Posterior Wall Velocity Research Articles

Systolic anterior motion of the mitral valve with and without asymmetric septal hypertrophy. Role of left ventricular posterior wall motion.

Abnormal systolic anterior (SAM) motion of the mitral valve without asymmetric hypertrophy of the interventricular septum was observed in 16 patients (group 1). 5 of the 16 patients had no other evidence of heart disease and the remaining 11 had a variety of cardiac disorders. Left ventricular dimensions, septal and posterior wall thickness, left ventricular ejection fraction, the mean velocity of circumferential fiber shortening, and the mean velocity of the posterior wall and septal contraction was measured by echocardiography in all patients in group 1. These measurements were compared with similar measurements in 14 patients with idiopathic hypertrophic subaortic stenosis (group 2) and in 11 normal subjects (group 3) to evaluate the role of the left ventricular contractility with particular reference to the left ventricular posterior wall motion in production of SAM. All patients with SAM (groups 1 and 2) showed significantly higher indexes of left ventricular contractility, particularly posterior wall velocity, and normalized mean posterior wall velocity, when compared to the normal subjects. The significantly higher posterior wall and the normalized mean posterior wall velocities in all patients with SAM suggest that the exaggerated systolic anterior motion of the left ventricular posterior wall plays an important role in production of SAM in the presence or absence of asymmetric septal hypertrophy.

Ventricular dynamics after surgical closure of VSD.

Twenty patients varying in age between 5 and 20 years at the time of surgical closure of VSD were studied 2 to 9 years postoperatively. Ventricular function was studied by echocardiography and measurement of systolic time intervals for the left and right ventricles and the findings were related to clinical and haemodynamic results of operation. The VSD was closed in all instances and the haemodynamic situation was normalized in all but 2 patients who had persisting pulmonary vascular disease. Right bundle branch block (RBBB) was recorded in 11 instances and in 5 there was an associated left axis deviation (LAD), suggesting left anterior hemiblock. LAD occurred as an isolated anomaly in another 2 patients. The heart size was within normal limits in all the patients. Abnormal septal motion (ASM) was recorded in 13 of the 20 patients, but other echocardiographic analyses, such as LV end-diastolic dimension, left atrial/aortic root ratio, posterior wall velocity index and maximal endocardial velocity, were all within predicted normal limits. There was an almost uniform prolongation of both left and right pre-ejection periods. left and right ejection period as a rule remained normal and gave an increased PEP/ET ratio, indicating the presence of postoperative ventricular dysfunction also in instances with complete normalization of the haemodynamic situation. Suggested background mechanisms for these findings are the frequent occurrence of conduction defects postoperatively, the likelihood of altered ventricular compliance and possibly also as a cause of ASM postoperative presence of an opened pericardial sac.

Left ventricular function in rheumatic mitral stenosis. Clinical echocardiographic study.

Echocardiography was used to examine the extent and significance of impairment in left ventricular function in 20 patients with rheumatic mitral stenosis. Indices of left ventricular performance--normalised mean rate of circumferential fibre shortening (Vcf), ejection fraction, normalised posterior wall velocity, and stroke volume were reduced. The impairment in left ventricular function was related to the degree of functional disability (NYHA), right ventricular dilatation, and left atrial enlargement. Vcf was inversely related to both the internal right ventricular diameter (r=-0.767, P less than 0.001) and the degree of left atrial enlargement (r=-0.554; P less than 0.05). The normalised velocity of the interventricular septum and the maximum systolic and diastolic endocardial velocities were also reduced. These results suggest that abnormalities in contractility of left ventricular myocardium are responsible for the impaired myocardial function in patients with mitral stenosis and that such impairment is clinically significant.

Echocardiographic study on diastolic posterior wall movement and left ventricular filling by disease category

The diastolic characteristics of the left ventricle with special reference to the patterns of left ventricular filling and diastolic posterior wall movement were studied echocardiographically in 95 patient with various cardiac conditions including constrictive pericarditis, idiopathic cardiomyopathy (CCM, HCM), valvular aortic stenosis (AS), mitral stenosis (MS), hypertension (HT), aortic insufficiency (AI), mitral insufficiency (MI), and in 20 normal subjects. 1. 1. Various types and severities of LV diastolic abnormalities were revealed by analyzing the patterns of posterior wall movement and LV filling in three diastolic phases-rapid filling period, slow filling period, and atrial filling period, respectively. 2. 2. Disturbances of posterior wall distension and LV filling during the rapid filling period with a compensatory augmentation of atrial contribution of LV filling were observed in most patients. These patients also showed a markedly decreased posterior wall velocity and LV filling rate during rapid filling period. 3. 3. E-F slope was significantly decreased in patients with MS, AS, and HCM. E-F slope correlated well with DPWV and RFR in most patients. In MS, however, DDR decreased to a disproportionate degree with a decrease in DPWV and RFR, probably due to the structural changes and decreased mobility of the mitral valve. From this study, we conclude that the patterns of the left ventricular filling and posterior wall movement during three phases of diastole obtained by echocardiography is useful in detecting left ventricular diastolic abnormalities.

Anatomical and Functional Features of Hypertrophied Left Ventricle Studied with M-mode and Real-time Cross-sectional Echocardiographies : SYMPOSIUM ON CURRENT TOPICS AND FUTURE PROSPECTS IN ECHOCARDIOGRAPHY

1)Left ventricular hypertrophy in hypertension is almost symmetric. However, the interventricular septum is slightly thicker than the posterior wall. In aortic regurgitation and mitral regurgitation the posterior wall is thicker than the interventricular septum. The above situation suggests a difference between the influence of pressure overloading to the heart and that of volume overloading. Hypertrophy in congestive cardiomyopathy is similar to that in aortic regurgitation. 2) The interventricular septum was thickened in all the examined cases of hypertrophic cardiomyopathy. In some cases the interventricular septum was mass-like, bulging into the left ventricular cavity and in some cases into the right ventricular cavity. 3) In the posterior wall of the left ventricle, various degrees and extents of hypertrophy are observed, with and without hypertrophy of the papillary muscle. In some cases, only one of the anterolateral and posteromedial papillary muscles is hypertrophied, but not the other. These findings reveal that a nonuniform hypertrophy develops not only in the septum and free wall, but also even in the papillary muscles. In one examined case a muscle bundle was hypertrophied, occupying a large space in the narrow ventricular cavity, but not the papillary muscle. 4) Motion of the hypertrophied ventricle especially the maximum velocity of the thickened posterior wall during rapid filling, is generally slow. There is a trend that the thicker the posterior wall, the slower the maximum velocity in rapid filling. However, the posterior wall velocity in cases of hypertrophic cardiomyopathy in diastole is generally slower than that in cases of hypertensive heart, even if the posterior wall thickness is the same in both conditions. 5) The mitral SAM consists of echoes of the mitral chordae which are shifted forwards by the hypertrophied papillary muscles sticking out anteriorly into the left ventricular cavity in systole. 6) The hypertrophied and maloriented papillary muscles occupying a large space in the narrow cavity possibly play an essential role in developing the intraventricular pressure gradient in cases of hypertrophic obstructive cardiomyopathy. 7) The obstructive and nonobstructive forms of hypertrophic cardiomyopathy do not seem to be essentially different, but with various manifestations, depending upon the locality and extent of nonuniform inappropriate hypertrophy, form a continuum.

Ultrasonodiagnosis of Subclinical Heart Failure by Increasing Afterload with Angiotensin II

In an attempt to diagnose latent heart failure, a transient increase of afterload to left ventricle was produced by angiotensin II, and the ventricular movement was assessed by echocardiography. Angiotensin II was administered in a dose of 0.075 micrograms/kg body weight. Blood pressure was elevated by 40.5 +/- 14.5 mmHg in 38 cases with latent heart failure and by 41.2 +/- 4.5 mmHg in 30 normal subjects. Yet, only in the former group, posterior wall excursion of left ventricle reduced from 11.4 +/- 2.4 mm to 7.3 +/- 2.3 mm and mean posterior wall velocity from 41.4 +/- 10.1mm/sec to 26.5 +/- 8.8 mm/sec. The rates of these reductions were inversely correlated to the rate of elevation of left ventricular endodiastolic pressure as determined in 5 cases by cardiac catheterization. There was no change in 30 subjects. The data indicate the usefulness of angiotensin-induced echocardiographic changes in detecting latent cadiac failure.

The effect of isosorbide dinitrate on left ventricular size, wall stress and left ventricular function in chronic refractory heart failure: An echocardiographic study

To determine the effect of a long-acting vasodilator isosorbide dinitrate (ID) on ventricular performance, 16 patients with refractory congestive heart failure underwent echocardiographic studies during control and for a period of 2 hours after the administration of 10 mg of sublingual ID. The effects of ID were seen in 5 to 10 minutes, reached maximum at 30 ± 3 minutes lasted for 60 minutes and dissipated thereafter. At the maximal drug effect, a significant decline in mean blood pressure (74 ± 2 versus 81 ± 3 mm Hg, p < 0.001), left ventricular afterload (228 × 10 3 ± 9 × 10 3 dynes/cm 2 versus 273 × 10 3 ± 12 × 10 3 dynes/cm 2 p < 0.001), end-diastolic dimension (5.90 ± 0.13 versus 6.40 ± 0.15 cm, p < 0.005) and end-systolic dimension (4.8 ± 0.15 versus 5.50 ± 0.17 cm, p < 0.001) occurred. These changes were associated with a significant increase in per cent fractional shortening (19 ± 2 per cent versus 14.5 ± 1.3 per cent, p < 0.001), mean rate of circumferential fiber shortening (VCF) (0.78 ± 0.06 versus 0.61 ± 0.05 circumferences per second (circ/sec) p < 0.001) and normalized mean posterior wall velocity (VPW) (0.65 ± 0.05 versus 0.47 ± 0.03 sec −1, p < 0.001) when heart rate was not significantly altered. All 16 patients were maintained on long-term ID therapy. Six of 16 patients (38 per cent) died within 17 to 270 days after the acute study. Nine of 16 patients have been followed for a period of three to 24 months and are clinically improved. These findings suggest that (1) ID reduces left ventricular size, preload and afterload, and improves ventricular performance; and (2) the use of ID might be of value as adjunctive therapy in acute/chronic management of refractory heart failure.

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.

The use of echocardiography in determination of reversible posterior wall asynergy

Recent studies have indicated that nitroglycerin can be delineate potentially reversible asynergic zones depicted ventriculographically. To assess the ability of the echocardiogram to detect reversible asynergy, posterior wall motion was assessed in 19 patients both echocardiographically and ventriculographically before and after nitroglycerin. Thirteen of the 19 patients demonstrated abnormal posterior wall motion both by echocardiography and ventriculography while six were normal by both techniques. In 4 of the 13 asynergic areas, posterior wall excursion improved following nitroglycerin (from 0.99 +/- .07 to 1.30 +/- .07 cm. by echocarciography (p less than .025) with a corresponding improvement in hemiaxis shortening from 12.0 +/- 6.1 per cent to 29.0 +/- 6.7 per cent (p less than .02). In contrast, in nine patients in whom inferior segment hemiaxis shortening was unchanged following nitroglycerin, posterior wall excursion by echocardiography was similarly not improved (1.01 +/- .03 cm. before and 1.02 +/- .03 cm. after nitroglycerin). The effect of nitroglycerin on posterior wall velocity paralleled changes in posterior excursion. The six patients with initially normal posterior excursion showed no significant change by either echocardiography or ventriculography following nitroglycerin. Thus, the echocardiogram is of considerable value in detecting both the presence and potential for improvement of asynergic posterior wall segments.

Interventricular septal motion and left ventricular function after coronary bypass surgery: Evaluation with echocardiography and radionuclide angiography

To evaluate interventricular septal motion and left ventricular function after coronary bypass graft surgery, 40 patients were studied early postoperatively and serially for up to 16 months with echocardiography and radionuclide angiography. Early after operation mean left septal excursion decreased significantly from 4.6 +/- 0.4 (standard error) to 0.8 +/- 0.6 mm (P less than 0.001), and left septal motion was abnormal in 23 of the 40 patients. Mean right septal excursion reversed from 2.1 +/- 0.5 to -2.1 +/- 0.5 mm early after operation in the 22 patients in whom these measurements could be made, and 15 patients showed paradoxical right septal excursion. At a mean of 4 months after operation, only 7 of 35 patients followed up had abnormal left septal motion, and mean left septal excursion had returned toward normal (3.6 +/- 0.7 mm); mean right septal excursion remained reversed (--1.1 +/- 0.7 mm), and 6 of the 14 patients followed up had paradoxical motion. In the 22 patients whose wall thickness could be measured, mean septal thickening during systole decreased significantly from 35 +/- 4 to 21 +/- 3 percent early after operation (P less than 0.01). During late follow-up septal thickening returned toward normal (32 +/- 4 percent). Mean normalized posterior wall velocity increased significantly after operation from 0.76 +/- 0.03 to 1.01 +/- 0.05 sec-1 (P less than 0.001), but posterior wall thickening remained unchanged. Left ventricular end-diastolic dimension and the radionuclide-determined left ventricular ejection fraction were unchanged postoperatively. It is concluded that (1) echocardiographically detected abnormal septal movement is frequent early after coronary bypass graft operation; (2) both decreased myocardial contraction in the septum and increased anterior movement of the whole heart contribute to this abnormality; (3) the abnormalities in septal movement decrease during late follow-up in many patients but persist in some patients; and (4) posterior wall function tends to increase early after operation and therefore overall left ventricular function remains normal.

Echocardiographic study on hypertrophic cardiomyopathy.

Echocardiographic study was performed on 21 cases with hypertrophic cardiomyopathy (HCM), 10 obstructive and 11 nonobstructive. Asymmetric septal hypertrophy was demonstrated in both obstructive and nonobstructive HCM. In all cases of HCM studied, the thickness of the interventricular septum was 1.4 cm or more (1.4-3.7 cm) and the ratio of septal to left ventricular posterior wall thickness was 1.4 or more (1.4-3.2). A systolic anterior movement of the mitral valve (SAM) was observed in obstructive cases only and characterized by a large backward component in late systole and an extreme approximation to the interventricular septum at its peak. Patients with HCM also showed abnormal echocardiographic indices of the left ventricular diastolic properties, such as the rate of diastolic descent of the mitral valve (DDR), mean diastolic posterior wall velocity (mPWVd), D/S ratio and mean rapid filling rate (mRFR). DDR correlated well with the ratio of rapid filling to total filling volume, rapid filling fraction, (r = 0.79, p less than 0.001), suggesting that reduced DDR in HCM was related with an abnormal left atrio-ventricular flow pattern. A significant correlation was also observed between mRFR and negative maximum dp/dt derived from the first derivative curve of the left ventricular pressure (r = o.68, p less than 0.005). Thus echocardiography was proved to be a valuable means for investigation of the left ventricular properties during early diastole.

Influence of acute alterations in heart rate and systemic arterial pressure on echocardiographic measures of left ventricular perfornmance in normal human subjects.

To study the effects of acute alterations in heart rate and systemic arterial pressure on the mean velocity of left ventricular circumferential fiber shortening (Vcf) and on mean posterior wall velocity (Vpw), we performed ultrasound studies in 25 normal human subjects between the ages of 21 and 29 years. When heart rate was augmented by the administration of intravenous atropine from 64 +/- 2.2 (SEM) to 98 +/- 2.7 beats/min, mean normalized Vcf increased from 1.22 +/- 0.05 to 1.38 +/- 0.06 circumferences (circ)/sec(P less than 0.001). Mean normalized Vpw increased from 0.76 +/- 0.03 to 0.89 +/- 0.04 sec-1 (P less than 0.001). Mean Vcf and mean Vpw uncorrected for end-diastolic diameter increased in a similar fashion (P less than 0.01). After atropine administration, systemic arterial pressure was augmented by means of a phenylephrine infusion in 23 subjects by an average of 39 mm Hg (range 20-50 mm Hg). During the phenylephrine infusion, average heart rate decreased from 96 +/- 2.6 to 91 +/- 3.1 beats/min (NS), while mean normalized Vcf declined from 1.38 +/- 0.06 to 1.09 +/- 0.05 circ/sec (P less than 0.001) and normalized Vpw from 0.89 +/- 0.04 to 0.65 +/- 0.04 sec-1 (P less than 0.001). Nonnormalized velocities exhibited similar alterations (P less than 0.01). We conclude that in the normal human subject mean Vcf and mean Vpw are sensitive to acute alterations in heart rate and systemic arterial pressure. Thus, when ultrasound measures are used for serial assessment of left ventricular performance, the level of heart rate and systemic arterial pressure at which studies are obtained must be considered. Further, the sequential use of atropine and phenylephrine, as described in this study, provides an experimental model for the evaluation of the effects of drug treatment and other interventions on left ventricular performance in man.

Noninvasive assessment of clinical response to oral propranolol therapy

Nineteen patients with severe but stable angina pectoris entered a double blind controlled study to evaluate the effect of orally administered propranolol on exercise tolerance measured with a bicycle ergometer, and left ventricular function measured by echocardiography and systolic time intervals. In the group treated with propranolol the dose was increased from 80 to 320 mg/day. Studies including determination of propranolol blood levels were obtained before treatment and for each dose of propranolol. With propranolol, 80 mg/day, total work performance increased by 128 percent from 765 ± 125 before treatment to 1,792 ± 285 kilopond-meters (mean ± standard error) ( P < 0.01). With 160 mg of propranolol daily, total work performance decreased, but remained higher than at control levels. In the group given propranolol, left ventricular function decreased progressively with increasing doses of the drug. As measured from the echocardiogram, maximal endocardial posterior wall velocity decreased 42 percent, from 72 ± 7 to 41 ± 4 mm/sec ( P < 0.02); ejection fraction decreased 13 percent, from 0.68 ± 0.01 to 0.59 ± 0.01; and end-diastolic volume increased 28 percent, from 79 ± 11 to 102 ± 9 ml/m 2 ( P < 0.05). The preejection period and the ratio between preejection period and left ventricular ejection time significantly increased with progressive dose increments. There was no correlation between blood level of propranolol and improved work performance. Exercise tolerance was maximally improved with doses of 80 to 160 mg/day. At higher dose levels left ventricular function deteriorated and exercise work decreased. Noninvasive assessment of left ventricular function proved more valuable than determination of drug blood levels in managing patients with angina pectoris and provided a guide to optimal adjustment of dosage.

Effect of inotropic agents on the localized dyskinesis of acutely ischemic myocardium. An experimental ultrasound study.

The response of the segmental dyskinesis of acutely ischemic myocardium to inotropic agents has not been well characterized. We studied this in detail in open-chest anesthetized dogs. Acute myocardial ischemia was produced by coronary ligation and confirmed by histologic studies. Ultrasound recordings obtained by direct reflection off the ischemic posterior wall revealed characteristic dyskinesis: aneurysmal bulging during isometric contraction and markedly reduced mean posterior wall velocity (PWVm), and excursion during ventricular ejection. Isoproterenol (I), norepinephrine (N), ouabain (O), glucagon (G), and propranolol (P) were then administered intravenously in graded doses. The response to these agents consisted of two discordant elements. There was a significant ( P &lt; 0.01) increase in aneurysmal bulging during isometric contraction with isoproterenol (5 ± 0 to 6 ± 0 mm) and ouabain (4 ± 0 to 5 ± 0 mm). However, during the ventricular ejection phase PWVm increased with isoproterenol (12 ± 1 to 26 ± 2 mm/sec), glucagon (12 ± 2 to 22 ± 2 mm/sec), norepinephrine (12 ± 1 to 17 ± 1 mm/sec), and ouabain (8 ± 1 to 12 ± 2 mm/sec). Simultaneous hemodynamic measurements showed the drugs elevated cardiac output (G &gt; I &gt; 0) and left ventricular dp/dt ( I &gt; G &gt; N). Inotropic agents thus have two opposing effects on the dyskinesis of acutely ischemic myocardium: increased aneurysmal bulging during isometric contraction, but improved wall velocity during ventricular ejection. The latter contributes to the drug-induced improvement in over-all ventricular performance and also indicates that acutely ischemic myocardium retains the capacity to respond to pharmacologic stimuli.

Posterior wall velocity: An unreliable index of total left ventricular performance in patients with coronary artery disease

Posterior wall velocity determined by use of echocardiography has been proposed as an index of total left ventricular performance in patients with ischemic heart disease. Accordingly, in 9 normal subjects and 39 patients with angiographically documented coronary artery disease, we compared mean endocardial posterior wall velocity determined by echocardiography with echocardiographic and biplane cineangiographic calculations of ejection fraction and the mean rate of circumferential fiber shortening (mean V CF), and with externally recorded systolic time intervals. All studies were performed on the same day in each patient. Mean endocardial posterior wall velocity averaged 4.6 cm/sec (range 2.9 to 8.7) and correlated poorly with echocardiographic ejection fraction ( r = 0.47), cineanglographic ejection fraction ( r = 0.26), cineangiographic mean V CF ( r = 0.47), the ratio of preejection period to left ventricular ejection time ( r = −0.35) and the preejection period corrected for heart rate ( r = −0.30). Substitution of maximal for mean endocardial posterior wall velocity did not improve the separation of normal from depressed left ventricular performance. Epicardial posterior wall velocity, a measurement more easily obtainable than endocardial posterior wall velocity, also did not correlate well with systolic time intervals or with ejection fraction or mean v cf derived from the echocardiogram and cineangiogram. Both endocardial and epicardial posterior wall velocity values were poorly reproducible on a day to day or a beat to beat basis. We conclude that neither endocardial nor epicardial posterior wall velocity, whether derived as a mean or a maximum, provides an accurate measure of total left ventricular performance in patients with coronary artery disease.

Ultrasound assessment of left ventricular function following aortocoronary saphenous vein bypass grafting.

Three serial determinations of left ventricular function were performed by echocardiographic techniques in ten patients undergoing aortocoronary saphenous vein grafting for occlusive coronary artery disease. There were significant increases in maximum posterior wall velocity, mean posterior wall velocity, amplitude of left ventricular wall excursion, and ejection fraction when the preoperative values were compared with those obtained one week and six weeks after surgery. Improvements in these indices seemed independent of heart rate and blood pressure and, therefore, probably reflected an improvement in ventricular function attributable to surgery. These data, of course, must be interpreted with care in patients with coronary artery disease who may have asynchronous ventricular contraction. The findings in this paper support previously reported data showing enhancement of ventricular function following aortocoronary saphenous vein grafting and provide a means for the serial evaluation of large numbers of patients by noninvasive techniques.

Assessment of left ventricular dimensions and function by echocardiography

Left ventricular dimensions and function indexes were measured in 40 patients with cardiac disease by both angiocardiographic and echocardiographic techniques. Good correlation was obtained between echocardiographic and angiographic values in 18 patients with technically excellent studies obtained by both techniques. The left ventricular echogram appears to be an effective technique for the noninvasive determination of left ventricular dimensions and volume. Echocardiographic indexes of ventricular function, including percent shortening of internal diameter, mean shortening velocity of internal diameter, ejection fraction, percent thickening of posterior wall and mean posterior wall velocity, distinguished between groups of patients with normal and abnormal left ventricular function. However, a single echocardiographic or angiographie measurement does not appear to provide selective data for the accurate functional classification of most individual patients.

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.