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Biomedical subjects

A Neumann

Publications and source records attributed to A Neumann.

At least 127 records · Page 7Linked to original sources
PubMed1986

Contrast echocardiography for evaluation of myocardial perfusion: effects of coronary angioplasty.

Assessment of viable myocardium before and after interventional therapy has become a critical issue in modern cardiology. This report describes a new contrast echocardiographic technique using conventional two-dimensional imaging during direct intracoronary injections of small volumes (1.5 to 2.0 cc) of sonicated Renografin-76. Contrast echocardiography was performed before and after coronary angioplasty in seven patients with single vessel coronary artery disease. Before angioplasty a contrast (that is, perfusion) defect was noted in all seven patients. This defect correlated with the anatomic distribution of the epicardial coronary stenosis. After angioplasty the mean gradient across the stenotic lesion decreased from 52 +/- 11 to 13 +/- 14 mm Hg (p less than 0.01) in association with a fall in the mean diameter of the lesion from 84 +/- 8 to 29 +/- 13% (p less than 0.001). Increased myocardial perfusion to the area of "contrast defect" was demonstrated in only five of the seven patients, despite hemodynamically and angiographically successful angioplasty. Thus, contrast echocardiographic techniques performed during interventional therapy and used in conjunction with standard coronary angiographic procedures may provide additional physiologic information regarding regional myocardial perfusion after attempts at revascularization.

Aged↗
PubMed1986

Myocardial mechanics in hyperthyroidism: importance of left ventricular loading conditions, heart rate and contractile state.

Hyperthyroidism has been reported to affect all of the major determinants of left ventricular performance in a manner that would augment ventricular shortening characteristics. The hypothesis tested in this study is that reduced afterload in conjunction with increased preload and heart rate, rather than augmented contractility, accounts for much of the increase in left ventricular performance noted previously in these patients. To investigate this hypothesis, 11 hyperthyroid patients were evaluated serially over 4 +/- 2 months. With therapy, serum total thyroxin (T4) decreased significantly (p less than 0.001). Ventricular hemodynamics were assessed by two-dimensional targeted M-mode echocardiograms and calibrated carotid pulse tracings. Ventricular preload was estimated by end-diastolic dimension, whereas afterload was measured as end-systolic wall stress. Overall left ventricular performance was quantitated by the extent and velocity of shortening, whereas myocardial work was assessed by ventricular systolic stress-length relations. With therapy, overall left ventricular performance declined (p less than 0.01). This change was associated with no change in end-diastolic dimension or end-systolic wall stress, and a 24% fall in heart rate (p less than 0.01). This latter finding has been shown previously to have no significant effect on left ventricular contractile state over the range of heart rates encountered in this study. In all cases, the end-systolic stress/rate-corrected shortening velocity relation fell with attainment of normal thyroid status, characteristic of a decline in contractility. There was a strong positive correlation between left ventricular contractility and serum thyroid hormone level (r = 0.83). In addition, ventricular minute work declined with therapy (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of acute lung injury and anesthesia on left ventricular mechanics.

Traditional left ventricular (LV) function curves are frequently depressed in patients with acute lung injury. Similar findings in pentobarbital sodium-anesthetized dogs with oleic acid lung injury (OALI) have been observed. To test the hypothesis that acute OALI produces a significant injury to the heart, the LV mechanics of pentobarbital-anesthetized dogs with (n = 6) and without (n = 6) OALI were evaluated. End-systolic force-length and force-velocity relations determined echocardiographically during afterload manipulation with sodium nitroprusside demonstrated a marked deterioration in LV shortening characteristics over 90 min in both groups of pentobarbital-anesthetized dogs. In contrast, LV mechanics studied using the same protocol in fentanyl-anesthetized dogs were unchanged in both the injured (n = 6) and noninjured (n = 6) lung groups. Comparisons with data acquired over a wide range of LV afterload from six conscious, instrumented dogs showed that LV contractile state was normal to slightly increased with fentanyl and markedly depressed with pentobarbital. Diastolic properties, as assessed by end-diastolic pressure-dimension relations, were essentially unchanged in all anesthetized animals. We conclude that OALI has no effect on LV systolic or diastolic mechanics; the LV dysfunction attributed to OALI in previous studies is due to an acute, severe cardiomyopathy induced by pentobarbital; and unlike pentobarbital, anesthesia with fentanyl has no discernible time-dependent effect on LV mechanics. These findings have important implications for future studies of canine cardiovascular physiology employing anesthetized animal preparations.

Anesthesia↗
PubMed1986

Systemic vascular resistance: an unreliable index of left ventricular afterload.

Systemic vascular resistance (SVR) is a frequently used clinical index of left ventricular afterload. However, SVR may not adequately assess left ventricular afterload (i.e., ventricular internal fiber load during systole) since it reflects only peripheral vasomotor tone. In contrast, left ventricular end-systolic wall stress (sigma es) reflects the combined effects of peripheral loading conditions and left ventricular chamber pressure, dimension, and wall thickness. To determine the relationship between SVR and sigma es, left ventricular afterload and contractility were pharmacologically altered in eight dogs instrumented with central aortic microtip and Swan-Ganz thermodilution catheters. Left ventricular wall thicknesses and dimensions were measured from two-dimensionally targeted M mode echocardiograms. Aortic, right atrial, and left ventricular end-systolic pressures as well as cardiac output were recorded. SVR and sigma es were determined under control conditions as well as during infusions of nitroprusside, methoxamine, dobutamine, and norepinephrine. Control data acquired before each drug infusion were similar. When compared with baseline values, SVR underestimated the magnitude of change in left ventricular sigma es by 22% when afterload alone was decreased (nitroprusside), 54% when afterload alone was increased (methoxamine), and 50% when afterload was decreased and contractility was augmented (dobutamine). Most importantly, when afterload was minimally decreased in association with augmented contractility (norepinephrine), SVR increased by 21% while sigma es fell by 9%. Thus, discordant changes in left ventricular afterload (i.e., sigma es) and SVR can occur during pharmacologic interventions. SVR is an unreliable index of left ventricular afterload, reflecting only peripheral arteriolar tone rather than left ventricular systolic wall force. This emphasizes the fact that a true measure of left ventricular afterload must consider the interaction of factors internal and external to the myocardium.

Animals↗
PubMed1986

[Tumor removal using performance ultrasound. Report of 50 brain tumor operations].

A report is given on the method of the tumour aspiration of cerebral tumours by means of power ultrasound. After classical exposure of the tumour--obligatory performance with physical-pharmacological reduction of the metabolism and in most cases under hypotension--the tumour is destroyed by ultrasonic power and simultaneously aspirated. A report is given on 50 cerebral tumour operations, which were carried out in Karl-Marx-Stadt within two years, using the tumour aspiration system "Aspirus 120". Finally the advantages of the method are summarised and dangers interpreted. At the end a valuation of the method is attempted and an outlook is given.

Brain↗
PubMed1986

Milrinone versus dobutamine: contribution of altered myocardial mechanics and augmented inotropic state to improved left ventricular performance.

Milrinone and dobutamine are positive inotropic agents with complex mechanisms of action. Traditional indexes of left ventricular function are unable to determine how much of the improvement in cardiac performance induced by these drugs is due to augmented inotropy and how much is the result of afterload reduction. Recently, the end-systolic wall stress (sigma es)-rate corrected velocity of fiber shortening (Vcfc) relationship has been shown to be a sensitive measure of contractility that is independent of preload while incorporating afterload. This index was measured in two groups of normal subjects (n = 8 per group) over a wide range of aortic pressures generated by administration of methoxamine before and during (1) milrinone or (2) dobutamine infusion. Studies were performed with the use of echocardiographic and calibrated carotid pulse tracings. Milrinone and dobutamine produced similar increases in overall left ventricular performance. Milrinone decrease end-systolic dimension (Des) by 15% and end-systolic pressure (Pes) by 22%, while increasing end-systolic wall thickness (hes) by 14%. This resulted in a 43% decline in left ventricular afterload as measured by sigma es. In contrast, dobutamine decreased Des by 11% while increasing hes by 14% and Pes by 22%. Despite the increase in left ventricular pressure, sigma es fell by 20%. Since afterload reduction alone results in increased left ventricular shortening, analysis of left ventricular performance was performed for both drugs at matched levels of sigma es under control and positive inotropic conditions. Twenty-nine percent of the improvement in Vcfc produced by milrinone was due to a decrease in afterload as compared with 18% of that produced by dobutamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Relation of electrocardiographic R-wave amplitude to changes in left ventricular chamber size and position in normal subjects.

Although exercise-induced changes in electrocardiographic R-wave amplitude have been ascribed to changes in left ventricular (LV) size, QRS axis, heart rate and ischemia, the physiologic mechanism remains unclear. To clarify the relation between R-wave amplitude and changes in LV size and position, simultaneous 9-lead electrocardiograms and targeted M-mode echocardiograms were recorded from 15 normal subjects. Recordings were made at rest, during Valsalva maneuver and during methoxamine infusion. LV diastolic dimension increased with methoxamine and decreased with Valsalva maneuver (p less than 0.001). R-wave amplitude in leads V5 and V6 varied directly with LV dimensions (p less than 0.001). The correlation coefficient between the change in R-wave amplitude in V5 or V6 and the change in LV dimension was 0.81 (p less than 0.01). No significant changes in R-wave amplitude were seen in electrocardiographic leads I, II, III, aVR, aVL, aVF or V1. Distance from the chest wall to the LV posterior wall correlated with change in R-wave amplitude (r = 0.79, p less than 0.001). Change from supine to left lateral position moved the left ventricle closer to the lateral chest wall in association with a 41 +/- 8% increase in R-wave amplitude in V5 and V6 (p less than 0.001). In conclusion, there is a direct and a dynamic relation between R-wave amplitude and LV chamber size. Chamber size and distance from the left ventricle to leads V5 or V6 interact as major determinants of R-wave amplitude.

Adult↗
PubMed1985

Physiologic assessment of the inotropic, vasodilator and afterload reducing effects of milrinone in subjects without cardiac disease.

Milrinone increases left ventricular (LV) shortening. Whether these changes result from vasodilation alone or from a combination of vasodilation and a positive inotropic action is controversial. Load-independent end-systolic indexes of LV contractility were measured over a wide range of aortic pressures generated by methoxamine infusion before and during milrinone administration. Sixteen studies were performed using echocardiography and calibrated carotid pulse tracings in 11 normal subjects. Milrinone loading doses of 30, 45 or 60 micrograms/kg were given intravenously over 10 minutes, followed by a maintenance infusion to achieve steady-state drug levels. Milrinone induced a dose-dependent decrease in baseline (i.e., before methoxamine) total systemic resistance (p less than 0.05) and afterload as measured by end-systolic wall stress (p less than 0.001). The associated changes in the end-systolic pressure-dimension, stress-shortening and stress-velocity of fiber shortening relations were characteristic of a positive inotropic intervention. All end-systolic indexes of LV contractility demonstrated greater inotropic effect at the higher milrinone plasma concentrations. Thus, load-independent indexes of LV contractility show that milrinone has a dose-related positive inotropic effect separate from its vasodilator (total systemic resistance) and afterload (end-systolic stress) reducing effects.

Adolescent↗
PubMed1985

Effects of loading conditions and contractile state (methoxamine and dobutamine) on left ventricular early diastolic function in normal subjects.

The influence of changes in preload, afterload and contractile state on left ventricular (LV) filling characteristics were examined. Normal subjects underwent echocardiographic determination of the peak rates of LV dimension change and wall thinning and their respective timing at rest, after preload augmentation with dextran, during increased afterload with methoxamine and during inotropic stimulation by dobutamine. These 2 peak velocities and their timing in diastole correlated well with each other and responded similarly to interventions. Increased preload resulted in higher peak velocities of dimension change and wall thinning, without changing the time in diastole at which they occur. Both peak velocities moved later into diastole with higher afterload; however, the overall change in magnitude was variable and without statistical significance. Inotropic stimulation resulted in faster rates of peak dimension change and wall thinning, which occurred at an earlier point in diastole. Examination of various measures of LV size and function over a wide range of preload and afterload conditions under a constant contractile state revealed a complex set of relations. The ratio of wall thickness-to-dimension at end-diastole showed the most significant relation to the peak rate of dimension change, whereas peak thinning was best correlated with fractional wall thickening. Both velocities were also significantly but more weakly related to other variables of systolic function. The timing of these peak velocities correlated most closely with the end-systolic wall stress and heart rate. Thus, LV filling and wall thinning depend in a complex fashion on loading conditions, heart rate and contractile state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Use of the calibrated carotid pulse tracing for calculation of left ventricular pressure and wall stress throughout ejection.

Calibrated carotid pulse tracings have been found previously to provide accurate estimates of end-systolic pressure. This study extends this technique to the estimation of arterial pressure throughout ejection. In twenty patients without aortic stenosis (age range 8 to 67 years), simultaneous recordings were made of the pressure tracing in the ascending aorta, externally recorded carotid pulse tracing, phonocardiogram, left ventricular echocardiogram, and peripheral blood pressure. Data were computer digitized and plots of arterial pressure were derived from the aortic pressure tracing (PA) and from the carotid pulse tracing (Pc). Left ventricular (LV) wall stress was then calculated throughout ejection using PA or Pc. The noninvasive estimation of pressure was excellent, with a maximum difference of 3.4 mm Hg between population means. This occurred within the first third of ejection. The wall stress calculations were similar, with a maximum mean population error of 3.5 gm/cm2 at 20% of ejection. The peak wall stress values had a mean difference of 1.4 gm/cm2; mean wall stress over the LV ejection period was 0.5 gm/cm2 higher when calculated from Pc than from PA. Thus, the carotid pulse tracing provides an accurate reproduction of the morphology of the pressure tracing recorded from the ascending aorta, and when calibrated by peripheral blood pressure measurement, it can be used to calculate LV pressure throughout ejection. These pressure estimates can be used to calculate wall stress throughout ejection with a high degree of accuracy.

Adolescent↗
PubMed1985

Left ventricular contractility and contractile reserve in humans after cardiac transplantation.

Limited data are available concerning left ventricular contractility and contractile reserve in the chronically denervated, transplanted human heart. This is primarily because of the inability of traditional tests of left ventricular performance to distinguish changes in contractility from alterations in ventricular loading conditions. In this study, load-independent end-systolic indexes of left ventricular contractility were measured by echocardiography and calibrated carotid pulse tracings in 10 patients who had undergone orthotopic cardiac transplant (age 48 +/- 4 years; interval from operation to study 1.2 +/- 0.8 years) and in 10 normal control subjects (age 25 +/- 4 years) matched for donor heart age (25 +/- 6 years). None of the transplant patients had evidence of rejection as determined by endomyocardial biopsy. Baseline left ventricular contractility was assessed over a wide range of afterload generated by infusion of methoxamine. Contractile reserve was measured as the response to an infusion of dobutamine plus methoxamine. Before afterload challenge, baseline left ventricular percent fractional shortening was higher for the transplant patients than for the control subjects (36.5 +/- 5.7% vs 32.1 +/- 2.1%; p less than .05). These differences occurred at a time that end-systolic wall stress (a measure of afterload) was significantly lower for the transplant patients (38 +/- 16 vs 50 +/- 9 g/cm2; p less than .05). When the left ventricular end-systolic pressure-dimension and stress-shortening relationships were determined for the transplant and control subjects, no differences in contractility or contractile reserve were noted. Thus the chronically denervated, transplanted, nonrejecting human left ventricle demonstrates normal contractile characteristics and reserve.

Adult↗
PubMed1985

Change in ventricular cavity size: differential effects on QRS and T wave amplitude.

Although many factors have been reported to change the R wave amplitude of the electrocardiogram (ECG), few observations have been made of the associated changes in T wave amplitude. We hypothesized that changes in R and T wave amplitude should parallel each other. To test this hypothesis, R and T wave amplitudes were measured in 15 normal subjects during increased and decreased left ventricular dimensions induced by infusion of methoxamine and by Valsalva maneuver, respectively, as well as during changes in the proximity of the left ventricle to the chest wall (i.e., shift in patient position from supine to left lateral position). Simultaneous nine-lead ECGs and two-dimensional-guided M mode echocardiograms of the left ventricle were recorded at rest and under each experimental condition. R wave amplitude increased as the left ventricular lateral wall moved closer to the V5 and V6 electrodes. Alterations in R wave amplitude seen with changes in left ventricular chamber size were primarily caused by radial movement of the left ventricle in relation to the chest wall. Proximity of the left ventricle to the chest wall was therefore a major determinant of R wave amplitude. In contrast, T wave amplitude varied directly with alterations in left ventricular chamber size but was unaffected by changes in proximity to the recording electrode on the chest wall. Left ventricular chamber size, and possibly the associated alteration in endocardial-to-epicardial surface area ratio, appeared to be the major determinants of T wave amplitude.

Adult↗
PubMed1985

Altered left ventricular mechanics in patients with valvular aortic stenosis and coarction of the aorta: effects on systolic performance and late outcome.

Despite similar degrees of left ventricular systolic hypertension shortening characteristics are usually greater in patients with congenital valvular aortic stenosis (VAS) than in patients with coarctation of the aorta (CoA). We hypothesized that these dissimilarities were caused by differences in myocardial mechanics rather than by alterations in contractile state. Eleven patients with VAS (ages 6 to 41 years) and 11 with CoA were matched for age, body surface area, and peak systolic ejection gradient. Results were compared with data from 22 normal subjects matched for age and body surface area. Echocardiographic tracings of the left ventricle were recorded in conjunction with left ventricular pressure measurements (VAS) or calibrated carotid pulse tracings (CoA and normal subjects). Peak and end-systolic wall stresses as well as left ventricular shortening fraction (% delta D) and rate-corrected velocity of fiber shortening (Vcfc) were calculated. No differences for left ventricular dimensions, heart rate or peak wall stress were present. Ventricular peak systolic pressures and wall mass were higher for the patients with VAS or CoA than for the normal subjects (p less than .001). These parameters did not differ between the VAS and CoA groups. The patients with VAS had higher % delta D and Vcfc than either the CoA or normal groups (p less than .01). Afterload, as quantified by end-systolic stress, was 41% lower than normal for the patients with VAS (p less than .001) and 13% higher than normal for those with CoA (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Adverse cardiac effects of acute alcohol ingestion in young adults.

Previous studies of the effects of acute alcohol ingestion in normal subjects have used measures of left ventricular performance that are altered by changes in preload and afterload and in contractile state. In studies involving nine healthy, young adults, we measured sensitive load-independent end-systolic indices of left ventricular contractility over a wide range of pressures generated by methoxamine infusion before and after oral alcohol administration. Echocardiography was used in conjunction with calibrated carotid pulse tracings. Alcohol ingestion resulted in a fall (p less than 0.01) in left ventricular end-diastolic dimension (a measure of preload), end-systolic wall stress (a measure of afterload), and systemic vascular resistance, while not changing the left ventricular shortening fraction. In contrast, the end-systolic pressure-dimension slope decreased (p less than 0.001) and the rate-corrected velocity of left ventricular fiber shortening at an end-systolic wall stress of 50 g/cm2 fell (p less than 0.001). Thus, when load-independent assessment of left ventricular contractility is done, acute alcohol ingestion has a myocardial depressant effect greater than previously suspected.

Adult↗