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Biomedical subjects

T Plappert

Publications and source records attributed to T Plappert.

At least 37 records · Page 2Linked to original sources
PubMed1991

Assessment of right and left ventricular function in terms of force development with gestational age in the normal human fetus.

OBJECTIVE: To assess right and left ventricular systolic function in normal human fetuses by cross sectional Doppler echocardiography to calculate the force developed by myocardial shortening. DESIGN: Cross sectional echocardiographic images of the aorta and pulmonary arteries were obtained prospectively in order to measure great vessel diameters and calculate their cross sectional areas. Doppler velocity signals were recorded from the proximal aorta and the proximal pulmonary artery and digitised to obtain peak velocity, acceleration time, flow velocity time integral during acceleration, and the flow velocity time integral for the whole of ejection. Right and left ventricular force development was estimated by Newton's equation in which force is defined as the product of mass and acceleration. PATIENTS: 58 normal human fetuses at a gestational age of from 20 to 42 weeks. RESULTS: The cross sectional area of the pulmonary artery was 20% greater than that of the aorta. Aortic acceleration time was longer than that in the pulmonary artery, and peak blood flow velocity in the aorta was consistently greater than that in the pulmonary artery. Right ventricular stroke volume was significantly greater than left ventricular stroke volume. The force developed by the right and left ventricles was, however, similar throughout the gestational period studied, increasing tenfold from 20 weeks' gestation to term (r = 0.74, p less than 0.0001; r = 0.75, p less than 0.0001) respectively. CONCLUSION: The development of right and left ventricular force in the human fetus is similar in spite of the greater volume handled by the right ventricle. This index of ventricular performance does not require calculation of ventricular volume and because it varies independently of ventricular geometry and heart rate it should prove useful in assessing cardiac function in the normal human fetus and in fetuses with ventricular dysfunction.

Blood Flow Velocity↗
PubMed1990

Effects of nifedipine on transmitral Doppler blood flow velocity profile in patients with concentric left ventricular hypertrophy.

To examine the effects of calcium channel blockade on left ventricular diastolic function, transmitral blood flow was evaluated by Doppler echocardiography following administration of sublingual nitroglycerin and nifedipine in 10 younger normal subjects and in 10 subjects with concentric left ventricular hypertrophy (LVH) and abnormal Doppler transmitral flow patterns. Nitroglycerin decreased peak early filling velocity (E velocity) in both normal (p less than 0.01) and LVH subjects (p less than 0.05) but did not significantly alter peak late filling velocity (A velocity), early filling velocity time integral (VTI E), or late velocity time integral (VTI A). In normal subjects, nifedipine decreased E velocity (p less than 0.01) but did not significantly change A velocity, VTI E, or VTI A. In LVH subjects nifedipine increased E velocity (p less than 0.05) as well as VTI E (p less than 0.05) and the ratio of VTI E/VTI A (p less than 0.05). Thus nifedipine, unlike nitroglycerin, improves the transmitral Doppler flow profile in patients with concentric LVH.

Adult↗
PubMed1990

Coronary atherosclerosis is associated with left ventricular dysfunction and dilatation in aortic stenosis.

Patients with aortic stenosis develop widely variable patterns of left ventricular hypertrophy and dysfunction. We postulated that coronary atherosclerosis (CAD) may be associated with impaired left ventricular function and chamber dilatation in patients with aortic stenosis. Left ventricular mass and volumes were quantified from two-dimensional echocardiography and correlated with coronary angiography in 78 patients with severe aortic stenosis and no previous myocardial infarction or regional wall motion abnormalities. Eighteen patients (group 1) had smooth coronary arteries, 25 patients had irregular coronary arteries with 50% or less stenosis (group 2), and 35 patients had obstructive CAD (group 3). Even though the calculated valve area was similar in all three study groups, group 1 patients had higher values for ejection fraction (65 +/- 9%, 51 +/- 17%, and 48 +/- 13%; p = 0.0002), systolic mass-to-volume ratio (9.2 +/- 3.9, 5.6 +/- 2.8, and 5.2 +/- 2.2; p = 0.0001), and cardiac index (2.9 +/- 0.7, 2.5 +/- 0.7, and 2.3 +/- 0.6 l/min.min2; p = 0.015) than patients in groups 2 and 3, respectively (mean +/- SD). Mean circumferential wall stress was inversely related to severity of CAD. Multivariate analysis showed that CAD is an independent predictor of ejection fraction and mass-to-volume ratio in this group of patients. Thus, in an elderly population with severe aortic stenosis, patients with both obstructive and nonobstructive CAD have an increased incidence of left ventricular enlargement and systolic dysfunction.

Aged↗
PubMed1990

Changes in placental blood flow in the normal human fetus with gestational age.

We assessed fetoplacental blood volume flow and placental resistance prospectively with Doppler sonography in 74 normal human fetuses of 19 to 42 wk gestation to determine the changes in placental perfusion with gestational age. Placental blood volume flow was assessed from the umbilical vein as the product of the mean flow velocity integral and the cross-sectional area of the umbilical vein. Placental resistance was assessed as the ratio of maximum systolic and minimum diastolic blood flow velocities from an umbilical artery. Umbilical vein blood volume flow increased exponentially (r = 0.86) with gestational age from 19 wk to term, and did not decrease in postdate fetuses. Umbilical vein blood volume flow increased linearly with fetal weight (r = 0.77), although volume flow per unit body weight changed little with gestational age. Umbilical artery velocity ratio decreased progressively, indicating diminishing placental resistance with gestational age, but did not correlate closely with umbilical vein blood volume flow. We submit that fetoplacental blood volume flow can be readily calculated directly from the umbilical vein with Doppler ultrasound and may provide a better index of placental perfusion than the umbilical artery velocity ratio.

Female↗
PubMed1989

Prospective Doppler echocardiographic evaluation of pulmonary artery diastolic pressure in the medical intensive care unit.

To test the hypothesis that the noninvasive evaluation of pulmonary regurgitation can provide accurate estimates of pulmonary artery (PA) diastolic pressures and PA wedge pressures, Doppler echocardiographic studies were performed immediately before bedside PA catheterization in 29 medical intensive care unit patients. The characteristic color flow Doppler signal of pulmonary regurgitation was detected in 19 (66%) patients. In 17 of the 29 patients (59%), the gradient between the right ventricle and PA at end-diastole could be calculated from the pulsed-wave Doppler signal of pulmonary regurgitation using the simplified Bernoulli equation. Right atrial pressure was then estimated by examination of the jugular venous pulse or by electronic transduction of the pressure signal from a previously placed central venous catheter. A noninvasive estimate of PA diastolic pressure was made by adding the clinical estimate of right atrial pressure to the end-diastolic pressure gradient across the pulmonary valve. Pulmonary artery catheterization was then performed and stripchart recordings were interpreted by a physician who was unaware of the noninvasively-estimated PA diastolic pressure. The PA diastolic pressure estimated by Doppler echocardiography correlated closely with that found at catheterization (r = 0.94, mean absolute difference 3.3 mm Hg). The noninvasive estimate of PA diastolic pressure also correlated with the PA wedge pressure (r = 0.87, mean absolute difference 3.8 mm Hg). Therefore, in 59% of medical intensive care unit patients, Doppler echocardiographic evaluation of pulmonary regurgitation allowed accurate noninvasive estimation of PA diastolic pressure.

Aged↗
PubMed1989

Peak left ventricular pressure during percutaneous aortic balloon valvuloplasty: clinical and echocardiographic correlations.

Peak left ventricular pressure during balloon inflation was measured in 20 patients who underwent balloon valvuloplasty for severe aortic stenosis to define the determinants of ventricular pressure development in response to increased loading conditions. The peak left ventricular pressure ranged from 150 +/- 5 to 386 +/- 22 mm Hg (mean +/- SD), was reproducible in each patient with each balloon inflation (mean coefficient of variation 7.8%) and correlated with concurrent echocardiographic measurements of ejection fraction (r = 0.89, p = 0.0001) and mass/volume ratio in systole (r = 0.91, p = 0.0001) or diastole (r = 0.88, p = 0.0001). Thirteen patients with class II or more severe congestive heart failure had lower values for peak left ventricular pressure than did those without failure (225 +/- 46 versus 305 +/- 45 mm Hg, p = 0.002), whereas no difference in rest left ventricular systolic pressure was seen between the two groups. The measurement of peak left ventricular pressure was inversely related to rest mean circumferential end-systolic wall stress (r = 0.52, p = 0.046). Thus, peak left ventricular systolic pressure measured during aortic valvuloplasty in humans correlates closely with traditional measures of left ventricular function. This measurement, which previously has been obtained only in experimental animal studies, is a simple and reproducible hemodynamic index that may provide new insights in studies of ventricular function and congestive heart failure in aortic stenosis.

Adult↗
PubMed1987

Doppler echocardiographic study of the frequency and severity of aortic regurgitation in hypertrophic cardiomyopathy.

Aortic regurgitation (AR) has been reported sporadically in hypertrophic cardiomyopathy (HC) but neither its frequency nor severity has been determined. Thirty-one consecutive patients with HC were evaluated by Doppler echocardiography over a 2-year period. Twenty-nine had echocardiographically normal aortic cusps and participated in the study; 2 had calcified aortic valves and were excluded. AR of grade I to grade II severity was demonstrated in 9 of 29 (31%) patients. Patients were divided into 2 groups: group 1 (n = 9) with AR and group 2 (n = 20) without AR. Group 1 patients were significantly older than group 2 patients (73 +/- 7 vs 60 +/- 17 years, p less than 0.05) and had larger end-diastolic (4.5 +/- 0.5 vs 4.0 +/- 0.7 cm, p less than 0.01) and end-systolic (2.7 +/- 0.4 vs 2.3 +/- 0.4, p less than 0.02) left ventricular dimensions. Left ventricular wall thickness, degree of asymmetric septal hypertrophy and left ventricular fractional shortening were similar in the 2 groups. Mitral regurgitation was more common in group 1 (100% vs 35%, p less than 0.005), although there were no differences in left atrial size between the 2 groups. The HC patients were compared with a control group of 23 normal subjects of similar age. There was no mitral regurgitation or AR in the normal subjects. Thus, nearly one-third of patients with HC had mild AR by Doppler. The AR most probably results from high-velocity systolic blood flow causing microscopic damage to the valve cusps.

Adult↗
PubMed1987

Longitudinal changes in left ventricular architecture and function in peripartum cardiomyopathy.

Left ventricular (LV) function was quantitated in 14 patients with peripartum cardiomyopathy, in 10 using 2-dimensional (2-D) echocardiography and in 4 radionuclide ventriculography, and values were compared with those in 11 normal women in the immediate postpartum period. LV end-diastolic and end-systolic volume indexes, LV wall mass index and ejection fraction were calculated during the acute phase of the illness and serially through long-term follow-up (mean 24 months). During the acute phase of illness there was marked LV dilatation: mean end-diastolic volume index was 95 +/- 22 ml/m2, vs 67 +/- 9 ml/m2 in control subjects (p less than 0.005), and mean end-systolic volume index was 66 +/- 18 ml/m2, compared to 27 +/- 5 ml/m2 in control subjects (p less than 0.001). Mean heart rates and mean systolic pressures in the patients with peripartum cardiomyopathy and the control subjects were similar, 91 +/- 24 vs 79 +/- 14 beats/min and 120 +/- 14 vs 117 +/- 10 mm Hg, respectively. LV wall mass index was higher, 139 +/- 38 vs 96 +/- 8 g/m2 (p less than 0.005), and ejection fraction much lower, 29 +/- 5% vs 67 +/- 5% (p less than 0.001), in control subjects. Five patients underwent endomyocardial biopsy during the acute illness, which showed interstitial fibrosis but no evidence of active inflammation. There was rapid and early improvement in LV function in 13 of 14 patients. Changes in LV volume, mass and ejection fraction all followed an exponential time course during LV remodeling.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Comparison of echocardiographic methods for assessment of left ventricular shortening and wall stress.

M-mode echocardiographic measurement of left ventricular fractional shortening and meridional wall stress has been used extensively alone and in combination to describe left ventricular systolic function. To determine whether the improved dimensional information afforded by two-dimensional echocardiography might result in shortening and stress calculations yielding a different view of left ventricular function, we compared two-dimensional and M-mode echocardiograms in 69 subjects (19 normal, 13 with aortic stenosis, 22 with aortic regurgitation and 15 with congestive cardiomyopathy). Fractional shortening was greater with M-mode than with two-dimensional echocardiography in all subjects, especially in those with cardiomyopathy (p less than 0.05). In aortic stenosis, two-dimensional shortening, at 24 +/- 5%, was reduced (p less than 0.05 versus normal), but M-mode shortening, at 34 +/- 5%, was not. M-mode estimates of meridional stress were higher than two-dimensional values, again especially in cardiomyopathy. Two-dimensional echocardiography enabled determination of long- and short-axis ratios, circumferential stress and the ratio of circumferential to meridional stresses. Circumferential stress was elevated in aortic stenosis at 302 +/- 65 X 10(3) dynes/cm2, suggesting afterload excess as the cause for the observed reduction in two-dimensional shortening. The more spherical cardiomyopathic hearts had a meridional to circumferential stress ratio closer to 1, such that use of meridional stress alone would overestimate effective afterload. It is concluded that M-mode and two-dimensional echocardiographic analyses of left ventricular shortening and stress produce different results. Two-dimensional echocardiographic methods may enhance the assessment of ventricular function, especially in patients with aortic stenosis and cardiomyopathy.

Adult↗
PubMed1987

Effects of heart rate on ventricular size, stroke volume, and output in the normal human fetus: a prospective Doppler echocardiographic study.

The effect of heart rate on cardiac output in the fetal heart is controversial. We used Doppler echocardiography to investigate the effects of increasing heart rate on stroke volume and ventricular output in the normal human fetal heart. Heart rate was increased in 25 human fetuses (mean age 36 weeks) by auditory stimulation with a sound emitter placed on the mother's abdomen. Aortic or pulmonary diameters were measured at valve level from two-dimensional echocardiographic images and cross-sectional areas were calculated. Blood flow velocity spectra from the pulmonary artery or aorta were digitized to obtain flow velocity integrals before and after auditory stimulation. Stroke volume was calculated as the product of the flow velocity integral and the area of the great vessel. Prestimulation mean heart rate was 132 +/- 8 beats/min and increased after auditory stimulation to 158 +/- 9 beats/min (p less than .001). Stroke volume decreased with the increase in heart rate from 3.7 +/- 1.4 ml before stimulation to 3.0 +/- 1.1 ml after stimulation (p less than .001), but ventricular output calculated as the product of stroke volume and heart rate remained unchanged (0.48 +/- 0.18 liter/min before vs 0.48 +/- 0.17 liter/min after stimulation). The decrease in stroke volume was accompanied by a decrease in ventricular end-diastolic area, although there was no change either in end-systolic area or fractional change in area. This study demonstrates that increases in heart rate within the physiologic range in the normal human fetus result in a decrease in ventricular size and stroke volume but no change in ventricular output or ventricular shortening.

Cardiac Output↗
PubMed1987

Early postoperative changes in left ventricular chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: a prospective two-dimensional echocardiographic study.

We prospectively studied 16 patients with isolated aortic stenosis and eight with isolated aortic regurgitation undergoing aortic valve replacement, using two-dimensional echocardiography preoperatively, intraoperatively, and 41 +/- 7 days postoperatively to calculate the intraoperative change in afterload, quantify the postoperative changes in left ventricular chamber size, architecture, load and function, determine whether the postoperative left ventricular remodeling correlated with the intraoperative change in afterload in aortic stenosis and aortic regurgitation, and assess whether preoperative afterload excess precluded postoperative improvement in left ventricular function. Preoperative left ventricular mass, end-systolic meridional and circumferential wall stresses, ejection fraction, and stress-shortening relations in patients with aortic stenosis and aortic regurgitation were similar. However, our patients with aortic regurgitation had severe systolic dysfunction, with ejection fraction less than 55% in all but one patient, compared with only 10 of 16 patients with aortic stenosis. Left ventricular end-diastolic volume, mass/volume ratio, and chamber shape were significantly different in patients with aortic stenosis and aortic regurgitation (174 +/- 64 vs 294 +/- 140 ml, p less than .01; 1.81 +/- 0.63 vs 1.14 +/- 0.18, p less than .01; and 0.59 +/- 0.09 vs 0.69 +/- 0.09, p less than .05, respectively). Intraoperative end-systolic meridional and circumferential stresses fell significantly in patients with aortic stenosis but remained unchanged in those with aortic regurgitation. The changes in left ventricular volume and ejection fraction during early postoperative remodeling (6 weeks) correlated with the intraoperative change in afterload in patients with aortic stenosis. In contrast, there was no intraoperative change in afterload in patients with aortic regurgitation and no significant changes in left ventricular volume, architecture, or function at 6 weeks or at 6 months. The differences in left ventricular remodeling and changes in function between patients with aortic stenosis and aortic regurgitation in the early postoperative period most probably relates to the major difference in intraoperative reduction in afterload, although a contributory role may have been played by the preoperative left ventricular dysfunction in those with aortic regurgitation that was underestimated by measurement of ejection fraction.

Adult↗
PubMed1986

Changes in intracardiac blood flow velocities and right and left ventricular stroke volumes with gestational age in the normal human fetus: a prospective Doppler echocardiographic study.

We used Doppler echocardiography to quantitate the changes in intracardiac blood flow velocities and right and left ventricular stroke volumes in 80 normal human fetuses from 19 to 40 weeks gestation. Blood flow velocity spectra across the aortic, pulmonary, tricuspid, and mitral valves were digitized to obtain peak velocities (m/sec) and flow velocity integrals. Aortic and pulmonary diameters were measured at valve level from two-dimensional echocardiographic images and cross-sectional area was calculated assuming a circular orifice. Ventricular stroke volume was calculated as the product of the cross-sectional area of a great vessel and the flow velocity integral through that vessel. The pulmonary arterial and aortic diameters increased linearly with gestational age (r = .82, r = .84), and pulmonary arterial diameter consistently exceeded aortic diameter. There was a positive relationship between stroke volume and gestational age: stroke volume increased exponentially from 0.7 ml at 20 weeks to 7.6 ml at 40 weeks for the right ventricle (r = .87) and from 0.7 ml at 20 weeks to 5.2 ml at 40 weeks for the left ventricle (r = .91). Similar results were obtained for right and left ventricular and combined cardiac outputs. In 44% of the fetuses it was possible to quantitate both right and left ventricular stroke volumes. There was a close correlation between right and left ventricular stroke volumes in these fetuses (r = .96) and right ventricular stroke volume exceeded left ventricular stroke volume by 28%.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1985

Relative wall thickness analysis by two-dimensional echocardiography.

M-mode echocardiographic relative wall thickness (RWT) has been used extensively as an index of left ventricular hypertrophy. To determine whether the more extensive tomographic sampling and enhanced spatial orientation provided by two-dimensional echocardiography (2DE) might improve the value of RWT analysis, we compared 2DE and M-mode RWT in 69 subjects (19 normals, 13 with aortic stenosis, 22 with aortic regurgitation, and 15 with congestive cardiomyopathy). M-mode results correlated relatively weakly with 2DE RWT (r = 0.62 at end diastole; r = 0.81 at end systole). End-systolic M-mode values were larger than 2DE results, while end-diastolic M-mode values were generally smaller than 2DE results (both p less than 0.001). Thus, in congestive cardiomyopathy M-mode RWT was larger than 2DE end-diastolic results and therefore failed to distinguish between cardiomyopathy, aortic regurgitation, and normals. We conclude that M-mode and 2DE analysis of RWT yield disparate results. Moreover, 2DE may enhance the value of RWT in the assessment of left ventricular hypertrophy due to volume overload and cardiomyopathy.

Adolescent↗
PubMed1985

Effects of reduced left ventricular mass on chamber architecture, load, and function: a study of anorexia nervosa.

We investigated the effects of reduction in left ventricular mass on cavity geometry, afterload, pump function, and exercise performance in 17 patients with anorexia nervosa and in 10 age-and sex-matched normal subjects. Left ventricular mass index determined by two-dimensional echo-cardiography was significantly lower than that in normal subjects (53 +/- 15 vs 79 +/- 18 g/m2; p less than .005). Left ventricular end-diastolic and end-systolic volume indexes were also reduced in patients with anorexia nervosa compared with normal subjects (49 +/- 11 vs 65 +/- 17 ml/m2, p less than .005; 14 +/- 5 vs 19 +/- 4 ml/m2, p less than .025). In spite of the reductions in left ventricular mass and volume indexes, left ventricular chamber architecture described as h/R ratio, mass to volume ratio, and short/long left ventricular axis ratio were normal. Left ventricular afterload assessed as end-systolic meridional and circumferential wall stress was normal (59 +/- 18 vs 79 +/- 19 dyne/cm2 X 10(3) and 170 +/- 26 vs 167 +/- 23 dyne/cm2 X 10(3)). Ejection fraction, percent fractional shortening, and the relationship between end-systolic wall stress and ejection fraction were all within normal limits. In seven patients restudied after a 15% to 20% weight gain, left ventricular mass and volume indexes increased significantly but end-systolic wall stress and ejection fraction did not change. Ten patients with anorexia nervosa and resting heart rates and systolic blood pressures significantly lower than control values underwent treadmill testing. Exercise duration, peak heart rate, peak systolic blood pressure, and peak oxygen consumption in these patients were all significantly lower than normal. The hypotensive effect of fasting resulted in an initial decrease in afterload, which was the stimulus for reduction in left ventricular mass. The left ventricular remodeling associated with the mass reduction occurred in such a way that (1) orthogonal, meridional, and circumferential wall stresses were normalized, (2) normal chamber shape and architecture were maintained, and (3) chamber function and stress-shortening relationships were preserved. Thus down-regulation of left ventricular mass per se, like up-regulation of left ventricular mass, is not associated with abnormal left ventricular function.

Adolescent↗
PubMed1983

Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results.

We performed a prospective anatomic validation study to determine the accuracy of left ventricular (LV) mass estimates from clinical two-dimensional echocardiographic (2-D echo) studies. In 21 subjects, antemortem 2-D echo LV mass determinations were compared with anatomic LV weight by postmortem chamber dissection. Major cardiac diagnoses included anatomic LV aneurysm in four, status post aneurysmectomy in one, transmural myocardial infarction in seven, congestive cardiomyopathy in five, rheumatic mitral disease in two, chronic severe mitral or aortic regurgitation in three, amyloid heart in two, and normal heart in three. Marked right-heart dilatation was present in 11 patients and LV thrombus in four. Regression equations derived in vitro for each 2-D echo instrument were used to correct LV mass estimates based on a short-axis, area-length method: uncorrected LV mass = 1.055 x k x 5/6 (AtLt - AcLc) + b, where At = total short-axis LV image area at the high papillary muscle level, Lc = endocardial LV length, k = an instrument-specific regression slope and b = an instrument-specific intercept. LV mass by 2-D echo correlated extremely well with actual LV weight (r = 0.93 slope = 0.85, SEE = 31 g, range 77-454 g). In contrast, M-mode echocardiographic LV mass estimates were less reliable (r = 0.86, SEE = 59 g) in these markedly distorted hearts. These 2-D echo LV mass results compare favorably with reported results from biplane angiography and M-mode echocardiography in more symmetric hearts. Thus, regression-corrected 2-D echo may be the method of choice for determining LV mass in man.

Echocardiography↗