Biomedical subjects

Patrick Segers

Publications and source records attributed to Patrick Segers.

46 records · Page 3Linked to original sources

PubMed2002

Design of a new pulsatile bioreactor for tissue engineered aortic heart valve formation.

Evidence has been gathered that biomechanical factors have a significant impact on cell differentiation and behavior in in vitro cell cultures. The aim of this bioreactor is to create a physiological environment in which tissue engineered (TE) aortic valves seeded with human cells can be cultivated during a period of several days. The bioreactor consists of 2 major parts: the left ventricle (LV) and the afterload consisting of a compliance, representing the elastic function of the large arteries, and in series a resistance, mimicking the arterioles and capillaries. The TE aortic valve is placed between the LV and the compliance. With controllable resistance, compliance, stroke volume and frequency, and hydrodynamic conditions can be changed over a wide physiological range. This study resulted in a prototype of a compact pulsatile flow system for the creation of TE aortic valves. In addition a biocompatibility study of the used materials is performed.

Aortic Valve↗

PubMed2002

Mock loop testing of On-x prosthetic mitral valve with Doppler echocardiography.

Previous in vitro testing (mainly in aortic position) and clinical experience (often based on Doppler echocardiographic observations) demonstrated an excellent hemodynamic behavior of the On-X valve. However, integrative studies including simultaneous hemodynamic pressure and flow measurements and Doppler echocardiography are lacking. Using our computer-controlled mock loop system, two samples of the Mitral 27/29 and one sample of the Conform-X Mitral 25/33 are tested in mitral position. Data include transvalvular pressure gradient and flow as well as transthoracic Doppler echocardiography. The valves are tested under three pressure conditions (ventricular systolic pressure of 100, 130, and 160 mm Hg) at three different heart rates (60, 100, and 140 beats/min). In addition, ventricular pressure conditions simulating fibrillation are imposed. Both valve types show similar hydrodynamic characteristics and have an effective orifice area of 2.1 cm2 and a performance index of 0.56 for a cardiac output of 3.5 L/min. Regurgitant volumes remain below 6 ml.

Coronary Circulation↗

PubMed2002

Effect of rotary blood pump failure on left ventricular energetics assessed by mathematical modeling.

In this study, we used a mathematical model to study the influence of backflow through a failing rotary blood pump. We performed simulations based on animal experiments that were published earlier by Nishida et al., who used the Medos Microdiagonal pump to assess the acute effect of sudden pump failure. The mathematical model consists of validated cardiac and arterial modules and a pump module. We could evaluate the influence of pump failure with mechanoenergetic parameters and wall stress obtained from model output. Simulations were performed at baseline and after 15 min of backflow in a control group and a heart failure group. Simulation results agreed well with the experiment. Stroke volume, aortic flow, and stress time integral increased significantly because of pump failure. However, total systemic flow and arterial pressure were not altered by backflow, and a life-threatening situation did not appear.

Animals↗

PubMed2002

Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity.

BACKGROUND: In aortic valve regurgitation (AR), aortic leak severity modulates left ventricle (LV) arterial system interaction. The aim of this study was to assess (1) how arterial elastance (E(a)), calculated as the ratio of LV end-systolic pressure and stroke volume, relates to arterial properties and leak severity and (2) the validity of E(a)/E(max) (with E(max) the slope of the end-systolic pressure-volume relation) as a heart-arterial coupling parameter in AR. METHODS AND RESULTS: Our work is based on human data obtained from a study on vascular adaptation in chronic AR. These data allowed us to assess the parameters of a computer model of heart-arterial interaction. In particular, total peripheral resistance (R) and aortic leak severity--expressed as leak resistance (R(L,ao))--were quantified for different patient subgroups (group I/IIa/IIb: E(max) = 2.15/0.62/0.47 mm Hg/mL; E(a) = 1.24/0.66/0.90 mm Hg/mL; R = 1.9/0.6/0.85 mm Hg.s/mL, R(L,ao) = 0.35/0.05/0.20 mm Hg.s/mL). A parameter study demonstrated that R(L,ao) was the main determinant of E(a). With all other parameters constant, valve repair would increase E(a) to 2.81, 1.08, and 1.54 mm Hg/mL in groups I, IIa, and IIb, respectively. For a given E(a)/E(max), LV pump efficiency (estimated as the ratio of stroke work and LV systolic pressure-volume area) was lower than the theoretical predicted value, except for the simulations with intact aortic valve. CONCLUSIONS: In AR, E(a) is determined by aortic leak severity rather than by arterial system properties. Using E(a)/E(max) as a coupling parameter in general or as a mechanico-energetic regulatory parameter in particular is questionable.

Aortic Valve Insufficiency↗

PubMed2002

The limitations of preload-adjusted maximal power as an index of right ventricular contractility.

UNLABELLED: Right ventricular (RV) dysfunction is an important cause of perioperative morbidity and mortality, particularly in cardiac surgery. However, assessment of RV contractility remains difficult in clinical practice. Our goal in this study was to examine the value of preload-adjusted maximal power (PWR(max)/end-diastolic volume [EDV](2); PAMP) as an alternative to the load-independent pressure-volume-derived indices of contractility in the RV. In anesthetized dogs, RV end-systolic elastance and preload-recruitable stroke work were studied as "gold standards" by using the conductance technique. PAMP was calculated with pulmonary artery flow and RV pressure measurements. Changes in these indices were compared after modulation of the inotropic state (dobutamine infusion; n = 12) and loading conditions (pulmonary artery and inferior caval vein occlusion; n = 14). All indices increased dose-dependently with dobutamine. PAMP was slightly influenced by preload reduction (the slope of the relation between PAMP and EDV was 0.00397 +/- 0.01026 W. mL(-3). 0.10(-4); mean +/- SD). PAMP decreased significantly during pulmonary artery banding (from 1.1 +/- 0.7 to 0.7 +/- 0.5 W. mL(-2). 0.10(-4); mean +/- SD), whereas end-systolic elastance and preload-recruitable stroke work did not change. We conclude that the value of PAMP as an index of RV contractility is limited in the open-chest/open-pericardium setting, primarily by its sensitivity to alterations in afterload. IMPLICATIONS: Preload-adjusted maximal power (PAMP), a load-independent contractile index in the left ventricle, could offer a solution to the problem of measuring right ventricular (RV) contractility in clinical practice. However, this study in open-chest dogs suggests that PAMP is unreliable for assessment of RV contractility because of its sensitivity to afterload changes.

Algorithms↗

PubMed2002

Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension.

OBJECTIVE: Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine. DESIGN: Prospective laboratory investigation using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: Seven adult beagle dogs weighing 8-14 kg. INTERVENTIONS: After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure. MEASUREMENTS AND MAIN RESULTS: Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion. CONCLUSIONS: In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.

Acute Disease↗

PubMed2002

Relation of effective arterial elastance to arterial system properties.

Effective arterial elastance (E(a)), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E(max), the slope of the LV end-systolic pressure-volume relation, E(a)/E(max) has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance (R; 0.6-1.8 mmHg x ml(-1) x s) and total arterial compliance (C; 0.5-2.0 ml/mmHg) covering the human pathophysiological range. E(a), E(a)/E(max,) LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E(a), R/T (where T is cycle length), and 1/C: E(a) = -0.13 + 1.02R/T + 0.31/C, indicating that R/T contributes about three times more to E(a) than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E(a) and E(a)/E(max) but can result in differences of 10% in stroke work and 50% in maximal power.

Aorta↗

PubMed2002

Excessive pressure in multichambered cuffs used for sequential compression therapy.

BACKGROUND AND PURPOSE: Pneumatic compression devices, used as part of the therapeutic strategy for lymphatic drainage, often have cuffs with multiple chambers that are inflated sequentially. The purpose of this study was to investigate (1) the relationship between cuff chamber pressure (P(chamber)) and the pressure on the cuff-skin interface (P(interface)) and (2) the mechanical interaction of cuff chambers and consequences for device control. SUBJECTS AND METHODS: In this study, we used 3 cylindrical (60-, 80-, and 100-mm-diameter) model limbs and 1 ellipsoidal model of the arm to test a commercially available pressure controller using "target pressures," indicated by the controller, of 30, 60, 80, and 100 mm Hg. We studied the time course of P(chamber) and P(interface) during the inflation sequence and the effect of local curvature on P(interface). RESULTS: Our data indicated that, overall, P(interface) is of the same order of magnitude as P(chamber). There was some effect of model diameter and shape, with the smaller curvatures yielding the highest P(interface). Cuff chamber interaction led to P(chamber) and P(interface) values in the most distal (first inflated) chamber that were up to 80% higher than the target pressure. For the 80-mm cylindrical model, for instance, pressure in this chamber reached 54, 98, 121, and 141 mm Hg, respectively, instead of the 30, 60, 80, and 100 mm Hg indicated by the controller. DISCUSSION AND CONCLUSION: The discrepancy between the target pressure, indicated by the controller, and the pressure measured inside the cuff chambers undermines the therapeutic control and efficacy of the pneumatic compression devices. Because the measured pressures were far beyond the pressure level indicated by the controller, it is recommended that pneumatic compression devices be used at much lower target pressures (<30 mm Hg) than those applied in clinical practice.

Analysis of Variance↗

PubMedDate not supplied

Hemodynamic modes of ventricular assist with a rotary blood pump: continuous, pulsatile, and failure.

Pulsatile operation of rotary blood pumps (RBPs) has received interest due to potential concern with nonphysiological hemodynamics. This study aimed to gain insight to the effects of various RBP modes on the heart-device interaction. A Deltastream diagonal pump (Medos Medizintechnik GmbH) was inserted in a cardiovascular simulator with apical-to-ascending aorta cannulation. The pump was run in continuous mode with incrementally increasing rotating speed (0-5000 rpm). This was repeated for three heart rates (50-100-150 bpm) and three levels of left ventricular (LV) contractility. Subsequently, the Deltastream was run in pulsatile mode to elucidate the effect of (de)synchronization between heart and pump. LV volume and pressure, arterial pressure, flows, and energetic parameters were used to evaluate the interaction. Pump failure (0 rpm) resulted in aortic pressure drops (17-46 mm Hg) from baseline. In continuous mode, pump flow compensated by diminished aortic flow, thus yielding constant total flow. High continuous rotating speed resulted in acute hypertension (mean aortic pressure up to 178 mm Hg). In pulsatile mode, unmatched heart and pulsatile pump rates yielded unphysiologic pressure and flow patterns and LV unloading was found to be highly dependent on synchronization phase. Optimal unloading was achieved when the minimum rotating speed occurred at end-systole. We conclude that, in continuous mode, a perfusion benefit can only be achieved if the continuous pump flow exceeds the preimplant (baseline) cardiac output. Pulsatile mode of support results in complex pressure and volume variations and requires accurate triggering to achieve optimal unloading.

Data Interpretation, Statistical↗

PubMedDate not supplied

Modeling ventricular function during cardiac assist: does time-varying elastance work?

The time-varying elastance theory of Suga et al. is widely used to simulate left ventricular function in mathematical models and in contemporary in vitro models. We investigated the validity of this theory in the presence of a left ventricular assist device. Left ventricular pressure and volume data are presented that demonstrate the heart-device interaction for a positive-displacement pump (Novacor) and a rotary blood pump (Medos). The Novacor was implanted in a calf and used in fixed-rate mode (85 BPM), whereas the Medos was used at several flow levels (0-3 l/min) in seven healthy sheep. The Novacor data display high beat-to-beat variations in the amplitude of the elastance curve, and the normalized curves deviate strongly from the typical bovine curve. The Medos data show how the maximum elastance depends on the pump flow level. We conclude that the original time-varying elastance theory insufficiently models the complex hemodynamic behavior of a left ventricle that is mechanically assisted, and that there is need for an updated ventricular model to simulate the heart-device interaction.

Animals↗