The relationship of transmembrane potential to surface morphology of human atrial muscle and cardiac hemodynamics.

A correlative study of transmembrane potential characteristics, surface morphological features of human atrial muscle, and cardiac hemodynamics was carried out in 41 patients, who were divided into 2 groups based on the level of the mean maximum diastolic potentials (MDP). Group A consisted of 19 patients with MDP values ranging from -60.0 to -82.0 mV (mean +/- S.D. = -65.70 +/- 6.63 mV). Group B included 22 patients who had abnormally low MDP (range -36.0- -58.5 mV, mean +/- S.D. = -48.14 +/- 6.72 mV). The differences in electrophysiological data were statistically significant. However, there were no significant differences in the hemodynamic data between the 2 groups. Furthermore, there was poor correlation between the electrophysiological and hemodynamic data in both groups. In group A, scanning and transmission electron microscopy revealed either no changes or only mild alterations in the surface morphology of the atrial myocardium. Various degrees of surface morphological changes, including a focal loss of the endothelium which was always associated with endocardial fibrosis, irregular thickening and lamination of the glycocalyx, disruption of the sarcolemma and complete destruction of the surface membrane structures were more often observed in group B. These results provide valuable evidence that sarcolemmal changes may underlie the electrophysiological alterations in diseased human atria. We suggest that the principal pathogenetic mechanisms leading to the transmembrane potential changes are the altered surface morphology of atrial myocardial cells, resulting from underlying disease processes.