Increase In Preload Research Articles

Uterine activity: implications for the condition of the fetus

The aim of this review is to provide more insight in the fetal mechanisms as a response to uterine contractions and to emphasize the importance of correct assessment of uterine activity (UA) patterns during labor. UA causes a decreased flow through the uterine artery. In the healthy uncompromised fetus, this will not cause fetal acidemia. The fetus has developed certain protection mechanisms to survive labor; (1) During a contraction, fetal preload increases and enables the fetus to maintain a constant blood flow through the umbilical artery and (2) UA increases the blood flow in the fetal middle cerebral artery, i.e., a brain sparing effect. The shortcoming of those protection mechanisms in the compromised fetus and in case of excessive UA increases the risk of adverse fetal outcome. The brain sparing effect will become more pronounced to compensate for the decreased umbilical artery blood flow and fetal oxygen saturation. Maintenance of normal UA, especially a sufficiently long relaxation time, is essential so that the supply of well oxygenated maternal blood to the intervillous space will be restored and the fetal cerebral oxygen saturation can remain stable. Adequate UA monitoring is a prerequisite for proper reading and interpretation of cardiotocograms. It alarms in cases of excessive UA and can help to prevent fetal acidemia. Uterine contraction monitoring deserves full attention in daily obstetric practice.

Effects of axial preload of ball bearing on the nonlinear dynamic characteristics of a rotor-bearing system

This research studies the effects of axial preload on nonlinear dynamic characteristics of a flexible rotor supported by angular contact ball bearings. A dynamic model of ball bearings is improved for modeling a five-degree-of-freedom rotor bearing system. The predicted results are in good agreement with prior experimental data, thus validating the proposed model. With or without considering unbalanced forces, the Floquet theory is employed to investigate the bifurcation and stability of system periodic solution. With the aid of Poincare maps and frequency response, the unstable motion of system is analyzed in detail. Results show that the effects of axial preload applied to ball bearings on system dynamic characteristics are significant. The unstable periodic solution of a balanced rotor bearing system can be avoided when the applied axial preload is sufficient. The bifurcation margins of an unbalanced rotor bearing system enhance markedly as the axial preload increases and relates to system resonance speed.

Left Ventricular Diastolic Function in Hemodialysis Patients: Role of Preload Increase Maneuver on Tissue Doppler Imaging Evaluation

Objective: Tissue Doppler imaging (TDI) has recently been proposed as a relatively preload-independent method to evaluate left ventricular diastolic function. We sought to investigate the higher-accuracy of TDI to assess diastolic function in end-stage renal disease (ESRD) patients on hemodialysis (HD) associated with a preload increase maneuver. Methods: Thirty-two consecutiveESRD patients (16 female, ages 48.8 ± 17.5 years, 14 ≤45 and 18 >45 years old) were evaluated. Measurements of E, A velocities and the E/A ratio from transmitral inflow pulsed wave Doppler, and E’, A’ velocities and the E’/A’ ratio from TDI were obtained 1 h before and 1 h after HD at baseline and with a preload increase maneuver. Results: The E/A ratio changed significantly in all patients aged >45 before and after HD with the preload increase maneuver. The E’/A’ ratio increased in all subjects with the preload increase maneuver before HD but did not change with the maneuver after HD in the euvolemic state in all patients. Conclusion: In ESRD patients on routine HD, TDI evaluation associated with a preload increase maneuver proved to be a more accurate method to identify diastolic dysfunction when the evaluation is performed in euvolemic patients after HD.

The following letters are in response to the Point:Counterpoint series “Hypoxic pulmonary vasoconstriction is/is not mediated by increased production of reactive oxygen species” that appears in this issue.

To the Editor : The underlying issue being discussed ([1a][1], [4][2]) seems much broader than simply the role of venoconstriction. It is really about the regulation of the magnitude of cardiac output. Thus while the argument put forth by Hainsworth and Drinkhill is fine as far as it goes, it fails

Biventricular myocardial adaptation to different training protocols in competitive master athletes

Background Conflicting data have been reported about the nature (physiologic versus pathologic) of left ventricular (LV) hypertrophy in master athletes. Aim of the study To analyze LV and right ventricular (RV) myocardial function in master athletes with LV hypertrophy induced by either endurance or strength training. Methods Standard Doppler echo and colour Doppler Myocardial Imaging (DMI) of LV and of RV basal lateral walls were performed in 40 competitive master (> 45 years) endurance athletes (ATE), in 20 master strength-trained athletes (ATS) and 25 age-matched healthy sedentary subjects, all males. By use of DMI, the following parameters of myocardial function were assessed: systolic peak velocities, precontraction time, contraction time, early (E m) and late ( A m) diastolic peak velocities, E m/ A m ratio, relaxation time. Results The two groups were comparable for age, but ATS at rest showed higher heart rate, systolic blood pressure, and body surface area. LV mass index did not significantly differ between the two groups of athletes. However, ATS showed increased wall thickness and relative wall thickness, while LV stroke volume and both LV and RV end-diastolic diameters were greater in ATE. All transmitral and transtricuspid Doppler indexes were higher in ATE. DMI analysis showed in ATE higher E m and E m/ A m ratio at the level of both RV and LV lateral walls. In the overall population of athletes, linear regression models evidenced independent positive association of RV peak E m velocity with both LV stroke volume and maximal workload achieved by bicycle ergometer (both p < 0.001). Conclusions RV early diastolic myocardial function is positively influenced by preload increase in master athletes and represents an independent determinant of cardiac performance during physical effort. Therefore, colour DMI may be taken into account to distinguish different cardiac adaptation to either endurance or strength sport training in master athletes.

Análise da função diastólica do ventrículo esquerdo em hipertensos sob variação de condições hemodinâmicas provocadas: estudo comparativo entre o doppler transmitral e tissular

To evaluate the behavior of LV diastolic displacement velocities of basal posterior septum near mitral ring segment obtained by tissue Doppler in relation to mitral flow velocities of hypertensive subjects, submitted to preload increase by left inferior limbs elevation for 5 minutes, and during 1 minute of handgrip (conditions 1 and 2, respectively). Twenty five outpatients (15 men, 52+/-11 years), with arterial hypertension > 3 years, by the transmitral flow Doppler variables: E, A and E/A, and of tissue Doppler: E', A' and E'/A', in basal situation and in conditions 1 and 2. For comparison of results in basal situation with conditions 1 and 2 a paired t test was applied. E(cm/s) varied from 68,88 +/- 11,94 to 75,82 +/- 15,71* and E'(cm/s) varied from 8,22 +/- 2,30 to 8,31 +/- 2,24 in condition 1 (p<0.05). In addition, a comparison of variation percent (%) of Doppler transmitral indices with corresponding tissue Doppler indices variation % showed a significant difference between E and E', with preload increase (p=0.01). Patients with left ventricular adaptation to systemic arterial hypertension showed less modification of the index E' than E, after preload increase maneuver, an evidence that may suggest its more ample utilization in the context of echocardiographic left ventricular diastolic function evaluation.

Timing of Surgical Intervention in Chronic Mitral Regurgitation

Timing of surgical intervention in chronic mitral regurgitation (MR) is a complex problem that has been studied extensively. Surgical technique in the treatment of MR has improved considerably over the last decades. Our knowledge of the pathophysiological mechanisms whereby MR exerts its deleterious effects on survival has also increased. Early reports in the literature and newer prospective studies suggest that severe MR is not a benign condition and that, left untreated, it has a high morbidity and eventually mortality. It therefore makes sense to periodically reexamine the rationale and safety of existing practice guidelines. The article by Rosenhek and colleagues1 in this issue of Circulation provides an interesting and important insight into the long-term outcomes when asymptomatic degenerative MR is managed in accordance with the current American College of Cardiology/American Heart Association guidelines.2 However, it is important in employing these guidelines to first understand the pathophysiological construct and studies that have led to their generation. Article p 2238 MR produces volume overload of the left ventricle and left atrium. The left ventricle develops eccentric hypertrophy whereby the sarcomeres elongate. Preload increases and the left ventricle dilates in order to maintain a normal forward flow. The increase in afterload resulting from left ventricular dilatation is offset by the fact that the ventricle is pumping much of its volume (regurgitant volume) into a low-impedance circuit (the left atrium). Therefore, afterload may be variably reduced initially in MR and typically only becomes elevated in later stages of the disease as left ventricular size increases further. Thus, ejection indices such as ejection fraction are not considered reliable measures of left ventricular contractile function and remain in the normal range when contractility is already impaired. Load-independent measures of contractile function, such as elastance, are more reliable. However, these measurements are both time consuming …

How to distinguish between ischemic and nonischemic postsystolic thickening: A strain rate imaging study

Ongoing myocardial thickening after aortic valve closure (postsystolic thickening = ε PST) is an established marker for the presence of segmental ischemia. However, ε PST may also be present in late activated segments and can be induced by pharmacological interventions or left ventricular pressure overload. The aim of this study was to determine if it is possible to distinguish between ischemic and nonischemic ε PST. In an experimental pig-model ( n = 11) regional radial deformation was measured in the inferolateral wall during either normal perfusion or regional ischemia using ultrasonic strain rate imaging. Ischemia was induced by active hypoperfusion of the circumflex coronary artery territory. Measurements were made at 1. baseline, and during 2. theodrenalin infusion, 3. dobutamine infusion 4. esmolol infusion and 5. during a preload increase induced by saline infusion. In all segments where thickening was ongoing after aortic valve closure, the amount of ε PST was calculated as the difference of maximal strain minus systolic strain. In addition, peak strain rate during the isovolumetric relaxation period was extracted. During normal coronary perfusion, 73% of all segments ( n = 40) developed ε PST. This physiological ε PST averaged 5 ± 2% and was most frequently induced during the esmolol infusion ( n = 11). Peak isovolumetric strain rate averaged −2.1 ± 0.5 s −1 in segments with physiological ε PST. During coronary hypoperfusion, 96% of the “at risk” segments developed ε PST. ε PST in the ischemic segments averaged 14 ± 3%, and was highest during the dobutamine infusion (25 ± 4%) and lowest during the esmolol infusion (5 ± 1%). In contrast to normally perfused segments, peak isovolumetric strain rate was positive in the ischemic segments and averaged 2.0 ± 0.5 s −1 in these pathologic segments with postsystolic strain. Using a cut-off value of ≥ 0 s −1 for isovolumetric strain rate, pathologic ε PST was detected with a sensitivity of 100% and a specificity of 87%. These experimental findings were confirmed by a subsequent clinical study with 6 patients with acute myocardial infarction (ischemic group) and 6 patients with arterial hypertension or aortic stenosis (nonischemic group). Ischemic and nonischemic postsystolic thickening can be precisely differentiated by extracting the polarity of the peak isovolumetric strain curve. (E-mail: strotmann_j@medizin.uni-wuerzburg.de)

Intraventricular Pressure Differences

Like all fluids, blood tends to flow from areas of high pressure to low pressure. This seemingly trite observation hides a great deal of sophisticated pathophysiology that we are only beginning to exploit diagnostically and potentially therapeutically. In this issue of Circulation , Yotti and colleagues have exploited a new noninvasive technique to measure the small pressure differences generated within the normal left ventricular outflow tract in systole, demonstrating the utility of such measurements in quantifying ventricular systolic function.1 Because the fluid dynamics concepts behind these methods remain obscure to many cardiologists, it is worth reviewing the theoretical underpinnings in the hope that they will be more widely applied on the basis of articles like those of Yotti et al and others. See p 1771 Cardiologists have become comfortable with the use of the Gorlin equation in the cardiac catheterization laboratory and the simplified Bernoulli equation in the echocardiography laboratory to characterize the severity of valvular stenosis. Both equations are based on the principle of conservation of energy, relating the pressure drop (potential energy) across the valve to the rise in velocity (kinetic energy) as blood rushes through it. Several special circumstances combine to make these simple equations particularly applicable to flow through a restrictive orifice, including lack of a significant friction factor (viscosity) and a lack of pressure recovery as the blood rushes out of the abrupt obstruction. One of the most important simplifications is the absence of a significant “inertial” component to flow through a restrictive orifice. That is, the amount of blood actually moving at high velocity is tiny compared with the volume of the overall column of blood in the left ventricular outflow tract. Thus, very little pressure is expended in getting that small mass moving, and all of the potential energy lost across the …

Acute progressive resistance exercise alters intracardiac pressure in ponies

AbstractFive male ponies (3–6 years, 208±11 kg) were used to examine the haemodynamic effects of resistance exercise. The experiment consisted of a 30 min catheterization period and a 15 min equilibration period followed by the test. Initially, the ponies stood quietly on a treadmill for collection of 5 min of baseline data. They then walked at 1.9 m s−1 for 1 min sets while carrying 0 kg, 67 kg or 134 kg of weight loaded on the saddle area. Weights were applied in a randomized order using a chain hoist and sling. The ponies rested unloaded for 2 min between sets and all cardiovascular parameters returned to baseline before beginning the next set. Haemodynamic measurements (heart rate (HR), carotid artery systolic (SP), diastolic (DP), pulse (PP) and mean pressure (MAP), right atrial pressure (RAP), right ventricular pressure (RVP) and right ventricular maximum rate of pressure rise (dP/dtmax)) were recorded continuously and data collected during the last 18 s of each set were averaged and analysed. HR increased (P&lt;0.05) with unloaded exercise (201%) and with increases in load (252 and 271% at 67 and 134 kg, respectively). RAP increased (P&lt;0.05) with exercise, with differences (P&lt;0.05) between the response to the 0 kg (66%), 67 kg (121%) and 134 kg (138%) loads. RVP increased (P&lt;0.05) incrementally with load during exercise (58, 110 and 136%, respectively), with differences (P&lt;0.05) between 0 versus 67 kg and 67 versus 134 kg. Right ventricular dP/dtmax increased (P&lt;0.05) incrementally and showed differences (P&lt;0.05) between loads (131, 191 and 252% at 0, 67 and 134 kg, respectively). There were increases (P&lt;0.05) in MAP (20%), SP (20%) and DP (27) with exercise, but no difference (P&gt;0.05) between the response to 67 versus 134 kg load (43 and 51%; 40 and 46%; 49 and 62, respectively). Pulse pressure did not change (P&gt;0.05) from baseline values. These data suggest that resistance exercise in the form of weight carried increases intraventricular pressure through a significant increase in both cardiac pre-load and after-load.

Spindle Housing Design Parameter Optimization Considering Thermo-Elastic Behaviour

This paper presents a simulation method for predicting thermo-elastic behaviours of spindle-bearing system and an optimization procedure for housing design parameters in relation to various spindle-bearing operating and surrounding conditions such as assembling tolerance, geometric dimension, cooling condition and thermal deformation. The numerical formulation of transient thermo-elastic behaviours as a function of major spindle-bearing system design parameters is developed using the design of experiment methodology. The spindle-bearing analysis program has also been suggested in this paper. The suggested modelling and optimization method not only considers thermal deformation or heat transfer, but eventually it includes the nature of thermo-elastic interaction within spindle, bearing, housing and surrounding conditions in terms of formulating the objective function describing thermo-elastic characteristics such as friction moment, heat generation, contact mechanism, thermal displacement, assembly tolerance change, bearing internal clearance and spindle stiffness change and the dynamically changing operating conditions of the spindle. In order to substantiate the method, this paper shows a numerical example of formulation and optimization results for spindle housing design parameters with consideration of thermo-elastic behaviours as the thermal displacement, the preload increase, and the preload fluctuation.

Right ventricular myocardial adaptation to different training protocols in top-level athletes.

The aim of this study was to analyze right ventricular (RV) myocardial function in competitive athletes with left ventricular (LV) hypertrophy induced by either endurance or strength training. Standard Doppler echo, maximal electrocardiogram (ECG) ergometric test, and pulsed tissue Doppler (TD) of LV mitral annulus and of RV tricuspid annulus were performed in 32 competitive endurance athletes (long-distance swimmers; ATE) and in 26 strength-trained athletes (short-distance swimmers; ATS), all males. By use of TD, the following parameters of myocardial function were assessed: systolic peak velocities (Sm), precontraction time, contraction time, early (Em) and late (Am) diastolic velocities, Em/Am ratio, and relaxation time. The two groups were comparable for age, but ATS at rest exhibited higher heart rate, systolic blood pressure, and body surface area. LV mass index did not significantly differ between the two groups. However, ATS characterized increased wall thickness and relative wall thickness, whereas LV stroke volume and both LV and RV end-diastolic diameters were greater in ATE. All transmitral and transtricuspid Doppler indexes were higher in ATE, with increased E/A ratios. TD analysis demonstrated in ATE higher Em and Em/Am ratio as well as longer relaxation time both at mitral and at tricuspid annulus level. In the overall population, distinct multiple linear regression models evidenced independent positive association between RV peak Em velocity and LV end-diastolic diameter (P < 0.001) as well as independent direct correlation of the same RV peak Em velocity with both LV stroke volume and maximal workload achieved by bicycle ergometer (both P < 0.001). Right ventricular early diastolic myocardial function is positively influenced by preload increase in athletes, and represents an independent determinant of cardiac performance during physical effort. Therefore, pulsed TD may be taken into account to distinguish different cardiac adaptation to either endurance or strength sport activities, and eventually to quantify RV adaptation degree to long-term training.

Systolic left ventricular function improves more by beta-blokade than losartan: the life study

Systolic left ventricular (LV) function is a predictor of cardiovascular morbidity and mortality and improvement of systolic LV function improves survival. However, it is unclear how to best improve systolic function. A total of 960 prospectively identified patients with essential hypertension and evidence of LV hypertrophy on a screening electrocardiogram underwent echocardiography at enrolment in the Losartan Intervention For Endpoint prevention in hypertension (LIFE) trial, of whom 939 had measurements at baseline and information about cardiovascular events during the 4.8 years mean follow-up. Comparing baseline with the patients last in-study echocardiogram, both treatments reduced LV relative wall thickness (−0.084±0.64 vs. −0.084±0.062, p=NS) similarly. Atenolol was associated with lesser decrease in endocardial fractional shortening (EFS, −2.5±5.8 vs. −1.6±5.8%, p<0.05) as well as stress-corrected EFS (−7.5±19.8 vs. −2.4±19.9, p<0.001). Treatment with atenolol was associated with greater increase in midwall shortening (MWS, 0.92±2.45 vs. 1.38±2.40%, p<0.01) as well as stress-corrected MWS (6.9±14.3 vs. 10.3±14.2%, p<0.001). Linear regression analyses with LV function measures as the dependent variable showed a trend towards independent effect of atenolol on MWS (β=0.089, p=0.011) and a trend towards independency on EFS (β=0.068, p=0.053) even when taking differences in heart rate into account. In similar linear regression models, adjusting for age, gender and heart rate change, atenolol remained associated with smaller decrease in stress-corrected EFS (−7.5±19.8 vs. −2.4±19.9%, p<0.001) and a greater increase in stress-corrected MWS (6.8±14.3 vs. 10.3±14.2%, p=0.001) compared to losartan. In a double-blind, randomized trial, antihypertensive therapy that reduced LV relative wall thickness reduced endocardial and increased midwall LV function. Atenolol treatment reduced EFS less and raised MWS more than losartan, attributable to greater heart rate reduction and consequent preload increase with atenolol. Losartan treatment increased stress-corrected MWS, an index of LV contractility, but atenolol did so even more, consistent with the additional beneficial effects of beta-blockade in heart failure trials.

Different involvement of right ventricular myocardial function in either physiologic or pathologic left ventricular hypertrophy: A Doppler tissue study

The aim of the study was to analyze right ventricular (RV) myocardial function in patients with left ventricular (LV) hypertrophy secondary to either hypertrophic cardiomyopathy (HC) or athletic endurance training. Doppler echocardiography and pulsed Doppler tissue imaging of the posterior septal wall, and mitral and tricuspid annulus were performed in 32 top-level endurance athletes (AT) and in 27 patients with HC, all men. LV mass index was comparable between the 2 groups. All transmitral Doppler indexes were higher in AT, whereas only tricuspid inflow peak E and E/A ratio were slightly decreased in the HC group. In the HC group, Doppler tissue analysis showed lower myocardial systolic and early-diastolic (Em) peak velocities, and longer time intervals at the level of all the analyzed segments, even after correction for age, heart rate, and LV mass index. Distinct multiple linear regression models revealed an independent positive association between RV peak Em velocity and LV end-diastolic diameter (β coefficient = 0.72, P <.0001) in AT, and an independent inverse correlation of the same peak Em velocity of tricuspid annulus with septal thickness (β = − 0.65, P <.001) in the HC group. Of interest, a RV Em peak velocity < 0.16 m/s differentiated AT and HC groups better than tricuspid Doppler (89% sensitivity and 93% specificity). In conclusion, Em RV myocardial function is positively influenced by preload increase in AT and negatively associated to increased septal thickness in patients with HC. Therefore, Doppler tissue imaging may represent a useful tool in the differential diagnosis between athlete's heart and HC, underlining the different involvement of RV myocardial function in either physiologic or pathologic LV hypertrophy. (J Am Soc Echocardiogr 2003;16:154-61.)

Dobutamine-inducible left ventricular obstruction: head-up tilt and autonomic balance

Background: Dobutamine-inducible left ventricular obstruction lacks a sound clinical meaning. This phenomenon may be related to an abnormal response of the heart to the sympathetic stimulation, and head-up tilt would elicit intraventricular obstruction in patients known to develop it during dobutamine administration, through the synergistic effects of reduced preload, hypercontractility, and reflex increase in the cardiac sympathetic tone. Methods: Twenty-one patients with normal coronaries and available dobutamine stress-echocardiography underwent 60°-head-up tilt on echocardiographic and electrocardiographic monitoring in drug-free and nitroglycerin infusion (0.3 mcg/kg/min) protocols. Twelve patients had (group 1: 7 males, aged 61±7 years), and nine had not (group 2: 3 males, aged 60±9 years) developed left ventricular obstruction during dobutamine stress-echocardiography. Doppler echocardiographic measurements of left ventricular diameters, function and outflow tract flow velocity were performed; power heart rate variability was analysed on short electrocardiographic recordings (low/high frequency ratio); plasma catecholamines were determined at baseline and during the tilt manoeuvres. Results: Intraventricular obstruction did not develop in group 1. There were baseline differences in ventricular dimensions and mitral early-to-late velocity ratio between group 1 and 2, but hemodynamic behaviour during either tilt manoeuvre was similar. Low/high frequency ratio, that was similar at baseline and similarly increased on head-up tilt, increased significantly less on nitroglycerin-tilt in group 1. No difference in plasma catecholamines was found. Conclusions: Reflex cardiovascular adaptive responses as those elicited by passive tilt are not involved in dynamic intraventricular obstruction in dobutamine-inducible obstruction patients, data indicating that left ventricular geometry and hypercontractility are not sufficient pathophysiological determinants.

Association between left ventricular structure and cardiac performance during effort in two morphological forms of athlete’s heart

Aim: The aim of the study was to evaluate in 263 competitive athletes possible correlations between changes induced by different sport activities in left ventricular (LV) structure and cardiac response during maximal physical effort. Methods: A total of 160 top-level endurance athletes (ATE; swimmers, runners; 28±4 years; 98 male) and 103 strength-trained athletes (ATS; weight-lifters, body-builders; 27±5 years; male), selected on the basis of training protocol (dynamic vs. static exercise), underwent standard Doppler echocardiography, heart rate variability analysis and maximal exercise stress test by bicycle ergometry. M- and B-mode echocardiographic LV measurements were determined at rest, while the following functional indexes were assessed during effort: maximal heart rate (HR), maximal systolic blood pressure (SBP) and maximal workload (Watts reached by bicycle test). Results: The two groups were comparable for age and sex, but ATS at rest showed higher HR, SBP, and body surface area (BSA). By echo analysis, LV mass index and ejection fraction did not significantly differ between the two groups. However, ATS showed increased sum of wall thickness (septum+posterior wall), relative wall thickness and LV end-systolic stress, while LV stroke volume and LV end-diastolic diameter ( P<0.01) were greater in ATE. HR variability analysis underlined in ATE increased indexes of vagal tone ( P<0.01). During maximal physical effort, ATE showed a better functional capacity, with greater maximal workload ( P<0.001) reached with lower maximal HR and SBP. After adjusting for HR, age, sex, BSA and SBP, distinct multiple linear regression models evidenced in ATE independent associations of maximal effort workload with LV end-diastolic diameter ( P<0.001), HR ( P<0.001) at rest and LV end-systolic stress ( P<0.01) were found in ATE. On the other hand, independent direct correlation of SBP max during effort with sum of wall thickness ( P<0.001), BSA ( P<0.05) and LV end-systolic stress ( P<0.001) was evidenced in ATS. Conclusions: LV structural changes in competitive athletes represent adaptation to hemodynamic overload induced by training and are consistent with different kinds of sport activity. Work capacity during exercise is positively influenced by preload increase in ATE, while increased afterload due to isometric training in ATS determines higher systemic resistance during physical effort.

Strain rate imaging for the assessment of preload-dependent changes in regional left ventricular diastolic longitudinal function

Background: Strain rate imaging is a new and intriguing way of displaying myocardial deformation properties by means of echocardiography. With high frame rate strain rate imaging we observed a spatial inhomogeneity in diastolic longitudinal strain rates in healthy persons. A base-to-apex time delay in diastolic lengthening could be seen both in early diastole and at atrial contraction. Methods and Results: We investigated this consistent finding and its dependence on loading conditions in 20 healthy volunteers. Propagation velocities of lengthening of 91 ± 31 cm/s (E-wave) and 203 ± 11 cm/s (A-wave) at rest (equal to time delays of 104 ± 29 ms and 56 ± 24 ms, respectively) increased significantly to 101 ± 27 cm/s (E) and 283 ± 17 cm/s (A) with lifting the volunteers' legs. Applying nitroglycerine sublingually and sitting upright significantly decreased propagation velocities (E-wave 76 ± 20 cm/s, A-wave 172 ± 93 cm/s and E-wave 66 ± 17 cm/s, A-wave 150 ± 64 cm/s, respectively). Free lateral walls showed a lower propagation velocity than septal walls. Conclusion: We conclude that the propagation velocities of left ventricular lengthening waves are dependent on preload changes and increase with increasing preload. (J Am Soc Echocardiogr 2002;15:13-9.)

Effect of a double intervertebral cage on the mechanical behavior of the lumbar spine

A three-dimensional nonlinear finite element model of the lumbar spine was developed. Paired threaded cages and a monosegmental internal spinal fixation device were integrated into the computer model. The model was loaded with such forces as apply during standing, as well as with pure moments in the three main anatomical planes, plus an additional preload. The latter was generated by shortening the distance between the pedicle screws on the longitudinal rod of the fixator. With the exception of torsional loading, an implant appreciably reduces the mobility in the segment concerned. At the loads studied, cages had only a minor impact on the movements and stresses in the adjacent regions, but a strong influence on the stresses in the endplates in contact with them. A preload increases these stresses dramatically. Contact conditions between vertebral body and cages also have a marked effect on the stress distribution in the corresponding vertebral endplate, especially in the case of extension loading. Owing to the preload, maximum stresses were higher for the rigid bond than when contact elements were used.

Reshaping the remodelled left ventricle: a new concept.

Based on the law of Laplace, transventricular tension members were designed to diminish wall stress by changing the left ventricle (LV) globular shape to a bilobular one, thus reducing the ventricular wall radius of curvature. This concept was tested in a model of congestive heart failure. Seven calves were used for the study (74.3+/-4.2 kg). Treatment efficacy was assessed with sonomicrometric wall motion analysis coupled with intraventricular pressure measurement. Preload increase was applied stepwise with tension members in released and tightened position. Tightening of the tension members improved systolic function for CVP>10 mmHg (dP/dt: 828+/-122 vs. 895+/-112 mmHg/s, P=0.019, for baseline and 20% stress level reduction respectively; wall thickening: 11.6+/-1.5 vs. 13.3+/-1.7%, P<0.001) and diastolic function (LV end-diastolic pressure: 15.9+/-4.8 vs. 13.6+/-2.7 mmHg, P<0.001, for CVP>10 mmHg; peak rate of wall thinning: -12.2+/-2.2 vs. -14+/-2.3 cm(2)/s, P<0.001 and logistic time constant of isovolumic relaxation: 48.4 +/-10.9 vs. 39.8+/-9.6ms, P<0.001, for CVP>5 mmHg). This less aggressive LV reduction method significantly improves contractility and relaxation parameters in this model of congestive heart failure.

Mechanoelectrical feedback: role of beta-adrenergic receptor activation in mediating load-dependent shortening of ventricular action potential and refractoriness.

Augmented preload increases myocardial excitability by shortening action potential duration (APD). The mechanism governing this phenomenon is unknown. Because myocardial stretch increases intracellular cAMP, we hypothesized that load-dependent changes in myocardial excitability are mediated by beta-adrenergic stimulation of a cAMP-sensitive K(+) current. The effects of propranolol on load-induced changes in electrical excitability were studied in 7 isolated ejecting canine hearts. LV monophasic APD at 50% and 90% repolarization (MAPD(50) and MAPD(90)) and refractoriness were determined at low (9+/-3 mL) and high (39+/-4 mL) load before and after beta-adrenergic blockade. During control, the MAPD(50) decreased from 193+/-26 to 184+/-26 ms with increased load, as did the MAPD(90) (238+/-28 to 233+/-28 ms), P</=0.04. Similar changes were observed in ventricular refractoriness. Treatment with propranolol completely abolished these load-induced effects. Myocardial catecholamine depletion with reserpine in 2 hearts also abolished changes in MAPD and excitability in response to increased preload. Increases in ventricular load mediate a decrease in ventricular APD and refractoriness through activation of the beta-adrenergic receptor. An increase in a cAMP-mediated K(+) current, possibly the slowly activating delayed rectifier I(Ks), may account in part for this form of mechanoelectrical coupling.