Mean Posterior Wall Velocity Research Articles

Effects of Nitroglycerin on Myocardial Excursions and Velocities in the Early Hours of Acute Myocardial Infarction

The effects of sublingual nitroglycerin on septal and left ventricular wall motion were determined by echocardiography in the early hours of acute myocardial infarction (MI) in 20 patients admitted via a mobile coronary care unit. Left ventricular and septal echoes were obtained in 11 patients with acute anterior MI and in 9 with acute inferior MI before and after administration of 500 micrograms sublingual nitroglycerin. In the group with acute anterior MI, nitroglycerin did not significantly affect the B-C excursion, posterior wall excursion, and mean posterior wall velocity. Nitroglycerin significantly increased (P less than 0.01), however, the systolic septal excursion, systolic septal velocity, diastolic septal excursion, and diastolic septal velocity. In the group with acute inferior MI, nitroglycerin significantly increased the B-C excursion (P less than 0.01); posterior wall excursion (P less than 0.01); mean posterior wall velocity (P less than 0.01); systolic septal excursion (P less than 0.01); diastolic septal excursion (P less than 0.05), and diastolic septal velocity (P = 0.01) but did not affect the systolic septal velocity. All measurements were obtained by use of a method of labeling and describing specific points of the wall motion that has been described recently.

Systolic and diastolic septal and posterior wall echocardiographic measurements in normal subjects.

M-mode echocardiographic measurement of septal and left ventricular excursions and velocities was attempted in 109 subjects. Seventy subjects had adequate echocardiograms enabling detailed measurement. Two groups of subjects were studied: a group of normal adults aged nineteen to seventy-eight years and a group of normal juveniles aged nine to eighteen years. The posterior wall excursion (PWE), systolic septal excursion (SSE), diastolic septal excursion (DSE), and diastolic septal velocity (DSV) did not differ in these groups. There were significant differences in the posterior wall excursion during isovolumetric contraction (B-Ce, p less than 0.002), mean posterior wall velocity (PWV mean, p less than 0.002), and systolic septal velocity (SSV, p = 0.05) between the two groups. The measurements were obtained by using the recently published method of the specific points for labeling and description of the wall motion.

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.

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.

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.

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.

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.

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.