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F W Prinzen

Publications and source records attributed to F W Prinzen.

At least 19 recordsLinked to original sources
PubMed2005

Electromechanics of paced left ventricle simulated by straightforward mathematical model: comparison with experiments.

Intraventricular synchrony of cardiac activation is important for efficient pump function. Ventricular pacing restores the beating frequency but induces more asynchronous depolarization and more inhomogeneous contraction than in the normal heart. We investigated whether the increased inhomogeneity in the left ventricle can be described by a relatively simple mathematical model of cardiac electromechanics, containing normal mechanical and impulse conduction properties. Simulations of a normal heartbeat and of pacing at the right ventricular apex (RVA) were performed. All properties in the two simulations were equal, except for the depolarization sequence. Simulation results of RVA pacing on local depolarization time and systolic midwall circumferential strain were compared with those measured in dogs, using an epicardial sock electrode and MRI tagging, respectively. We used the same methods for data processing for simulation and experiment. Model and experiment agreed in the following aspects. 1) Ventricular pacing decreased systolic pressure and ejection fraction relative to natural sinus rhythm. 2) Shortening during ejection and stroke work declined in early depolarized regions and increased in late depolarized regions. 3) The relation between epicardial depolarization time and systolic midwall circumferential strain was linear and similar for the simulation (slope = -3.80 +/- 0.28 s(-1), R2 = 0.87) and the experiments [slopes for 3 animals -2.62 +/- 0.43 s(-1) (R2 = 0.59), -2.97 +/- 0.38 s(-1) (R2 = 0.69), and -4.44 +/- 0.51 s(-1) (R2 = 0.76)]. We conclude that our model of electromechanics is suitable to simulate ventricular pacing and that the apparently complex events observed during pacing are caused by well-known basic physiological processes.

Algorithms↗
PubMed2004

Comparison of the effects of dexmedetomidine and esmolol on myocardial oxygen consumption in dogs.

BACKGROUND AND OBJECTIVE: The beta-adrenergic blocker esmolol and the alpha 2-adrenergic agonist dexmedetomidine have the potential to decrease perioperative myocardial ischaemia. The pathophysiological mechanisms involved in these anti-ischaemic properties have not been thoroughly studied. We compared the effects of esmolol and dexmedetomidine on two indices of overall myocardial oxygen demand and on directly measured myocardial oxygen consumption of the left anterior coronary artery territory. METHODS: Eleven mongrel dogs were instrumented to measure aortic and left ventricular pressure, aortic and left anterior coronary artery flow and myocardial wall thickening. Variables related to myocardial oxygen metabolism were also determined. Measurements were performed during four sequential experimental conditions in each dog (Control 1: esmolol; Control 2: dexmedetomidine). RESULTS: Esmolol and dexmedetomidine decreased haemodynamic indices of myocardial oxygen demand to a similar extent: esmolol decreased the rate-pressure product by 16+/-3% and the pressure-work index (PWI) by 16+/-3%, dexmedetomidine decreased the rate-pressure product by 26+/-3% and the PWI by 16+/-7%. However, these similar decreases resulted from different haemodynamic effects of the two study drugs. Dexmedetomidine had a more pronounced bradycardic effect than esmolol (P = 0.01) and increased systolic aortic pressure (SAP) by 15+/-4% while esmolol decreased SAP by 8+/-2% (P < 0.01). dP/dt(max) and regional myocardial area decrease were lower after esmolol than after dexmedetomidine. Neither drug had an effect on myocardial oxygen consumption. CONCLUSIONS: Esmolol and dexmedetomidine decreased two haemodynamic indices of overall myocardial oxygen demand to a similar extent but neither drug decreased directly measured myocardial oxygen consumption in the territory of the left anterior descending artery.

Adrenergic alpha-Agonists↗
PubMed2003

Homogeneity of cardiac contraction despite physiological asynchrony of depolarization: a model study.

The use of mathematical models combining wave propagation and wall mechanics may provide new insights in the interpretation of cardiac deformation toward various forms of cardiac pathology. In the present study we investigated whether combining accepted mechanisms on propagation of the depolarization wave, time variant mechanical properties of cardiac tissue after depolarization, and hemodynamic load of the left ventricle (LV) by the aortic impedance in a three-dimensional finite element model results in a physiological pattern of cardiac contraction. We assumed that the delay between depolarization for all myocytes and the onset of crossbridge formation was constant. Two simulations were performed, one in which contraction was initiated according to the regular depolarization pattern (NORM simulation), and another in which contraction was initiated after synchronous depolarization (SYNC simulation). In the NORM simulation propagation of depolarization was physiological, but wall strain was unphysiologically inhomogeneous. When simulating LV mechanics with unphysiological synchronous depolarization (SYNC) myofiber strain was more homogeneous and more physiologic. Apparently, the assumption of a constant delay between depolarization and onset of crossbridge formation results in an unrealistic contraction pattern. The present finding may indicate that electromechanical delay times are heterogeneously distributed, such that a contraction in a normal heart is more synchronous than depolarization.

Anisotropy↗
PubMed2002

Transmural gradients of cardiac myofiber shortening in aortic valve stenosis patients using MRI tagging.

Aortic valve stenosis impairs subendocardial perfusion with a risk of irreversible subendocardial tissue damage. A likely precursor of damage is subendocardial contractile dysfunction, expressed by the parameter TransDif, which is defined as epicardial minus endocardial myofiber shortening, normalized to the mean value. With the use of magnetic resonance tagging in two short-axis slices of the left ventricle (LV), TransDif was derived from LV torsion and contraction during ejection. TransDif was determined in healthy volunteers (control, n = 9) and in patients with aortic valve stenosis before (AVSten, n = 9) and 3 mo after valve replacement (AVRepl, n = 7). In the control group, TransDif was 0.00 +/- 0.14 (mean +/- SD). In the AVSten group, TransDif increased to 0.96 +/- 0.62, suggesting impairment of subendocardial myofiber shortening. In the AVRepl group, TransDif decreased to 0.37 +/- 0.20 but was still elevated. In eight of nine AVSten patients, the TransDif value was elevated individually (P < 0.001), suggesting that the noninvasively determined parameter TransDif may provide important information in planning of treatment of aortic valve stenosis.

Aged↗
PubMed2001

Remodeling by ventricular pacing in hypertrophying dog hearts.

OBJECTIVE: Asynchronous electrical activation of the left ventricle (LV), induced by ventricular pacing (VP), reduces mechanical load in early- and enhances it in late-activated regions. Consequently, chronic VP leads to asymmetric hypertrophy. We investigated whether such locally induced myocardial hypertrophy also occurs in the presence of pressure overload hypertrophy (POH). METHODS: POH was induced by aortic banding in puppies. At age 9 months, seven dogs were paced at the right ventricular (RV) apex at physiological heart rate for 6 months (POH-pace group), while four POH dogs served as POH-control group. Changes in volume of the LV cavity and the total LV wall and of five LV wall sectors were measured by means of 2D-echocardiography and X-ray marker detection. RESULTS: During the last 6 months of the protocol the volume of the five LV wall sectors increased in the POH-control group, ranging from 27+/-9 to 30+/-5% (mean+/-S.D.). In POH-pace animals sector wall volume in the four sectors at intermediate to long distance from the pacing site increased to a similar extent (ranging from 31+/-16 to 35+/-17%), but wall volume in the early-activated apical septum increased significantly less (17+/-21%). In these hearts myocyte diameter was significantly smaller in the apical septum than in the lateral LV wall. The regional difference in wall volume changes (19+/-21%) was significantly smaller in the POH-pace group than in chronically paced, non-hypertrophic, canine hearts in a previous study from our laboratory (43+/-14%). CONCLUSIONS: In hypertrophying hearts chronic pacing at the RV apex suppresses the development of hypertrophy in the early-activated apical septum but does not cause additional hypertrophy in late-activated regions, as is the case in non-hypertrophic hearts. The latter suggests that the local growth response is reduced in hypertrophying hearts.

Analysis of Variance↗
PubMed2001

High-resolution functional imaging with ultrasound contrast agents based on RF processing in an in vivo kidney experiment.

Knowledge of the relative tissue perfusion distribution is valuable in the diagnosis of numerous diseases. Techniques for the assessment of the relative perfusion distribution, based on ultrasound (US) contrast agents, have several advantages compared to established nuclear techniques. These are, among others, a better spatial and temporal resolution, the lack of exposure of the patient to ionizing radiation and the relatively low cost. In the present study, US radiofrequency (RF) image sequences are acquired, containing the signal intensity changes associated with the transit of a bolus contrast agent through the microvasculature of a dog kidney. The primary objective is to explore the feasibility of calculating functional images with high spatial resolution. The functional images characterize the transit of the contrast agent bolus and represent distributions of peak time, peak value, transit time, peak area, wash-in rate and wash-out decay constant. For the evaluation of the method, dog experiments were performed under optimized conditions where motion artefacts were minimized and an IA injection of the contrast agent Levovist was employed. It was demonstrated that processing of RF signals obtained with a 3.5-MHz echo system can provide functional images with a high spatial resolution of 2 mm in axial resolution, 2 to 5 mm in lateral resolution and a slice thickness of 2 mm. The functional images expose several known aspects of kidney perfusion, like perfusion heterogeneity of the kidney cortex and a different peripheral cortical perfusion compared to the inner cortex. Based on the findings of the present study, and given the results of complimentary studies, it is likely that the functional images reflect the relative perfusion distribution of the kidney.

Animals↗
PubMed2000

Blood flow distributions by microsphere deposition methods.

The art and science of the use of deposition markers for the estimation of blood flow distributions throughout the body and within organs is reviewed. Development of diffusible tracer techniques started 50 years ago. Twenty years later, radioactive 15 micron microspheres became the standard marker. Early studies on small animals, fetal sheep in 1967 and rats in 1976, provoked much of the technical development. Needs for avoiding the use of radioactivity, for having long lasting labels, and for providing higher spatial resolution, are driving the continuing exploration of newer techniques using colored and fluorescent microspheres and molecular deposition markers. Strengths and weaknesses of the various methods are compared.

Animals↗
PubMed1999

Hyperoxia and local organ blood flow in the developing chick embryo.

1. Hyperoxia can cause local vasoconstriction in adult animal organs as a protective mechanism against hyperoxia-induced toxicity. It is not known at what time during development this vasoconstrictor capacity is present. Therefore, we measured the cardiac output (CO) distribution in different organs during a period of acute hyperoxia (100 % O2) in the developing chick embryo. 2. Fertile eggs were divided into five incubation time groups (10 and 11, 12 and 13, 14 and 15, 16 and 17, and 18 and 19 days of a normal incubation time of 21 days). Eggs were opened at the air cell and a catheter was inserted into a branch of the chorioallantoic vein for injections of 15 microm fluorescent microspheres during normoxia and at the end of 5 min (test group 1; n = 39) or 20 min (test group 2; n = 21) of hyperoxia exposure (100 % O2). The fraction of CO to an organ was calculated as the fluorescence of the organ sample divided by the sum of the fluorescence of all organs. 3. Only in 18- and 19-day-old embryos did hyperoxia cause a decrease in the fractions of CO to the heart and carcass, and an increase in those to the yolk-sac and chorioallantoic membrane. This response was more pronounced after 20 min (test group 2) than after 5 min (test group 1) of hyperoxia with an additional decrease in the fractions of CO to the brain, intestine and liver (test group 2). 4. These data indicate that local mechanisms for hyperoxia-induced vasoconstriction in the heart, brain, liver, intestine and carcass develop late, during the final 15 % of the incubation period, in the developing chick embryo.

Animals↗
PubMed1999

Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging.

OBJECTIVES: The purpose of this study was to determine the spatial distribution of myocardial function (myofiber shortening and work) within the left ventricular (LV) wall during ventricular pacing. BACKGROUND: Asynchronous electrical activation, as induced by ventricular pacing, causes various abnormalities in LV function, perfusion and structure. These derangements may be caused by abnormalities in regional contraction patterns. However, insight into these patterns during pacing is as yet limited. METHODS: In seven anesthetized dogs, high spatial and temporal resolution magnetic resonance-tagged images were acquired in three orthogonal planes. Three-dimensional deformation data and LV cavity pressure and volume were used to determine midwall circumferential strain and external and total mechanical work at 192 sites around the left ventricle. RESULTS: During ventricular pacing, systolic fiber strain and external work were approximately zero in regions near the pacing site, and gradually increased to more than twice the normal value in the most remote regions. Total mechanical work, normalized to the value during right atrial pacing, was 38 +/- 13% (right ventricular apex [RVapex] pacing) and 61 +/- 23% (left ventricular base [LVbase] pacing) close to the pacing site, and 125 +/- 48% and 171 +/- 60% in remote regions, respectively (p < 0.05 between RVapex and LVbase pacing). The number of regions with reduced work was significantly larger during RVapex than during LVbase pacing. This was associated with a reduction of global LV pump function during RVapex pacing. CONCLUSIONS: Ventricular pacing causes a threefold difference in myofiber work within the LV wall. This difference appears large enough to regard local myocardial function as an important determinant for abnormalities in perfusion, metabolism, structure and pump function during asynchronous electrical activation. Pacing at sites that cause more synchronous activation may limit the occurrence of such derangements.

Animals↗
PubMed1999

Kinematic analysis of left ventricular deformation in myocardial infarction using magnetic resonance cardiac tagging.

The Magnetic Resonance (MR) tagging technique provides detailed information about 2D motion in the plane of observation. Interpretation of this information as a reflection of the 3D motion of the entire cardiac wall is a major problem. In finite element models of the mechanics of the infarcted heart, an infarcted region causes motional asymmetry, extending far beyond the infarct boundary. Here we present a method to quantify such asymmetry in amplitude and orientation. For this purpose images of a short-axis cross-section of the ejecting left ventricle were acquired from 9 healthy volunteers and 5 patients with myocardial infarction. MR-tags were applied in a 5 mm grid at end-diastole. The tags were tracked by video-image analysis. Tag motion was fitted to a kinematic model of cardiac motion. For the volunteers and the patients the center of the cavity displaced by about the same amount (p = 0.11) during the ejection phase: 3.8 +/- 1.4 and 3.0 +/- 0.9 mm (mean +/- sd), respectively. Cross-sectional rotation and the decrease in cross-sectional area of the cavity were both greater in the volunteers than in the patients: 6.4 +/- 1.5 vs. 3.0 +/- 0.8 degrees (p < 0.001), and 945 +/- 71 vs. 700 +/- 176 mm2 (p = 0.02), respectively. In the patients, asymmetry of wall motion, as expressed by a sine wave dependency of contraction around the circumference, was significantly enlarged (p = 0.02). The proposed method of kinematic analysis can be used to assess cardiac deformation in humans. We expect that by analyzing images of more cross-sections simultaneously, the 3D location and the degree of infarction can be assessed efficiently.

Biomechanical Phenomena↗
PubMed1999

Mapping propagation of mechanical activation in the paced heart with MRI tagging.

The temporal evolution of three-dimensional (3-D) strain maps derived from magnetic resonance imaging (MRI) tagging were used to noninvasively evaluate mechanical activation in the left ventricle (LV) while seven canine hearts were paced in situ from three different sites: the base of the LV free wall (LVb), the right ventricular apex (RVa), and the right atrium (RA). Strain maps plotted against time showed the evolution of shortening over the entire LV midwall and were used to generate mechanical activation maps showing the onset of circumferential shortening. RA pacing showed rapid synchronous shortening; LVb pacing showed a wave front of mechanical activation propagating slowly and steadily from the pacing site, whereas RVa pacing showed regions of rapid and slower propagation. The mechanical (M) activation times correlated linearly with the electrical (E) activation (M = 1.06E + 8.4 ms, R = 0.95). The time for 90% activation of the LV was 63.1 +/- 24.3 ms for RA pacing, 130.2 +/- 9.8 ms for LVb pacing, and 121.3 +/- 17.9 ms for RVa pacing. The velocity of mechanical activation was calculated for LVb and RVa pacing and was similar to values reported for electrical conduction in myocardium. The propagation of mechanical activation for RVa pacing showed regional variations, whereas LVb pacing did not.

Animals↗
PubMed1998

Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall.

BACKGROUND: Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. METHODS AND RESULTS: Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2+/-10.6 to 113+/-16.5 ms acutely and to 133.8+/-25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27+/-15% and 15+/-17%, respectively. The early-activated LV free wall became significantly (17+/-17%) thinner, whereas the late-activated septum thickened significantly (23+/-12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39+/-13%. In paced animals, cardiomyocyte diameter was significantly (18+/-7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. CONCLUSIONS: Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.

Animals↗
PubMed1998

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time.

1. The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. 2. Fertilized eggs were studied at three incubation times (10-13 days, 14-16 days and 17-19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 micron fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. 3. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (-3 to -65 % of baseline), yolk-sac (-46 to -77 % of baseline) and carcass (-6 to -33 % of baseline). 4. The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. 5. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

Animals↗
PubMed1998

Imaging asynchronous mechanical activation of the paced heart with tagged MRI.

A method for imaging the rapid temporal-spatial evolution of myocardial deformations in the paced heart is proposed. High time resolution-tagged MR images were obtained after stimulation of the myocardium with an MR-compatible pacing system. The images were analyzed to reconstruct dynamic models of local 3D strains over the entire left ventricle during systole. Normal canine hearts were studied in vivo with pacing sites on the right atrium, left ventricular free wall and right ventricular apex. This method clearly resolved local variations in myocardial contraction patterns caused by ventricular pacing. Potential applications are noninvasive determination of electrical conduction abnormalities and the evaluation of new pacing therapies.

Animals↗
PubMed1998

Estimates of regional work in the canine left ventricle.

Assessment of the magnitude of regional myocardial work requires knowledge of regional fiber stress and fiber shortening. The theoretical development and experimental validation of a method is presented which used values of estimated active and passive fiber stress according to a fluid-fiber model, and measured fiber strain values. This enables the construction of regional stress-strain diagrams, a regional analog of the pressure-volume area model by Suga and co-investigators, which can be linked to regional oxygen consumption. In the left ventricle, either normally or asynchronously activated, the method yields reliable data on strain and active and passive fiber stress. The relation between estimated regional work and myocardial oxygen demand is in quantitative agreement with previously reported relations between global oxygen demand and measured pressure-volume area. During coronary artery occlusion, however, these values were less reliable, which might be due to inaqdequate knowledge of the (passive) material properties of the myocardium.

Animals↗
PubMed1998

Optimization of ventricular function by improving the activation sequence during ventricular pacing.

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowprobe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 +/- 5 ms during sinus rhythm and increased to 110 +/- 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8% +/- 7% and 15% +/- 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex (15% +/- 16%, 10% +/- 12% [P < 0.05], and 15% +/- 10%, respectively) and LV base pacing (11% +/- 12% [P < 0.05], 3% +/- 12%, and 3% +/- 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.

Animals↗
PubMed1998

Fluorescent microspheres are superior to radioactive microspheres in chronic blood flow measurements.

The accuracy of the fluorescent (FM) and radioactive microsphere (RM) techniques is similar in acute experiments but has not been established in chronic experiments. In the present study various combinations (at least pairs) of FM and/or RM labels were injected simultaneously between 2 mo and 5 min before each animal was killed. Blood flow was determined in many organs. Intramethod mean difference and variation did not change over time for FM but increased significantly for RM (from 1.8 +/- 1.4 to 25.6 +/- 21.8% and from 4.4 +/- 3.2 to 32.4 +/- 23.0% at 5 min and 2 mo, respectively). Also the FM-RM intermethod mean difference and variation increased (from -0.5 +/- 8.5 to 40.8 +/- 23.8% and from 23. 6 +/- 4.6 to 71.8 +/- 34.3%, respectively). After 2 mo, blood flow estimations were 20-50% lower with the various RM, whereas brain and liver blood flow values varied even more between isotopes. Underestimation started within 1 day for 51Cr and within 2 wk for 141Ce, 95Nb, and 85Sr. We conclude that FM are superior to RM for blood flow determination in experiments lasting longer than 1 day, presumably because of leaching of isotopes from RM.

Animals↗