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PubMed1978

[Procedural aspects and indications for using stimulation of the heart in the therapeutic clinic].

Temporary endocardial decelerating stimulation of the heart was conducted 151 times in 57 patients with various tachysystolic disorders of the rhythm. The values of central and intracardiac hemodynamics were studied in some patients against the background of decelerating stimulation. Definite groups of patients were distinguished according to the results of decelerating stimulation. In 17 patients decelerating stimulation of the heart served as an independent method of treatment of cardiac arrhythmias the underlying factor of which was the re-entry mechanism. In 11 patients paired and combined stimulation of the ventricles promoted the normalization of the values of hemodynamics and myocardial metabolism which had occurred against the background of severe disorders of the rhythm. In 14 patients with marked electric instability of the myocardium due to various causes, decelerating stimulation allowed time to be gained for choosing and carrying out adequate drug therapy.

Adolescent↗
PubMed1981

[Fetal mechanocardiogram studied by systolic time intervals in ultrasonic doppler fetal heart valve signals using new multistylus recorder system (author's transl)].

Continuous and on-line recording of ultrasonic Doppler fetal heart valve signals were investigated simultaneously with FHR and uterine contraction during labor in 57 cases using new multistylus recorder system 1) Electromechanical intervals of normal cases were found in FHR-baseline that T-Ao, Mc-Ac, T-Ac and Ao-Ac showed prolongation with FHR decrease when starting point of cardiac cycle was exposed by "T", but T-Mc, Mc-Ao and Ac-Mo had no particular relation to FHR. T-Ao showed large variation, but no relation to gestational age. Ac-Mo was almost constant. Early deceleration showed elongation of T-Ao during FHR decrease in 2 cases but no change in 1. Small variation of Ao-Ac was noted in each FHR range. Mild variable deceleration showed elongated T-Ao, Mc-Ao and T-Mc in 13 cases but unchanged in 1. Ao-Ac had large variation in each FHR range. At the acceleration, 2 cases had T-Ao prolongation but a case no change. Ac-Mo values were almost constant during deceleration and acceleration. 2) In 5 abnormal cases diagnosed by late deceleration, severe variable deceleration or bradycardia, 4 showed continuous shortening of T-Ao. One had prolongation after its shortening. Two cases showed abnormal Ao-Ac values in some FHR range.

Computers↗
PubMedDate not supplied

[Phonocardiographic and Doppler echocardiographic study on the mechanism of the presystolic murmur in mitral stenosis, especially the relationship to mitral inflow dynamics].

The cause of the "presystolic murmur" in mitral stenosis was investigated by phonocardiography and continuous wave Doppler echocardiography in 31 patients with mitral stenosis and sinus rhythm classified into two groups: 18 patients with and 13 without "presystolic murmur". 1. The "presystolic murmur" group demonstrated high frequency vibrations preceding the first heart sound coinciding with the initial low frequency component of the first heart sound recorded at the apex in both groups. 2. There were two types of "presystolic murmur": The first type observed in three of the 18 patients occurred during the accelerated phase of the atrial (A) wave of mitral inflow signals and lasted until the first heart sound. The A wave velocity in mitral inflow signals was high at the onset and peak, and rapidly decreased after the peak. The second type observed in 15 patients occurred during the decelerated phase of the A wave and lasted until the first heart sound. The A wave velocity in mitral inflow signals was low at the onset, but high at the peak and rapidly decreased after the peak. 3. The mitral orifice area tended to be smaller in all patients with "presystolic murmur". The peak flow velocity, deceleration rate of the A wave, and maximal pressure gradient across the mitral valve during atrial contraction were significantly increased in all patients with "presystolic murmur". 4. Five patients with newly developed "presystolic murmur" after amyl nitrite inhalation had an increased initial low frequency component of the first heart sound coinciding with the latter half of "presystolic murmur". The rate of increase in the peak flow velocity and the deceleration rate of the A wave were significantly larger and the maximal atrioventricular pressure gradient during atrial contraction tended to be larger in these five patients than those in five who did not develop "presystolic murmur". 5. The peak flow velocity, deceleration rate of the A wave and the maximal atrioventricular pressure gradient during atrial contraction had increased 1 year later compared with those immediately after cardioversion of atrial fibrillation, and newly developed "presystolic murmur" appeared according to the recovery of left atrial mechanical function. These results suggest that the latter half of "presystolic murmur" originates from augmentation and prolongation of the initial low frequency component of the first heart sound up to the audible range caused by the sudden deceleration of mitral inflow velocity due to left ventricular contraction, and that the early half of "presystolic murmur" is the atriosystolic murmur produced by the increase in mitral inflow velocity during atrial contraction.

Blood Flow Velocity↗
PubMed1984

Braking of fast and accurate elbow flexions in the monkey.

The processes responsible for braking fast and accurate elbow movements were studied in the monkey. The movements studied were made over different amplitudes and against different inertias . All were made to the same end position. Only fast movements that showed the typical biphasic or triphasic pattern of activity in agonists and antagonists were analysed in detail. For movements made over different amplitudes and at different velocities there was symmetry between the acceleration and deceleration phases of the movements. For movements of the same amplitude performed at different velocities there was a direct linear relation between peak velocity and both the peak acceleration (and integrated agonist burst) and peak deceleration (and integrated antagonist burst). The slopes of these relations and their intercept with the peak velocity axis were a function of movement amplitude. This was such that for large and small movements of the same peak velocity and the same end position (i) peak acceleration and phasic agonist activity were larger for the small movements and (ii) peak deceleration and phasic antagonist activity were larger for the small movements. The slope of these relations and the symmetry between acceleration and deceleration were not affected by the addition of an inertial load to the handle held by the monkey. The results indicate that fast and accurate elbow movements in the monkey are braked by antagonist activity that is centrally programmed. As all movements were made to the same end position, the larger antagonist burst in small movements, made at the same peak velocity as large movements, cannot be due to differences in the viscoelastic contribution to braking (cf. Marsden, Obeso & Rothwell , 1983).(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1980

Fetal heart rate patterns in infants in whom necrotizing enterocolitis develops: a preliminary report.

Perinatal changes in fetal heart rate (FHR) were monitored in infants in whom necrotizing enterocolitis (NEC) developed. Eleven of 16 monitoring strips indicated severe FHR changes consistent with perinatal hypoxia, two indicated mild changes, two indicated tachycardia alone, and only one was normal. Severe variable FHR decelerations indicating umbilical cord compression occurred in four cases, persistent late FHR decelerations occurred in two cases, persistent late and severe variable FHR decelerations occurred in two cases, prolonged bradycardia occurred in two cases, and bradycardia with persistent late FHR decelerations occurred in one case. These findings confirm that NEC does occur in infants with perinatal hypoxia and indicate that intestinal ischemia may occur before delivery and after delivery from hypoxia and acidosis from lung disease, exchange transfusion, or sepsis. Perinatal monitoring may become an important determinant in identifying the infant in whom NEC will develop.

Enterocolitis, Pseudomembranous↗
PubMed2000

Two-phase model of the kinetics of growth of Rhizopus oligosporus in membrane culture.

An empirical model was developed to describe a growth profile occurring in solid-state fermentation (SSF), namely that consisting of an initial period of rapid acceleration followed by an extended period of deceleration. This kinetic profile is not adequately described by the logistic model. The empirical model is based on the concept of active and nonactive hyphal segments. Exponential and deceleration growth phases are modeled. The model parameters can be determined directly from the dry-weight profile and they depend on the growth medium present. The model suggests that, at the instant the culture enters the deceleration phase, there is a 71% to 86% decrease in the number of actively extending hyphal tips and that, during the deceleration phase, there is an exponential decay in the number of active hyphal segments, with a first-order decay constant of 0.042 to 0.072 h(-1).

Biomass↗
PubMed1993

Growth pattern in the Apert syndrome.

In this paper, we demonstrate that a discernible and unique growth pattern characterizes the Apert syndrome. The keys to understanding Apert newborn measurement values are brain size and cranial configuration. Both true megalencephaly and coronal synostosis are present at birth. Thus, the head is unusually heavy and the cranium is disproportionately high. Mean newborn length and weight are above the normal 50th centile. Of our newborn patients, 16% exceeded 4,000 g in weight. Preterm infants were appropriate or slightly large for gestational age. A biphasic linear growth pattern was found. In childhood, deceleration of linear growth occurs so that most values fall between the 5th and 50th centiles. From adolescence to adulthood, deceleration becomes more pronounced. This 2-step linear growth deceleration results in large measure from rhizomelic shortness of the lower limbs. Puberty takes place within the normal time frame. Although a disproportionate amount of the megalencephaly accounts for the dramatic increase in head height, the widely patent midline calvarial defect, allowing the brain to expand anteriorly into the metopic area, and some increase in the head breadth permit the mean head circumference at birth to normalize slightly above the 50th centile. During the growth period, the head circumference was studied in surgically unoperated Apert patients from the 1960s and earlier. The natural history of the growing cranium consists of gradual deceleration in head circumference from slightly above the 50th centile at birth to within or at -2 SD later on.

Acrocephalosyndactylia↗
PubMed2003

Mechanisms of force and power production in unsteady ricochetal brachiation.

Brachiators travel by swinging beneath handholds, and it is not obvious how these animals manage to accelerate and decelerate in a horizontal direction, especially when moving rapidly. Most previous analyses focused on brachiation in highly constrained laboratory conditions that induced steady-state locomotion. Emerging understanding of brachiation suggests that much of gibbon locomotory behavior and morphology must be considered within the context of the complexities of the natural environment: the forest canopy is three-dimensional, with high variation in handhold availability and properties. The goal of this paper is to quantify the active mechanisms by which gibbons can dynamically control their velocity. Force production and kinematics were analyzed from a white-handed gibbon Hylabates lar during ricochetal brachiation. Both the mechanisms of force production and power input may be inferred for accelerating and decelerating brachiation by combining force data with kinematics. Examples of steady-state, accelerating, and decelerating ricochetal brachiation are highlighted. Gibbons are able to produce net horizontal impulses by releasing early (resulting in a loss of potential energy, but an accelerating horizontal impulse) or delaying release (associated with an increase in potential energy, and a decelerating horizontal impulse). Torque about the shoulder, leg-lifting (or dropping), and elbow flexing (or straightening) are discussed as potential mechanisms for controlling energy within the brachiating system. Of these possibilities, leg-lifting and arm-flexing were observed as mechanisms of adding mechanical energy. Net energy loss, and substantial torques about the shoulder, were not observed.

Acceleration↗
PubMed2004

Evaluation of myocardial performance index to predict mild rejection in cardiac transplantation.

BACKGROUND: Early diagnosis of heart transplant rejection is mandatory, since even mild rejection can rapidly progress to more severe rejection. Noninvasive diagnosis of heart transplant rejection still remains a challenge. HYPOTHESIS: The purpose of the study was to determine a possible association between myocardial performance index (MPI) and biopsy score of the heart transplant. METHODS: This is a retrospective cohort analysis of 99 complete Doppler echocardiographic studies from 24 consecutive patients (23 men) performed within 24 h of endomyocardial biopsy. Mean age of the cohort was 50 +/- 9 years and mean time from transplantation was 19 +/- 21 months (1-81). All patients were in sinus rhythm. Myocardial performance index was calculated as the ratio of isovolumic contraction time plus isovolumic relaxation time divided by ejection time. Left ventricular dimensions, left ventricular mass, ejection fraction, and a number of Doppler indices (E-point velocity, A-point velocity, deceleration time, and deceleration slope) were also measured. The International Society for Heart and Lung Transplantation (ISHLT) grading system was used for the classification of endomyocardial biopsies. RESULTS: Myocardial performance index was significantly prolonged (0.60 +/- 0.13, 0.68 +/- 0.08, 0.75 +/- 0.20, in biopsy scores 0, IA, and IB, respectively; p<0.001). Isovolumic contraction time was significantly prolonged; isovolumic relaxation time was not significantly changed. Ejection time and deceleration time were significantly shortened. Multivariate stepwise regression analysis revealed that MPI and deceleration time were the only independent predictors of biopsy score (r=0.48, F=10.53, p<0.0001). CONCLUSION: Myocardial performance index seems to be a useful adjunct in the follow-up of cardiac transplant patients. These preliminary data suggest that a larger study may be indicated to clarify the relevance of myocardial performance index.

Adult↗
PubMed1985

Prediction in the oculomotor system: smooth pursuit during transient disappearance of a visual target.

Eye movements were recorded in human subjects who tracked a target spot which moved horizontally at constant speeds. At random times during its trajectory, the target disappeared for variable periods of time and the subjects attempted to continue tracking the invisible target. The smooth pursuit component of their eye movements was isolated and averaged. About 190 ms after the target disappeared, the smooth pursuit velocity began to decelerate rapidly. The time course of this deceleration was similar to that in response to a visible target whose velocity decreased suddenly. After a deceleration lasting about 280 ms, the velocity stabilized at a new, reduced level which we call the residual velocity. The residual velocity remained more or less constant or declined only slowly even when the target remained invisible for 4 s. When the same target velocity was used in all trials of an experiment, the subjects' residual velocity amounted to 60% of their normal pursuit velocity. When the velocity was varied randomly from trial to trial, the residual velocity was smaller; for target velocities of 5, 10, and 20 deg/s it reached 55, 47, and 39% respectively. The subjects needed to see targets of unforeseeable velocity for no more than 300 ms in order to develop a residual velocity that was characteristic of the given target velocity. When a target of unknown velocity disappeared at the very moment the subject expected it to start, a smooth movement developed nonetheless and reached within 300 ms a peak velocity of 5 deg/s which was independent of the actual target velocity and reflected a "default" value for the pursuit system. Thereafter the eyes decelerated briefly and then continued with a constant or slightly decreasing velocity of 2-4 deg/s until the target reappeared. Even when the subjects saw no moving target during an experiment, they could produce a smooth movement in the dark and could grade its velocity as a function of that of an imagined target. We suggest that the residual velocity reflects a first order prediction of target movement which is attenuated by a variable gain element. When subjects are pursuing a visible target, the gain of this element is close to unity. When the target disappears but continued tracking is attempted, the gain is reduced to a value between 0.4 and 0.6.

Adult↗
PubMed1987

Mechanism of growth retardation of the adenocarcinoma EO 771.

Growth retardation of tumors has been predominantly described by an increase of the "cell loss factor" phi. However, this cell loss factor alone merely reflects the growth deceleration without giving information on the mechanism that causes growth retardation. In the present study a quantitative analysis of the mechanism causing growth retardation of the adenocarcinoma EO 771 has been carried out by determining separately the components of the cell loss factor phi, namely the cell production rate and the cell loss rate of the tumor cell population. For this purpose the alteration of the histology of the tumor (proportion of necrotic tumor tissue, tumor cell density) and the proliferative capacity of the tumor cell population as a function of the tumor size was studied by applying morphometric and cell kinetic methods. The results show that growth deceleration is due to a decrease of the cell production rate kappa p and a simultaneous increase of the cell loss rate kappa l. Both processes contribute to about the same extent to the growth deceleration of the tumor cell population. In early tumor growth deceleration is mainly due to a prolongation of the cycle time of the tumor cells, in later phases of tumor growth to an increasing probability of the tumor cells to decycle leading to a decrease of the growth fraction GF and an increase of the cell loss rate kappa l.

Adenocarcinoma↗
PubMed1995

Density and age-specific mortality.

Age-specific mortality rates decelerate at older ages in laboratory populations in the Medfly Ceratitis capitata. This has been interpreted by Carey et al. (1992) to reflect a slowing of the aging process, but might also be explained by declining adult density. Here it is argued that the density explanation, as presented by Graves and Mueller (1993), is unpersuasive for several reasons: extrapolations from Drosophila to Medflies are unjustified; the range of densities they studied is 2-120 times higher than that used in other studies; they ignore data on Medflies held in isolation, which rule out density effects; their own data suggest that initial cohort density has no effect on mortality rates at older ages, which is the relevant part of the life cycle; their experiment is too small to provide accurate estimates of mortality; new Medfly experiments executed at multiple densities show decelerating and then declining mortality rates at advanced ages for all densities. When Drosophila survivorship experiments are done on a sufficiently large scale they also show a deceleration of mortality at older ages that is not attributable to density effects. The deceleration of mortality rates is most likely a real facet of aging, and will have to be taken into consideration in any synthesis of the genetics and evolution of aging.

Aging↗
PubMed1994

Prognostic value of Doppler echocardiographic assessment of left ventricular filling in idiopathic dilated cardiomyopathy.

The relation of left ventricular (LV) diastolic filling with the clinical outcome in patients with idiopathic dilated cardiomyopathy (IDC) was examined. LV diastolic filling was assessed by Doppler echocardiography in 57 patients with IDC at the time that the diagnosis was established by angiocardiography. Patients were followed for 29 +/- 16 months. Fifteen patients died: 12 due to progressive congestive heart failure and 3 suddenly. Four other patients underwent cardiac transplantation because of progressive heart failure (1-year survival 86%). Patients who died of congestive heart failure or underwent cardiac transplantation had a steep increase and decrease in the early filling phase as compared with survivors; the peak early Doppler velocity was higher (0.84 +/- 0.16 vs 0.65 +/- 0.21 m/s; p < 0.005), and the deceleration time of the early velocity peak was shorter (117 +/- 26 vs 188 +/- 62 ms; p < 0.001) than in survivors. Surviving patients and those who died suddenly showed similar patterns of LV filling. Deceleration time and peak early Doppler velocity were the strongest predictors of survival as compared with systolic function and clinical status in a Cox proportional-hazards analysis. Patients with a shortened deceleration time (< or = 140 ms) had a significantly reduced 2-year survival rate of 52% (confidence interval 34 to 71%) as compared with those with a longer deceleration time (94%; confidence interval 89 to 98%) (p < 0.001). Evidence was presented for a relation between LV filling and survival in patients with IDC.

Actuarial Analysis↗
PubMed1976

Antepartum fetal heart rate and uterine activity studies: I. Preliminary report of accelerations and the oxytocin challenge test.

A series of 344 antepartum fetal heart rate studies in 209 high-risk patients is described. The importance of evaluation of accelerations of the fetal heart rate as well as periodic decelerations associated with uterine activity is demonstrated. Our data suggest that the absence of accelerations of the fetal heart rate during the recording period may be associated with increased perinatal morbidity. Late decelerations may occur in the same recording session as accelerations of the fetal heart rate. The association of late decelerations of the fetal heart rate with no accelerations during the recording session is highly suggestive of increased perinatal morbidity. In high-risk patients, accelerations of the fetal heart rate and no late decelerations with uterine activity are a reassuring finding, with 91 per cent of patients showing no increased perinatal morbidity.

Adolescent↗
PubMed1979

The role of a trial of labor with a positive contraction stress test.

During a 28 month period 812 patients underwent antepartum FHR testing. Twenty-eight patients had a positive CST. There were two antepartum fetal deaths and 11 patients had a cesarean section without a trial of labor. Fifteen patients had a trial of closely monitored labor (continuous FHR and fetal scalp blood sampling when indicated) and 11 of these (73%) were delivered vaginally. The CST records were examined for: per cent late deceleration, baseline FHR, presence of FHR accelerations, duration of the latency period (time from onset of contraction to onset of deceleration), and amplitude of deceleration. The absence of accelerations (nonreactive CST) and a latency period of less than 45 seconds both predicted persistent late deceleration during labor or fetal death in utero but statistical significance was found only for the latter parameter.

Apgar Score↗
PubMed1981

The prediction of intrapartum fetal metabolic acidosis by fetal heart rate monitoring.

Fetal heart rate characteristics during the 8 hours prior to delivery have been studied in 200 patients in whom the fetus had evidence of a metabolic acidosis at delivery, and compared to those in 200 patients in whom the fetus had a normal acid-base at delivery. Baseline fetal heart rate moderate bradycardia and tachycardia, decreased baseline variability, and decreased fetal heart rate accelerations are predictors of intrapartum fetal hypoxia with metabolic acidosis. Marked patterns of total decelerations and late decelerations are predictive of intrapartum fetal hypoxia with metabolic acidosis. The probability of fetal metabolic acidosis in the presence of a marked pattern of total decelerations is 25%, and with late decelerations it is 48%, in a population of high-risk pregnancies.

Acidosis↗
PubMed1985

Effects of hypoxemic events on breathing, body movements, and heart rate variation: a study in growth-retarded human fetuses.

In 14 growth-retarded human fetuses, breathing and body movements were studied before, during, and after late heart rate decelerations. Heart rate variation was measured before and after the decelerations. Breathing and body movements were significantly reduced during and after the deceleration. Heart rate variation was reduced after the decelerative episode. Since late heart rate decelerations are presumably signs of acute fetal hypoxemia, there is evidence that these reductions are caused by hypoxemia. The results suggest, furthermore, that just as in fetal sheep, these changes might be mediated by a change in brain activity state.

Female↗
PubMed1992

Numeric analysis of heart rate variation in intrauterine growth-retarded fetuses: a longitudinal study.

OBJECTIVE: We attempted to determine changes occurring with time in fetal heart rate and its variation in fetuses with intrauterine growth retardation in whom late antepartum fetal heart rate decelerations eventually develop. STUDY DESIGN: Thirteen fetuses with intrauterine growth retardation were studied over a median period of 25 days. One-hour fetal heart rate records were made two to five times per week and were analyzed numerically. Fetal movements were recorded by the women. RESULTS: On average long-term fetal heart rate variation decreased gradually with time and fell below the norm (30 milliseconds) at about the same time decelerations appeared. Mean heart rate showed a slight but statistically significant increase after the occurrence of decelerations. There were large interfetal differences in all parameters studied. CONCLUSION: In fetuses with intrauterine growth retardation a decrease in long-term fetal heart rate variation is a rather late sign of impairment that coincides with the occurrence of late decelerations. In the surveillance of the fetus with intrauterine growth retardation it might be most appropriate to use each fetus as its own control.

Female↗