It would appear from this study that one can determine the contour of the left atrial pressure pulse curve by recording esophageal pulsations at the level of the left atrium with the technique which has been described. This relationship between the intra-atrial pressure pulse contour and the contour of the esophageal pressure pulse tracing (piezocardiogram) has been demonstrated by two kinds of evidence. The first evidence consisted of a study in animals wherein simultaneous recordings were made of left atrial pressure curves and curves of esophageal pressure pulsations. These studies showed that all phases of the atrial pressure curve were transmitted to the esophageal curve. The second type of evidence consisted in a comparison between direct intra-atrial pressure tracings which had been obtained by other investigators in human beings with mitral valve disease and the esophageal piezocardiograms which had been obtained by us in other human beings who also had mitral valve disease. This evidence, though circumstantial in a sense, appeared to us to be strongly convincing. Absolutely conclusive proof in human beings of the identity between the two sets of curves could be obtained only by simultaneous recording of the direct atrial and esophageal pressure curves in the same individual during mitral valve surgery. We have not yet been able to accomplish this. On the basis of the comparative evidence discussed above, it was possible to tentatively divide the piezocardiographic tracings into three categories, namely, predominant mitral insufficiency, mitral stenosis without insufficiency, and mitral stenosis with insufficiency. Tracings of patients with mitral insufficiency were characterized by a positive pressure wave which began its ascent in ventricular systole, rose progressively, and reached a peak in late systole just prior to the opening of the mitral valve. The pressure then declined precipitously. This wave contour corresponded very closely to the findings of Wiggers 4, 5 in animals with experimentally induced mitral insufficiency. He emphasized that the increase in atrial pressure and volume due to regurgitation did not reach substantial proportions in the early phases of ventricular systole. The greatest amount of regurgitation occurred during the latter phases of ventricular ejection, increasing even as ventricular pressure began to fall. The tracings of patients who had mitral stenosis with no insufficiency were characterized by a sharp, early systolic pressure peak and either a plateaulike sustained pressure elevation during the remainder of ventricular systole or a fall in pressure followed by a rounded wave of low amplitude. The tracings of patients with combined mitral stenosis and insufficiency were characterized by an early systolic pressure peak followed by a secondary rise in pressure beginning in mid-systole which then formed a secondary pressure peak in late systole. This secondary peak was often higher than the primary peak. Though we have shown that the contours of the esophageal and intra-atrial pressure curves are very similar, we do not wish to imply that one can determine the actual level of pressure within the atrium with this technique. Other techniques which have been applied to the study of mitral valve disease, such as cardiac catheterization, 6,7,8 particularly the recording of the pulmonary capillary pressure, 9,10 and electrokymography, 11 supply vital information about cardiopulmonary dynamics. However, none of these yields the type of information about the contour and range of variation of the left atrial pressure pulsation that this technique of esophageal recording does. We feel, therefore, that it offers useful, direct information about the nature of the impairment of the mitral valve.
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