An attempt was made to determine whether mitral regurgitation could be detected and its severity evaluated semiquantitatively by newly developed real-time two-dimensional Doppler flow imaging in 109 patients who underwent left ventriculography. In the Doppler flow imaging technique, Doppler signals due to blood flow in the cardiac chambers are processed using a high speed autocorrelation technique, so that the direction, velocity and turbulence of the intracardiac blood flow are displayed in the color-coded mode on the monochrome B-mode echocardiogram in real time. Mitral regurgitant flow was imaged as a jet spurting out from the mitral valve orifice into the left atrial cavity. It was noted that the regurgitant jet in the left atrial cavity had a variety of orientations and dynamic features when studied by the present technique. The sensitivity of the technique in the detection of mitral regurgitation was 86% as compared with that of left ventriculography. Mitral regurgitation in the false negative cases was mostly mild. On the basis of the farthest distance reached by the regurgitant flow signal from the mitral valve orifice, the severity of regurgitation was graded on a four point scale and these results were compared with those of angiography. A significant correlation (r = 0.87) was found between Doppler imaging and angiography in the evaluation of the severity of mitral regurgitation. A similar result was obtained for the evaluation based on the area covered by the regurgitant signals in the left atrial cavity. Thus, noninvasive semiquantitative evaluation by real-time two-dimensional Doppler flow imaging appears to be a promising clinical technique.

In some patients with mitral stenosis, a smoke-like echo is observed in the left atrial cavity. The present study in 116 consecutive patients with rheumatic mitral valve disease investigated the echocardiographic features and clinical significance of this echo. The smoke-like echo is characterized by the following echocardiographic features: 1) it is composed of numerous microechoes; 2) it curls up slowly in the enlarged left atrial cavity; and 3) it vanishes as soon as it pours into the ventricular cavity. Hemostasis in the left atrial cavity was considered to be an important underlying condition for development of the echo. Hemorheologic conditions indicated that the shear rate of blood flow in the left atrial cavity was calculated to be low enough for the development of red blood cell aggregation. These conditions suggest that the source of the smoke-like echo might be aggregated cells due to hemostasis in the left atrial cavity. Left atrial thrombi were detected in many patients who had this echo in the left atrial cavity. Although it has not been conclusively determined that the presence of the smoke-like echo is a necessary condition for thrombus formation, this echo appears to be closely related to thrombus formation in the left atrial cavity. It is concluded that the presence of this echo indicates severe left atrial hemostasis and is a warning for thrombus formation.

The aim of the present study was to elucidate the mechanisms of mitral regurgitation accompanying myocardial infarction. Severity and site of mitral regurgitation was evaluated by the real-time two-dimensional Doppler flow imaging technique in 81 patients with old myocardial infarction. The incidence of mitral regurgitation did not depend on the region of infarction. There was, however, a close relationship between the site of regurgitation and the region of infarction. In patients with mitral regurgitation spurting from the posteromedial area of the valve, the inferior wall was involved in infarction without exception and in some of these patients, the posteromedial papillary muscle was also found to be affected by myocardial infarction; in those with regurgitation spurting from the anterolateral area, the anterior wall showed asynergy. On the other hand in patients with mitral regurgitation spurting from the central area, the region of infarction varied. In these patients, however, the larger the diameter of the mitral anulus, the more severe the grade of regurgitation. The extent of asynergy was another factor related to the severity of mitral regurgitation. Both longitudinally and transversely, broad infarction leads to the enlargement of the mitral anulus. However, even if the mitral anulus is not so dilated, severe involvement of either commissural area results in severe mitral regurgitation from the same commissural side. Thus, there are two major causative factors of mitral regurgitation: (1) asynergy of the papillary muscle or the ventricle that results in mitral regurgitation located in the commissural area of the same side as asynergy, and (2) enlargement of mitral anulus, which results in regurgitation from the central area of the orifice. The mechanisms of mitral regurgitation unveiled in the present study will contribute much to the clarification of the concept of so-called papillary muscle dysfunction." Circulation 76, No. 4, 777-785, 1987. MITRAL REGURGITATION is frequently observed in patients with myocardial infarction. Since it develops in the absence of any lesions in the mitral valve leaflet, its pathogenesis has been explained by the concept of "papillary muscle dysfunction" proposed by Burch et al. 1 At present, papillary muscle dysfunction is thought to be a sequence of unsuccessful coordination of the whole mitral apparatus (which is composed of the anulus, leaflets, chordae tendineae, papillary muscles, and the left ventricular wall), rather than a mere disorder of the papillary muscle. However, the concept of papillary muscle dysfunction is a rather theoretical one and its existence has not been proven from the point of view of functional anatomy. The purpose of this present study was to elucidate the pathogenesis of mitral regurgitation observed in patients with old myocardial infarction by assessment of the topographic features of regurgitation with a realtime two-dimensional Doppler flow imaging technique as well as two-dimensional echocardiography. Materials and methods...

No abstract

To elucidate the mechanism of regional hemostasis in the left ventricular (LV) cavity during myocardial infarction, the blood pathway in LV cavity was examined with contrast echocardiography injected from the left atrium before and after coronary ligation in nine canines. Before coronary ligation, contrast echoes spread over LV cavity with one rush. After ligation, smokelike echoes indicating hemostasis were observed at the apical middle of the LV cavity in five dogs with apical akinesis and at the apical area in four dogs with apical dyskinesis. The contrast echoes did not reach the apex within one diastolic period but turned upward to the outflow tract in the middle of the cavity in all dogs. In the cardiac beats that followed, some contrast echoes spread slowly toward the apex, forming a thin layer along the posterior wall in cases with akinesis but not in cases with dyskinesis. The area separated from the blood pathway developed where the smokelike echoes had been developed. Tachycardia exaggerated the abnormality of blood pathway and widened the contrast echo-free area. The abnormal pathway of the blood in apical myocardial infarction develops hemostasis in the apex. This should be one of the mechanisms of thrombus formation in myocardial infarction. (Circulation 1988;78:157-164)