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PubMed1980

Intensity of sensation related to activity of slowly adapting mechanoreceptive units in the human hand.

1. Impulses were recorded from single afferent fibres in the median and ulnar nerves of human subjects. The response of slowly adapting mechanosensitive units with receptive fields in the glabrous skin of the hand were studied when rectangular indentations of varying amplitudes and invariant time duration were delivered. Simultaneously the subject was asked to estimate the magnitude of his sensation associated with the stimuli.2. Stimulus-response plots of the afferent units were constructed and compared with the psychophysical magnitude estimation plots.3. The stimulus-response data of the afferent units fell along monotonous curves which were largely decelerating when stimuli above the static threshold were taken into account. When responses below the static threshold were taken into account many plots were S-shaped.4. The psychophysical plots were monotonous and either decelerating, linear or accelerating.5. Power functions were fitted to the two sets of data. The group average differed considerably with regard to the exponent of the fitted functions which was 0.7 for the neural and 1.0 for the psychophysical function.6. There was considerable variation between shapes of curves derived from individual test points. The range of exponents for the neural function was 0.26-1.92 and for the psychophysical function 0.36-2.09. The variation in psychophysical functions was partly accounted for by relatively stable inter-subject differences, whereas no such inter-subject difference was evident for the neural functions, which seemed to vary randomly.7. There was no indication of a correlation between the shapes of the neural functions and the shapes of the psychophysical functions when data from individual subjects or individual test points were compared. Moreover, when two groups of data were considered, one with accelerating and one with decelerating psychophysical functions, the associated neural functions did not differ between the two groups.8. It was concluded that the hypothesis of a close agreement between the stimulus-response functions of slowly adapting mechanoreceptors in the human hand and the psychophysical magnitude estimation functions is not tenable. This was evident when average group data were compared as well as when data from individual subjects and individual target points were compared. The findings suggest that the shapes of the psychophysical magnitude estimation functions are highly dependent on central mechanisms and are not a direct function of the properties of the afferent units as has been claimed in previous investigations.

Adult↗
PubMed1993

Organization of motor output in slow finger movements in man.

1. Slow finger movements were analysed in normal human subjects with regard to kinematics and EMG activity of the long finger muscles. Surface EMG from the finger extensor and flexor muscles on the forearm was recorded along with angular position and angular velocity during voluntary ramp movements at single metacarpophalangeal joints. Angular acceleration was computed from the velocity record. 2. It was found that movements were not smooth but characterized by steps or discontinuities, often recurring at intervals of 100-125 ms, yielding velocity and acceleration profiles dominated by 8-10 Hz cycles. The discontinuities were manifest from the very first trial and thus not dependent on training. Their amplitude and amount varied between subjects but were relatively stable for the individual subject. 3. The 8-10 Hz cycles were seen with voluntary ramp movements of widely varying velocities, higher velocities being associated with larger steps recurring with the same repetition rate as the small steps of slow voluntary ramps. Maximal step amplitude observed was more than one order of magnitude larger than physiological tremor. 4. The individual 8-10 Hz cycle was asymmetrical in that decelerations usually reached higher peaks than the preceding acceleration, suggesting that the antagonist contributed with a braking action. Moreover, in very slow voluntary ramps, the movement cycles were often interspaced by periods of zero velocity, providing a highly non-sinusoidal velocity profile. 5. The EMG of the agonist and the antagonist muscles was modulated in close relation to the accelerations and decelerations respectively of the individual movement cycle. These modulations were present in both extensor and flexor muscles, although they were more consistent and usually more prominent in the former. 6. The findings indicate that a feature of slow finger movements was an 8-10 Hz periodic output to the muscular system, suggesting that slow finger movements are implemented by a series of biphasic force pulses, involving not only the shortening agonist muscle propelling the movement, but the antagonist muscle as well whose activity increased shortly after the agonist and contributed to a sharp deceleration of the individual step of movement. 7. It is proposed, as a hypothesis, that this biphasic motor output may reflect a similar organization of the descending motor command for slow finger movements. Hence, this command would include a series of biphasic pulses, concatenated at a rate of 8-10 per second and a pulse-height regulator capable of setting the size of the pulse and thus the overall speed of the movement.

Adult↗
PubMed1999

A delayed wave of death from reproduction in Drosophila.

Mortality rates typically increase rapidly at the onset of aging but can decelerate at later ages. Reproduction increases the death rate in many organisms. To test the idea that a delayed impact of earlier reproduction contributes to both an increase in death rates and a later deceleration in mortality, the timing of the surplus mortality produced by an increased level of egg production was measured in female Drosophila. Reproduction produced a delayed wave of mortality, coincident with the sharp increase in death rates at the onset of aging and the subsequent deceleration of mortality. These results suggest that aging has evolved primarily because of the damaging effects of reproduction earlier in life, rather than because of mutations that have detrimental effects only at late ages.

Aging↗
PubMed2000

Serial assessment of left ventricular diastolic function after Fontan procedure.

OBJECTIVE: To assess longitudinal changes in systemic ventricular diastolic function late after the Fontan procedure. DESIGN AND PATIENTS: Prospective study of 13 patients at 2.8 (2.0) years (early) and again at 11.4 (2.0) years (late) after the Fontan procedure by Doppler echocardiography with simultaneous ECG, phonocardiogram, and respirometer. SETTING: Tertiary paediatric cardiac centre. RESULTS: The isovolumic relaxation time (IVRT) was significantly longer, and E wave deceleration time, E and A wave velocities, and E:A velocity ratio were reduced compared to normal both early and late after the procedure. The mean (SD) z score of IVRT decreased significantly from +2.50 (1.00) to +1.24 (0.80) (p = 0.002), and the z score of the E wave deceleration time decreased from -1.69 (1.31) to -2.40 (1.47) (p = 0.03) during follow up. The A wave deceleration time also tended to decrease (early 80 (12) ms v late 73 (11) ms, p = 0.13) with increased follow up. There were no changes of the E and A wave velocities and E:A velocity ratio. The E wave velocity was inversely related to IVRT both early (r = -0.82, p = 0.001) and late (r = -0.59, p = 0.034) after the operation. The prevalence of diastolic flow during isovolumic relaxation decreased from 85% (11/13) to 38% (5/13) (p = 0.04), while that of mid diastolic flow increased from 23% (3/13) to 77% (10/13) (p = 0.02) between the two assessments. CONCLUSIONS: Left ventricular diastolic function remains highly abnormal late after the Fontan procedure. The longitudinal changes demonstrated on follow up are compatible with reduction of left ventricular compliance in addition to persisting abnormalities of relaxation.

Blood Flow Velocity↗
PubMed2001

Four year follow up of aortic valve replacement for isolated aortic stenosis: a link between reduction in pressure overload, regression of left ventricular hypertrophy, and diastolic function.

OBJECTIVE: To evaluate changes in left ventricular function and the impact of ventricular hypertrophy and pressure gradient early and late after aortic valve replacement in patients with isolated aortic stenosis. DESIGN: 41 patients with isolated aortic stenosis and normal systolic function underwent cross sectional and Doppler echocardiography two months before and two weeks and four years after aortic valve replacement. RESULTS: Early after the operation, left ventricular mass index (mean (SD)) decreased from 187 (44) g/m(2) to 179 (46) g/m(2), because of a reduction in end diastolic diameter (p < 0.05). Aortic pressure gradients were reduced, as expected. Isovolumic relaxation time was reduced from 93 (20) ms to 78 (12) ms, and deceleration time from 241 (102) ms to 205 (77) ms (p < 0.05). At four years, left ventricular mass index was further reduced to 135 (30) g/m(2) (p < 0.01) as a result of wall thickness reduction in the interventricular septum (from 14 (1.6) mm to 12 (1.4) mm, p < 0.01) and the posterior wall (from 14 (1.6) mm to 12 (1.3) mm, p < 0.01). Diastolic function, expressed by a reduction in isovolumic relaxation time from 93 (20) ms to 81 (15) ms (p < 0.01) and deceleration time from 241 (102) ms to 226 (96) ms (p < 0.05), remained improved. Prolonged isovolumic relaxation time was associated with significant septal and posterior wall hypertrophy (wall thickness > 13 mm) (p < 0.05), whereas prolonged deceleration time was related to high residual gradient (peak gradient > 30 mm Hg ) (p < 0.01). CONCLUSIONS: Left ventricular diastolic function improves early after surgery for aortic stenosis in parallel with the reduction in the aortic gradient. However, prolongation of Doppler indices of myocardial relaxation and ventricular filling is observed in patients with significant left ventricular hypertrophy and a residual pressure gradient early after surgery. At four years postoperatively, diastolic function remains improved.

Aged↗
PubMed2004

Relation between aortic stiffness and left ventricular diastolic function in patients with hypertension, diabetes, or both.

OBJECTIVE: To evaluate aortic function and its relation to left ventricular diastolic function in patients with hypertension, diabetes, or both, without coronary artery disease. METHODS: Study groups were composed of 27 healthy participants and 25 patients with hypertension, 24 with diabetes, and 18 with hypertension and diabetes. Coronary artery disease was excluded in all of the study participants. Aortic strain and distensibility were calculated from the aortic diameters measured by echocardiography and blood pressure obtained by sphygmomanometry. RESULTS: There were significant differences between the control and the patient groups (hypertensive, diabetic, and diabetic-hypertensive) in aortic strain (mean (SD) 18 (8)% v 11 (7)%, 9 (3)%, and 8 (3)%, respectively, p < 0.001) and distensibility (10 (5.1) v 3.1 (1.5), 5.1 (2.8), and 2 (0.9) cm2/dyn/10(3), respectively, p < 0.001). In a multivariate analysis, the parameter most closely related to the deceleration time in the control group was aortic distensibility (standardised beta coefficient -0.50, p = 0.002, overall R2 = 0.25). In the patient group, the parameter most closely related to deceleration time was also aortic distensibility (standardised beta coefficient -0.36, p = 0.009, overall R2 = 0.13). Even though the study group variable was entered in to the multivariate model, aortic distensibility was found to be the parameter most closely related to deceleration time (standardised beta coefficient -0.48, p < 0.001, overall R2 = 0.22). CONCLUSION: Aortic stiffness is increased in patients with hypertension, diabetes, or both even after the exclusion of coronary artery disease. Aortic stiffness and left ventricular diastolic dysfunction are also associated in these patients.

Aorta, Thoracic↗
PubMed1996

Effects of gradual volume loading on left ventricular diastolic function in dogs: implications for the optimisation of cardiac output.

BACKGROUND: Volume loading is commonly used to adjust preload and optimise cardiac output. It is difficult to monitor preload at the bedside because filling affects ventricular diastolic function and consequently end diastolic pressure, which is the variable used to monitor preload. OBJECTIVE: To assess the effects of gradual volume loading on the different components of left ventricular diastolic function---filling velocities, relaxation, and chamber compliance---to identify how excessive loading produces diastolic dysfunction. METHODS AND RESULTS: Eight mongrel dogs, anaesthetised and mechanically ventilated with both the chest and the pericardium closed, were studied during basal conditions (B), during gradual volume loading with physiological saline---5 ml/kg (VL5), 10 ml/kg (VL10), and 15 ml/kg (VL15)---and during infusion of isosorbide dinitrate (10 g/kg/min) started after the VL15 load was achieved. Dogs were monitored haemodynamically and by transthoracic Doppler echocardiography to assess peak modal velocities of the E and A waves, E/A ratios, and the deceleration time of the E wave. M mode recordings of aligned mitral and aortic valve motion were also obtained to calculate the isovolumic relaxation time. Effects of volume loading on ventricular diastolic function seemed to occur in two phases. Small and moderate volume loads (VL5 and VL10) promoted early ventricular filling, increasing E wave velocities, improving the mean (SD) E/A ratio from 1.95 (0.3) (B) to 2.0 (0.27) (VL5) and 2.6 (0.3) (VL10) (P < 0.00005), prolonging the E wave deceleration time, and only slightly increasing ventricular diastolic pressures. These changes suggest an improvement in ventricular compliance. Extreme volume loads (VL15) produced an abrupt reduction in early ventricular filling, which was transfered to late in diastole, by decreasing E wave velocity, by increasing A wave velocity, and by decreasing E/A ratio from 2.6 (0.3) (VL10) to 0.8 (0.05) (VL15) (P < 0.00005). The E wave deceleration time was shortened and left ventricular diastolic pressures were much increased, all suggesting a deterioration in chamber compliance. All these restrictive changes were promptly reversed by the perfusion of isosorbide dinitrate. The isovolumic relaxation time steadily increased with volume loading. CONCLUSIONS: Small and moderate volume loads improved ventricular diastolic function by promoting early ventricular filling and increasing ventricular compliance. Extreme volume loads promptly induced a diastolic restrictive pattern, transferring filling to the second part of diastole (increasing dependence on atrial contraction) and reducing ventricular compliance. These changes in ventricular diastolic function were independent of simultaneously measured haemodynamic systolic performance and were promptly reversed by isosorbide dinitrate, which after extreme loading promoted early filling, myocardial relaxation, and improved chamber compliance.

Animals↗
PubMed2003

RV instantaneous intraventricular diastolic pressure and velocity distributions in normal and volume overload awake dog disease models.

Intraventricular diastolic right ventricular (RV) flow field dynamics were studied by functional imaging using three-dimensional (3D) real-time echocardiography with sonomicrometry and computational fluid dynamics in seven awake dogs at control with normal wall motion (NWM) and RV volume overload with diastolic paradoxical septal motion. Burgeoning flow cross section between inflow anulus and chamber walls induces a convective pressure rise, which represents a "convective deceleration load" (CDL). High spatiotemporal resolution dynamic pressure and velocity distributions of the intraventricular RV flow field revealed time-dependent, subtle interactions between intraventricular local acceleration and convective pressure gradients. During the E-wave upstroke, the total pressure gradient along intraventricular flow is the algebraic sum of a pressure decrease contributed by local acceleration and a pressure rise contributed by a convective deceleration that partially counterbalances the local acceleration gradient. This underlies the smallness of early diastolic intraventricular gradients. At peak volumetric inflow, local acceleration vanishes and the total adverse intraventricular gradient is convective. During the E-wave downstroke, the strongly adverse gradient embodies the streamwise pressure augmentations from both local and convective decelerations. It induces flow separation and large-scale vortical motions, stronger in NWM. Their dynamic corollaries on intraventricular pressure and velocity distributions were ascertained. In the NWM pattern, the strong ring-like vortex surrounding the central core encroaches on the area available for flow toward the apex. This results in higher linear velocities later in the downstroke of the E wave than at peak inflow rate. The augmentation of CDL by ventriculoannular disproportion may contribute to E wave and E-to-A ratio depression with chamber dilatation.

Animals↗
PubMed1981

Mechanisms of mitral valve motion during diastole.

To examine the mechanisms of mitral valve motion in mid diastole and at closure, we simultaneously measured mitral flow (electromagnetic), valve motion (echo), and atrioventricular pressures (micromanometer). Peak valve excursion (E point) occurs early 46 +/- 7 ms) after opening and always precedes peak flow; therefore, mid-diastolic closing motion (EF slope) is not due to flow deceleration or vortex formation. Large variations in peak flow are accompanied by small variations in valve excursion (coefficient of variation 41 vs. 12%, respectively). We conclude that the valve overshoots its equilibrium position and that the chordae produce tension on the valve during diastole. This approach is supported by data from papillary muscle rupture, prolonged P-R interval, and mathematical modeling. We offer a valve-closure theory unifying chordal tension, flow deceleration, and vortices, with chordal tension as a necessary condition for the proper function of the other two. Nevertheless, prolonged periods of diastasis and ventricular premature contractions indicate that competent valve closure may occur in the absence of vortices and flow deceleration.

Animals↗
PubMed2002

Evidence that the superior colliculus participates in the feedback control of saccadic eye movements.

There is general agreement that saccades are guided to their targets by means of a motor error signal, which is produced by a local feedback circuit that calculates the difference between desired saccadic amplitude and an internal copy of actual saccadic amplitude. Although the superior colliculus (SC) is thought to provide the desired saccadic amplitude signal, it is unclear whether the SC resides in the feedback loop. To test this possibility, we injected muscimol into the brain stem region containing omnipause neurons (OPNs) to slow saccades and then determined whether the firing of neurons at different sites in the SC was altered. In 14 experiments, we produced saccadic slowing while simultaneously recording the activity of a single SC neuron. Eleven of the 14 neurons were saccade-related burst neurons (SRBNs), which discharged their most vigorous burst for saccades with an optimal amplitude and direction (optimal vector). The optimal directions for the 11 SRBNs ranged from nearly horizontal to nearly vertical, with optimal amplitudes between 4 and 17 degrees. Although muscimol injections into the OPN region produced little change in the optimal vector, they did increase mean saccade duration by 25 to 192.8% and decrease mean saccade peak velocity by 20.5 to 69.8%. For optimal vector saccades, both the acceleration and deceleration phases increased in duration. However, during 10 of 14 experiments, the duration of deceleration increased as fast as or faster than that of acceleration as saccade duration increased, indicating that most of the increase in duration occurred during the deceleration phase. SRBNs in the SC changed their burst duration and firing rate concomitantly with changes in saccadic duration and velocity, respectively. All SRBNs showed a robust increase in burst duration as saccadic duration increased. Five of 11 SRBNs also exhibited a decrease in burst peak firing rate as saccadic velocity decreased. On average across the neurons, the number of spikes in the burst was constant. There was no consistent change in the discharge of the three SC neurons that did not exhibit bursts with saccades. Our data show that the SC receives feedback from downstream saccade-related neurons about the ongoing saccades. However, the changes in SC firing produced in our study do not suggest that the feedback is involved with producing motor error. Instead, the feedback seems to be involved with regulating the duration of the discharge of SRBNs so that the desired saccadic amplitude signal remains present throughout the saccade.

Action Potentials↗
PubMed2005

Neurons in V1, V2, and PMLS of cat cortex are speed tuned but not acceleration tuned: the influence of motion adaptation.

We studied neurons in areas V1, V2, and posteromedial lateral suprasylvian area (PMLS) of anesthetized cats, assessing their speed tuning using steps to constant speeds and acceleration and deceleration tuning using speed ramps. The results show that the speed tuning of neurons in all three cortical areas is highly dependent on prior motion history, with early responses during speed steps tuned to higher speeds than later responses. The responses to speed ramps are profoundly influenced by speed-dependent response latencies and ongoing changes in neuronal speed tuning due to adaptation. Acceleration evokes larger transient and sustained responses than subsequent deceleration of the same rate with this disparity increasing with ramp rate. Consequently, there was little correlation between preferred speeds measured using speed steps, acceleration or deceleration. From 146 recorded cells, the proportion of cells that were clearly speed tuned ranged from 69 to 100% across the three brain areas. However, only 13 cells showed good skewed Gaussian fits and systematic variation in their responses to a range of accelerations. Although suggestive of acceleration coding, this apparent tuning was attributable to a cell's speed tuning and the different stimulus durations at each acceleration rate. Thus while the majority of cells showed speed tuning, none unequivocally showed acceleration tuning. The results are largely consistent with an existing model that predicts responses to accelerating stimuli developed for macaque MT, which showed that the responses to acceleration can be decoded if adaptation is taken into account. However, the present results suggest future models should include stimulus-specific adaptation and speed-dependent response latencies.

Acceleration↗
PubMed2005

Motor cortex neural correlates of output kinematics and kinetics during isometric-force and arm-reaching tasks.

We recorded the activity of 132 proximal-arm-related neurons in caudal primary motor cortex (M1) of two monkeys while they generated either isometric forces against a rigid handle or arm movements with a heavy movable handle, in the same eight directions in a horizontal plane. The isometric forces increased in monotonic fashion in the direction of the force target. The forces exerted against the handle in the movement task were more complex, including an initial accelerating force in the direction of movement followed by a transient decelerating force opposite to the direction of movement as the hand approached the target. EMG activity of proximal-arm muscles reflected the difference in task dynamics, showing directional ramplike activity changes in the isometric task and reciprocally tuned "triphasic" patterns in the movement task. The apparent instantaneous directionality of muscle activity, when expressed in hand-centered spatial coordinates, remained relatively stable during the isometric ramps but often showed a large transient shift during deceleration of the arm movements. Single-neuron and population-level activity in M1 showed similar task-dependent changes in temporal pattern and instantaneous directionality. The momentary dissociation of the directionality of neuronal discharge and movement kinematics during deceleration indicated that the activity of many arm-related M1 neurons is not coupled only to the direction and speed of hand motion. These results also demonstrate that population-level signals reflecting the dynamics of motor tasks and of interactions with objects in the environment are available in caudal M1. This task-dynamics signal could greatly enhance the performance capabilities of neuroprosthetic controllers.

Animals↗
PubMed1993

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation.

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

[The cardiotocographic score of Hammacher in computer analysis].

OBJECTIVE: After the quantitative, fully computerized evaluation of cardiotocography (CTG) after G.S. Dawes had yielded reliable results, an investigation was to be carried out to see whether a semiquantitative CTG analysis together with a CTG score (K. Hammacher) produced similarly useful results, too. METHODS: The last 120 directly recorded intrapartum CTG minutes (HP 8040A, 80300A) of 393 vaginally delivered fetuses were evaluated by simple means (magnifying glass, dividers, Plexiglas sliding caliper). The number of turning points, the bandwidth and the mean frequency level were determined for each individual CTG minute. Further, all decelerations were registered numerically (start, end and depth of decelerations), both qualitatively (28 key positions) and quantitatively. The CTG score of Hammacher was programmed in Fortran IV and integrated as a subroutine into a larger software system. RESULTS: Score 4 was noted most frequently (35.4%) during the last 30 min ante partum. The score values 10, 11, 12, 14, 15, 16, 17 and 18 were not seen at all. On the basis of the 'percent distribution of points' of the three score components, it could be shown that the decelerations were numerically overrepresented in comparison with the two other factors. The rank correlation between the score value and the relevant blood pH of the umbilical artery was highly significant (p << 0.001). The scoring of the CTG rises perceptibly only above pH 7.15. The sensitivity of score < or =4 is 87.2% for pH 7. 10 and 100% for pH 7.00. CONCLUSIONS: The interpretation of the cardiotocogram by means of the Hammacher score, which is based on a semiquantitative evaluation, yields clinically useful results. These may further be improved by changing the score structure. Beside the fully computerized analysis, the semiquantitative CTG analysis is able to finally determine the reliability of this monitoring method.

Acidosis↗
PubMedDate not supplied

Diastolic spectrum of left-ventricular hypertrophy: the impact of etiology and coronary artery disease on Doppler transmitral velocity.

UNLABELLED: Diastolic filling of hypertrophied left ventricles has frequently been observed by Doppler methods. We hypothesized that filling characteristics in hypertrophy vary with etiology and concurrent ischemia. For patients with hypertrophy, the left-ventricular ejection fraction was > 0.47 +/- 0.16, end-diastolic pressure was > 15 +/- 2 mm Hg, end-diastolic volume index was < 96 +/- 12 ml/m2 and left-ventricular mass index was 127 +/- 7 g/m2. Peak E (early) and peak A (late) diastolic velocities and E-wave deceleration time, respectively, were as follows (significant unless otherwise indicated): normal subjects (NS), 79 +/- 9 and 82 +/- 19 cm/s, and 151 +/- 7 ms; cardiomyopathic hypertrophy, 63 +/- 16, 83 +/- 15 (NS) and 193 +/- 63, aortic stenosis without coronary disease, 110 +/- 10, 128 +/- 12 and 158 +/- 22 (NS); aortic stenosis with coronary disease, 57 +/- 12, 86 +/- 26 (NS) and 187 +/- 39; hypertension without coronary disease, 107 +/- 9, 128 +/- 9 and 143 +/- 22 (NS); hypertension with coronary disease, 58 +/- 12, 84 +/- 26 (NS) and 189 +/- 29. CONCLUSIONS: Hypertrophied left ventricles filled with two diastolic Doppler patterns: a relaxation abnormality with low peak E and delayed deceleration in hypertrophic cardiomyopathy, and a compliance abnormality with tall peak E and normal deceleration in pressure overload hypertrophy. When coronary artery disease occurred with pressure overload hypertrophy, impaired relaxation was the dominant pattern. Therefore, in addition to the known physiologic influences on diastolic filling, the etiology and presence of coronary artery disease modulate the configuration of transmitral velocities into hypertrophied ventricles.

Aortic Valve Stenosis↗
PubMed1992

Fetal cerebral blood flow velocity during labour. Preliminary report.

The authors have tried to ascertain in a preliminary study if monitoring of fetal cerebral blood flow velocity during labour could identify a situation threatening the fetal brain, which could justify a compulsory fetal extraction. Nine patients were explored at term during labour. The Doppler signal was recorded using the abdominal route at the level of the fetal internal carotid. The diastolic carotid index was used (DCI = D/S). In 5 cases, fetal heart rate (FHR) was normal during labour and the DCI was on average comparable for each of the patients and the mean DCI (20.1 +/- 1%) was in close agreement with the values normally seen after 33 weeks of amenorrhoea during pregnancy. The case of isolated deceleration shows that deceleration causes an almost instant drop in the telediastolic flux, but the index increases more rapidly than could be expected from the increase in cardiac frequency if this phenomenon were of purely cardiogenic origin. In the case of bradycardia, it was noticed that during the return to the initial FHR frequency, the DCI was much higher than during the measurements performed before bradycardia. In the 1st case of pathological FHR, the index was very high and remained elevated during all the observation period. The fetus presented at birth a normal Apgar score as well as normal blood pH and neurological examination. In the 2nd case of pathological FHR, the FHR was abnormal with decelerations, the DCI increased rapidly and remained high.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1986

Pulsed Doppler findings in patients with coarctation of the aorta.

We used combined two-dimensional and pulsed Doppler echocardiography to examine 37 infants and children with coarctation of the aorta and 19 normal subjects. The ages ranged from 1 day to 16 years. We compared the differences between the Doppler flow signal from the ascending aorta and the descending aorta below the coarctation in each patient, as well as the differences between the corresponding flow signals in the aorta of patients with coarctation and normal subjects. Six variables were measured from each Doppler signal: acceleration slope (peak rate of acceleration), acceleration time (time from onset of flow to the peak systolic frequency), antegrade flow time, peak systolic frequency, peak velocity of flow, and deceleration slope (peak rate of deceleration). In patients with coarctation, each of these variables was significantly different in the descending aorta compared with the ascending aorta. There was a decrease in the acceleration slope (14 +/- 13 vs 87 +/- 67 kHz/sec) (mean +/- SD), peak systolic frequency (1.8 +/- 1.0 vs 5.2 +/- 1.9 kHz), peak velocity of flow (0.70 +/- 0.40 vs 1.4 +/- 0.44 m/sec), and deceleration slope (11 +/- 11 vs 27 +/- 12 kHz/sec). There was also a prolongation of the acceleration time (140 +/- 50 vs 88 +/- 22 msec) and antegrade flow time (330 +/- 120 vs 270 +/- 50 msec). In addition, these variables in the descending aorta of patients with coarctation were significantly different from those in the descending aorta of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1996

Right ventricular diastolic dysfunction in heart failure.

BACKGROUND: Left ventricular (LV) diastolic dysfunction is common in heart failure and is an important predictor of prognosis and mortality. Less attention has been paid to right ventricular (RV) diastolic function. In this study, we compared RV diastolic function in a large cohort of patients with heart failure (HF) with two groups: patients with pulmonary hypertension and normal LV function (the PHT group) and normal subjects. METHODS AND RESULTS: Transtricuspid and pulmonary artery flow were assessed by two-dimensional Doppler echocardiography at maximum inspiration and expiration in 185 subjects: 114 symptomatic HF patients (ejection fraction < 0.5), 31 PHT patients (pulmonary artery systolic pressure > 40 mm Hg), and 40 normal subjects. A subset was matched for age and heart rate. The results showed a high prevalence of RV diastolic abnormalities: HF patients had lower tricuspid E-A ratios, lower peak E-wave velocity, and prolonged RV isovolumic relaxation time (all P< .0001). Tricuspid E-wave deceleration time was significantly shorter only in those who had an LV restrictive filling pattern. The PHT group had similar findings. Compared with a normal range, more than half of the patients had lower tricuspid E-A ratios (HF, 55%; PHT, 69%), and 61% of HF and 58% of PHT patients had a prolonged RV isovolumic relaxation time. In the PHT group, RV diastolic parameters (E-wave deceleration time, E-A ratio, and isovolumic relaxation time) correlated significantly with pulmonary artery systolic pressure (P< .05). In the HF group, however, only tricuspid E-wave deceleration time correlated significantly with pulmonary artery systolic pressure, and HF patients with normal pulmonary artery systolic pressures had significantly lower tricuspid E-A ratios and prolonged RV isovolumic relaxation times compared with normal subjects. A close correlation existed between individual RV and LV diastolic parameters, suggesting that LV diastolic dysfunction may directly affect RV function, but there was no relation between LV size or systolic function and RV diastolic dysfunction. CONCLUSIONS: RV diastolic function is frequently abnormal in HF patients, and this is not related to elevated pulmonary artery systolic pressure alone, although high pulmonary artery pressure by itself also is associated with impaired RV diastolic function. Assessment of the role of right ventricular diastolic function in determining the symptoms and prognosis of heart failure is warranted.

Diastole↗