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T Delhaas

Publications and source records attributed to T Delhaas.

At least 19 recordsLinked to original sources
PubMed2006

Towards model-based analysis of cardiac MR tagging data: relation between left ventricular shear strain and myofiber orientation.

Many cardiac pathologies are reflected in abnormal myocardial deformation, accessible through magnetic resonance tagging (MRT). Interpretation of the MRT data is difficult, since the relation between pathology and deformation is not straightforward. Mathematical models of cardiac mechanics could be used to translate measured abnormalities into the underlying pathology, but, so far, they even fail to correctly simulate myocardial deformation in the healthy heart. In this study we investigated to what extent (1) our previously published three-dimensional finite element model of cardiac mechanics [Kerckhoffs, R.C.P., Bovendeerd, P.H.M., Kotte, J.C.S., Prinzen, F.W., Smits, K., Arts, T., 2003. Homogeneity of cardiac contraction despite physiological asynchrony of depolarization: a model study. Ann. Biomed. Eng. 31, 536-547] can simulate measured cardiac deformation, and (2) discrepancies between strains in model and experiment are related to the choice of the myofiber orientation in the model. To this end, we measured midwall circumferential strain E(cc) and circumferential-radial shear strain E(cr) in three healthy subjects using MRT. E(cc) as computed in the model agreed well with measured E(cc). Computed E(cr) differed significantly from measured E(cr). The time course of E(cr) was found to be very sensitive to the choice of the myofiber orientation, in particular to the choice of the transverse angle. Discrepancies between circumferential-radial shear strain in model and experiment were reduced strongly by increasing the transverse angle in the original model by 25%.

Adult↗
PubMed2006

Stenting of hypoplastic aortic segments with mild pressure gradients and arterial hypertension.

OBJECTIVE: To determine the safety, feasibility and effectiveness of stent expansion of hypoplastic aortic segments with pressure gradients in patients with arterial hypertension. DESIGN: Non-randomised prospective clinical trial. SETTING: Tertiary referral centre, congenital cardiac unit. PATIENT SELECTION: 20 consecutive patients (median age 14.5 years, range 11.6-38.8 years) with arterial hypertension and a hypoplastic segment of the aorta. Seventeen patients had successful previous arch interventions in a coarctation site. INTERVENTIONS: Stent deployment in hypoplastic arch segments. MAIN OUTCOME MEASURES: Gradient across the aortic arch; complications early and during follow up; residual hypertension. RESULTS: 23 stents were deployed: 13 in the cross and 10 in the isthmus. The mean gradient across the aortic arch decreased from 16 (SD 6) (median 17) to 3 (4) (median 1) mm Hg (p < 0.001). In a few patients a mild gradient persisted just distal to the left carotid artery due to residual orificial narrowing or acute angulation. No complications occurred during or after the procedure. During follow up of 2.2 years (range 0.2-4.8 years) arterial hypertension resolved in 10 patients and 10 required residual drug treatment with better control of blood pressures. CONCLUSIONS: Pressure loss due to residual hypoplastic aortic segments can be treated effectively and safely with stent expansion. Some patients remain mildly hypertensive and require additional drug treatment.

Adolescent↗
PubMed2003

[Hypertrophic cardiomyopathy: from diagnosis to prevention].

In a 55-year-old man, his two sons aged 32 and 30 years and a 3-year-old grandchild, a gene mutation related to an increased chance of hypertrophic cardiomyopathy was found. The adults had complaints of cardiac arrhythmias varying from dizziness to cardiac arrest and received medication; a defibrillator was also implanted in the case of the sons. Familial hypertrophic cardiomyopathy can be diagnosed in an early stage with DNA screening methods. At that time 'patients' (carriers) often do not exhibit symptoms. This offers the possibility of taking therapeutic measures to prevent or slow down the disease process. However, the scientific basis for preventive therapy is inadequate, so that medical-ethical dilemmas arise which can affect the decision-making process with respect to genetic testing. Additional research must lead to satisfactory preventive therapies, so that in the future the genetic diagnosis 'hypertrophic cardiomyopathy' can be effectively translated into disease prevention.

Adult↗
PubMed2003

Modeling the relation between cardiac pump function and myofiber mechanics.

Complexity of the geometry and structure of the heart hampers easy modeling of cardiac mechanics. The modeling can however be simplified considerably when using the hypothesis that in the normal heart myofiber structure and geometry adapt, until load is evenly distributed. A simple and realistic relationship is found between the hemodynamic variables cavity pressure and volume, and myofiber load parameters stress and strain. The most important geometric parameter in the latter relation is the ratio of cavity volume to wall volume, while actual geometry appears practically irrelevant. Applying the found relationship, a realistic maximum is set to left ventricular pressure after chronic pressure load. Pressures exceeding this level are likely to cause decompensation and heart failure. Furthermore, model is presented to simulate left and right ventricular pump function with left-right interaction.

Adaptation, Physiological↗
PubMed2003

Supraventricular tachycardia: an incidental diagnosis in infants and difficult to prove in children.

AIMS: To determine (a) the age distribution at first clinical supraventricular tachycardia (SVT) presentation; (b) the time interval between first clinical suspicion and electrocardiographic proof of SVT; c) the most indicative symptoms and signs of SVT; and (d) the SVT mechanism and its age distribution according to surface ECG. METHODS: The records of 55 children (32 males and 23 females) with electrocardiographically proven SVT but without congenital heart disease were reviewed. RESULTS: At diagnosis, 27 patients (49%) were younger than 1 y (infants), and 28 (51%) were older than 1 y (children). Only a quarter of infants presented with symptoms. The majority (20/27), however, were detected during routine investigation without having any complaints. Children presented with symptoms (mostly palpitations) in almost 90% of cases. Despite these symptoms, the median time interval between first clinical presentation suggestive of SVT and electrocardiographic proof of SVT was 138 d. Using surface ECG, we were unable to show any age-dependency of the SVT mechanism in our study group. CONCLUSION: In infants SVT is a chance finding; SVT can only be proven electrocardiographically with a median delay of 138 d, despite the presence of symptoms; SVT using a (concealed) accessory pathway is the most common mechanism.

Adolescent↗
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

Long term complications of inferior vena cava thrombosis.

AIM: To evaluate the long term outcome after paediatric inferior vena cava (IVC) thrombosis. METHODS: A combined retrospective and prospective study on infants and children with IVC thrombosis treated at Aachen and Maastricht University Hospitals between 1980 and 1999. RESULTS: Forty patients were enrolled, including four with preceding cardiac catheterisation, 18 with central venous saphenous lines, and an additional eight with umbilical venous catheters. Six patients died within three months of diagnosis; one patient was lost to follow up. Twelve of the remaining 33 patients had suffered from limited IVC thrombosis; during follow up (for up to nine years) none showed persisting caval obstruction (successful thrombolysis, n = 2; spontaneous recanalisation, n = 10). The remaining 21 patients presented with extensive IVC thrombosis. During follow up (for up to 18 years) complete restitution was found in only four cases (one thrombolysis, two surgery, one spontaneous recanalisation). Persisting iliac and/or caval venous obstruction occurred in 17 patients, including six with thrombolysis. Varicose veins were found in 12, and post-thrombotic syndrome in seven of these cases. According to Kaplan-Meier analysis, 30% of patients with persisting venous disease will develop post-thrombotic syndrome within 10 years of the thrombotic event. CONCLUSIONS: Infants and children with extensive IVC thrombosis are at high risk for persisting venous disease and serious long term complications. Prospective trials are urgently needed to establish effective treatment strategies and to improve long term prognosis. Central venous catheters, contributing to IVC thrombosis in the majority of cases reported here, should be inserted only if essential.

Adolescent↗
PubMed1999

Differential responses of adult cardiac fibroblasts to in vitro biaxial strain patterns.

Different patterns of extracellular matrix (ECM) remodeling in the heart are thought to be dependent on altered mechanical and chemical conditions and can contribute to cardiac dysfunction. Cardiac fibroblasts are the primary regulators of the ECM and may respond to mechanical factors in vitro. We hypothesized that different types of in vitro strains, e.g. tensile or compressive, can stimulate different functional responses in cultured adult rat cardiac fibroblasts. In this study, we first showed that a single step in strain applied by a uniaxial stretch system stimulated collagen III and fibronectin mRNA levels and transforming growth factor-beta(1) (TGF-beta(1)) activity in the adult phenotype of rat cardiac fibroblasts. Two-dimensional deformations were measured by tracking fluorescent microspheres attached to the substrate and cultured cells. For 10% uniaxial strain, mean principal strains were 0. 104 +/- 0.018 in the direction of stretch and -0.042 +/- 0.013 in the perpendicular direction, verifying that the fibroblasts were simultaneously subjected to tensile (positive) and compressive (negative) strains. Furthermore, these cells were also subjected to area change and to shear. In order to examine the distinct effects of different types of deformation on cardiac fibroblasts, an equibiaxial stretch system was used to apply either pure tensile or compressive area strains, in the absence of shear. Magnitudes of equibiaxial strain were selected to apply local cell area changes identical to those applied in the uniaxial system. Results showed that pure tensile and compressive area strains induced divergent responses in ECM mRNA levels. TGF-beta(1) activity was dependent on the magnitude of applied area strain regardless of the mode of deformation. These findings demonstrate that adult cardiac fibroblasts may respond differently to varied types of mechanical loading, suggesting that ECM remodeling may be locally regulated by specific mechanical stimuli in the heart.

Animals↗
PubMed1998

Transitory spinal cord swelling in a 6-year-old boy with Guillain-Barré syndrome.

A 6-year-old boy developed progressive motor weakness and areflexia. The clinical picture, combined with electrophysiological findings, indicated a diagnosis of Guillain-Barré syndrome (GBS). MRI on admission revealed spinal cord swelling and increased signal intensity within the cord. It is concluded that, since a degree of central nervous system involvement can occasionally be part of the spectrum of GBS, swelling of the spinal cord without contrast enhancement does not exclude a diagnosis of GBS.

Child↗
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↗
PubMed1997

Benign recurrent intrahepatic cholestasis (BRIC): evidence of genetic heterogeneity and delimitation of the BRIC locus to a 7-cM interval between D18S69 and D18S64.

Benign recurrent intrahepatic cholestasis (BRIC) is an autosomal recessive liver disease characterized by multiple episodes of cholestasis without progression to chronic liver disease. The gene was previously assigned to chromosome 18q21, using a shared segment analysis in three families from the Netherlands. In the present study we report the linkage analysis of an expanded sample of 14 BRIC families, using 15 microsatellite markers from the 18q21 region. Obligate recombinants in two families place the gene in a 7-cM interval, between markers D18S69 and D18S64. All intervening markers had significant LOD scores in two-point linkage analysis. Moreover, we identified one family in which the BRIC gene seems to be unlinked to the 18q21 region, or that represents incomplete penetrance of the BRIC genotype.

Cholestasis, Intrahepatic↗
PubMed1996

An equibiaxial strain system for cultured cells.

We developed a device that applies homogeneous equibiaxial strains of 0-10% to a cell culture substrate and quantitatively verified transmission of substrate deformation to cultured cardiac cells. Clamped elastic membranes in both single-well and multiwell versions of the device are uniformly stretched by indentation with a plastic ring, resulting in strain that is directly proportional to the pitch-to-radius ratio. Two-dimensional deformations were measured by tracking fluorescent microspheres attached to the substrate and to cultured adult rat cardiac fibroblasts. For nominal stretches up to 18%, strains along circumferential and radial axes were equal in magnitude and homogeneously distributed with negligible shear. For 5% stretch, circumferential and radial strains in the substrate were 0.046 +/- 0.005 and 0.048 +/- 0.004 [not significant (NS)], respectively, and shear strain was 0.001 +/- 0.003 (NS). Calibration of both single-well and multiwell versions permits strain selection by device rotation. The reproducible application and quantification of homogeneous equibiaxial strain in cultured cells provides a quantitative approach for correlating mechanical stimuli to cellular transduction mechanisms.

Animals↗
PubMed1996

Regional wall mechanics in the ischemic left ventricle: numerical modeling and dog experiments.

The mechanics of the ischemic left ventricle during a complete cardiac cycle were simulated using a finite-element model accounting for the thick-walled ventricular geometry, the fibrous nature of the myocardial tissue, and the dependency of active muscle fiber stress on time, strain, and strain rate. Ischemia was modeled by disabling the generation of active stress in a region comprising approximately 12% of total wall volume. In the model simulations, the approximately 12% reduction in the amount of normally contracting tissue resulted in an approximately 25% reduction in stroke work compared with the normal situation. The more-than-proportional loss of stroke work may partly be attributed to storage of elastic energy in the bulging ischemic region. Furthermore the mechanical performance in the nonischemic border zone deteriorated because of reduced systolic fiber stress (if fibers were in series with those in the ischemic region) or reduced fiber shortening (if fibers were parallel). The deformation pattern of the ventricle was asymmetric with respect to the ischemic region because of the anisotropy of the myocardial tissue. Epicardial fiber shortening in and around the ischemic region, as predicted from the model simulations, was in qualitative agreement with shortening, as measured in four dogs in which ischemia was induced by occlusion of the distal part of the left anterior interventricular coronary artery.

Animals↗