Posterior Wall Excursion Research Articles

LEFT VENTRICULAR DYSFUNCTION IN RHEUMATIC MITRAL REGURGITATION: AN ECHOCARDIOGRAPHIC ASSESSMENT

Echocardiograms (E) in mitral regurgitation (MR) are thought to show exaggerated interventricular septal excursion (IVSE) and posterior wall excursion (PWE), suggesting that LV function is unimpaired. E from 15 patients (pts) with rheumatic MR were compared to those from 20 normal (N) children to delineate any segmental variation in LV function. The following measurements are defined: (1)Fractional shortening (FS)= (D-S)/D × 100 where D and S are end-diastolic and end-systolic diameters; (2)Posterior wall fractional shortening (PFS)=PWE/D × 100; (3)Septal fractional shortening (SFS)= IVSE/D × 100; (4)Ratio of SFS/PFS (R). Pts were divided into group A with LA/Ao ratio ≥1.5:1 and group B with LA/Ao <1.5:1. FS was similar In all groups: 39±5 in A, 37±4 in B, and 38±4 in N. In contrast SFS was Increased in A(22±2) compared to B and N(17±3), and R was significantly increased (p<.001) in A(l.1±0.3) compared to B and N(both 0.6±0.1). On the other hand, PFS was diminished significantly (p<.001) in A(20±3) compared to N and B (28±3). In summary, in MR with LA/Ao ratio>, 5:1, SFS and R were clearly increased and PWE diminished. Hyperdynamic septal motion may, therefore, be a compensatory mechanism for posterior wall dysfunction in mitral regurgitation. Furthermore, frequently used estimates of LV function, including FS and ejection fraction, would fail to detect this regional dysfunction.

Clinical and angiographic implications of a depressed echocardiographic ejection fraction in coronary artery disease.

AbstractTo evaluate the clinical and angiographic implications of a depressed echocardiographic ejection fraction (EF) in coronary artery disease, 45 patients with an echocardiographic EF &lt; 0.50 were studied with complete cardiac catheterizations. Most of the patients had clinical evidence of a prior myocardial infarction, cardiomegaly, and/or congestive heart failure. All had coronary arteriographic evidence of multivessel disease and either reduced cardiac output, elevated left ventricular end‐diastolic pressure, or both. Reduction in percentage of echocardiographic dimensional shortening closely paralleled reduction in echocardiographic EF. Forty of the 45 patients (89%) had an angiographic EF less than 0.50. There was considerable scatter of angiographic EF's with echocardiographic EF's between 0.40 and 0.50, limiting the usefulness of these latter values. However, 23 of the 24 patients (96%) with an echocardiographic EF less than 0.40 had an angiographic EF less than 0.40, and there was a linear relationship between these echocardiographic and angiographic values with a correlation coefficient (r) = 0.54 (SEE = ±0.15, p&lt;0.05). All of the 12 patients with both reduced septal and reduced posterior wall excursion on the echocardiogram had both abnormal echocardiographic and angiographic ejection fractions, and 10 of the 12 had EF &lt; 0.40 by both techniques. Our study suggests that coronary artery disease patients with extensive left ventricular dysfunction can be identified noninvasively, and the echocardiographic EF may be useful in deciding whether such patients may require special cardiac catheterization procedures to evaluate contractile reserve if cardiac surgery is being considered.

Echocardiographic detection of regional myocardial infarction: an experimental study.

Posterior wall velocities have been advanced as a useful technic for the assessment of left ventricular function. To evaluate the echocardiographic effects of regional myocardial infarction on posterior wall motion (PWM), measurements were obtained in 22 open-chest dogs. Coronary artery ligation produced infarction of the apex in 11 dogs (group I) and the posterior wall in 11 dogs (group II). Echoes were thus received from noninfarcted myocardium in group I and from infarcted myocardium in group II. Postinfarct recordings in group I showed no significant changes in posterior wall velocities or excursion. In contrast, group II showed striking changes in the contour of PWM with a large initial posterior displacement (aneurysmal bulging) during isometric contraction, followed by a slow anterior movement during ventricular ejection and then a rapid anterior recoil motion during isometric relaxation. Mean posterior wall velocity fell from 31 ± se 3 mm/sec preinfarct to 13 ± 4 postinfarct ( P &lt; 0.01); from 33 ± 4 to 21 ± 5 mm/sec during atrial pacing pre- and postinfarction ( P &lt; 0.05); from 30 ± 3 to 18 ± 3 mm/sec during volume loading with dextran 20 ml/kg ( P &lt; 0.01); and from 32 ± 4 to 5 ± 2 mm/sec during aortic constriction ( P &lt; 0.01). Corresponding reductions in posterior wall systolic excursion were observed. Simultaneous hemodynamic measurements revealed moderate depression of ventricular performance in group II, but there was no significant correlation between the changes in hemodynamic parameters and echocardiographic velocities following infarction. We conclude that the marked changes in PWM following posterior infarction were due to echocardiographic detection of dyskinesis in the infarcted area rather than to generalized changes in ventricular function. Posterior wall velocities are not a reliable index of left ventricular performance when localized dyskinesis, as indicated by abnormal PWM, is present.

Independent effects of heart rate and exercise on left ventricular wall movement measured by reflected ultrasound

Movement of the posterior wall of the left ventricle was assessed using an ultrasound technique in 11 normal subjects at rest and immediately after maximal erect exercise. Maximal posterior wall velocity was measured as the maximal slope of the wall movement from the end-diastolic position to the end-systolic position, and posterior wall excursion was measured as the maximal amplitude of movement anteriorly. Maximum posterior wall velocity increased from a mean of 37 mm/sec at rest to 96 mm/sec after exercise ( P < 0.001), and posterior wall excursion increased from 4.00 mm at rest to 6.8 mm after exercise ( P < 0.001). The effect of heart rate alone on posterior wall movement was evaluated using the technique of atrial pacing. Increasing the heart rate in 6 patients resulted in a reduction in both posterior wall velocity and excursion. At identical heart rates in 5 patients there was a significant increase in both posterior wall velocity and excursion during exercise compared to atrial pacing. It is suggested that changes in posterior wall movement reflect alterations in left ventricular function independent of heart rate, and that these changes can be measured by reflected ultrasound.

Changes in left ventricular wall movement after acute myocardial infarction measured by reflected ultrasound.

Serial measurements of left ventricular posterior wall movement were made in eight patients with acute myocardial infarction by an ultrasound technique. Maximum posterior wall velocity and excursion were decreased during the first 36-hour period after infarction. In two patients a reduction in posterior wall velocity was associated with an increased pulmonary artery pressure and as the pressure returned towards normal the posterior wall motion also improved. It is suggested that this method provides a convenient, non-invasive bedside assessment of left ventricular function after acute myocardial infarction.

Ultrasonic measurement of left ventricular wall motion in acute myocardial infarction.

The time-motion representation of the echogram was used to evaluate the left ventricular posterior wall motion in myocardial infarction. The left ventricular posterior wall echo was obtained in 10 normal subjects and 26 patients with chest pain admitted to a coronary care unit, including 11 with acute myocardial infarction (group 1), nine with old myocardial infarction (group 2), and six with chest pain of miscellaneous origin (group 3). The total amplitude of posterior wall excursion, left ventricular isometric contraction time, left ventricular systolic ejection time, and mean posterior wall velocity (ratio of posterior wall excursion to ejection time) were measured. By using the measurements of posterior wall excursion, mean posterior wall velocity, and isometric contraction time, group 1 patients were differentiated from those of groups 2 and 3 and from the normal subjects (all P &lt; 0.01). The data from patients in groups 2 and 3 were not statistically different from those of normal subjects. The measurements obtained by the time-motion curve of the left ventricular posterior wall echo appear to be of value in the bedside evaluation of acute myocardial infarction.

Ultrasound measurements of ventricular wall motion following administration of vasoactive drugs

The analog presentation of the echocardiogram was used to record left ventricular posterior wall motion in 19 patients given vasoactive drugs at the time of cardiac catheterization. In 13 patients, an infusion of isoproterenol produced significant increases in posterior wall excursion (16 percent), mean posterior wall velocity (54 percent) and maximal posterior wall velocity (73 percent). Anticipated mean increases in heart rate, cardiac output and maximal rate of left ventricular pressure rise were also observed while end-diastolic pressure fell. Atropine produced similar changes in 2 patients except for a slight (10 percent) fall in wall excursion. The pressure-velocity relations expressed by plotting maximal posterior wall velocity against the temporally related left ventricular systolic pressure demonstrated an upward and rightward shift after administration of these drugs, suggesting a positive inotropic effect. In contrast, methoxamine produced a slight, early fall in the velocity indexes, and left ventricular systolic pressure rose 16 percent, resulting in a rightward and somewhat downward shift in the pressure-velocity relation. This study indicates that ultrasound cardiography is sensitive to drug-induced changes in posterior wall motion.

Ultrasonic determination of left ventricular wall motion in normal man: Studies at rest and after exercise

The analogue presentation of the echocardiogram was used to measure parameters of left ventricular wall motion in 25 normal males at rest and in 20 individuals after moderate exercise. Characteristic tracings of posterior wall motion, recorded by this technique, are discussed with relation to ventricular pressure and geometric events during the cardiac cycle. Following exercise, significant increases (p < 0.001) in posterior wall excursion and velocity were evident with only a fair correlation (r = 0.48) between increments in maximal wall velocity and heart rate. It is suggested that measurements of posterior wall motion with reflected ultrasound may provide an innocuous means of assessing changes in ventricular contractility.