marker for endothelial damage. LAA specimens were obtained immediately after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacement. Right atrial appendage (RAA) specimens were similarly obtained as controls for individual patients. The specimens were fixed in 2.5% glutaraldehyde solution overnight, stored in Sorensen's phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documented the most advanced lesion in each specimen as follows: (1) "minimal" changes, with minimal disruption of the endocardium; (2) "intermediate" changes or prethrombotic lesions; and (3) "advanced" changes, with endocardial disruption and thrombotic lesions. Plasma levels of vWf were also measured (enzyme-linked immunosorbent assay) in all patients, and results were compared with those of age- and sex-matched healthy control patients.
RESULTS: Advanced changes were more frequently seen in the endocardium of the 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 =.00167). Similarly, the LAA from patients with mitral stenosis had a higher proportion 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 significant. Plasma vWf levels were significantly higher in patients with MV disease 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 earlier 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 compared with mitral regurgitation. These anatomic appearances may contribute to the risk of intra-atrial thrombus formation in patients with mitral valve disease, especially if AF is present.