Theo Arts

Bio: Theo Arts is an academic researcher from Maastricht University. The author has contributed to research in topics: Ventricle & Blood flow. The author has an hindex of 50, co-authored 151 publications receiving 7974 citations. Previous affiliations of Theo Arts include Eindhoven University of Technology.

Wall shear stress--an important determinant of endothelial cell function and structure--in the arterial system in vivo. Discrepancies with theory.

Abstract: It has been well established that wall shear stress is an important determinant of endothelial cell function and gene expression as well as of its structure. There is increasing evidence that low wall shear stress, as present in artery bifurcations opposite to the flow divider where atherosclerotic lesions preferentially originate, expresses an atherogenic endothelial gene profile. Besides, wall shear stress regulates arterial diameter by modifying the release of vasoactive mediators by endothelial cells. Most of the studies on the influence of wall shear stress on endothelial cell function and structure have been performed in vitro, generally exposing endothelial cells from different vascular regions to an average wall shear stress level calculated according to Poiseuille's law, which does not hold for the in vivo situation, assuming wall shear stress to be constant along the arterial tree. Also in vivo wall shear stress has been determined based upon theory, assuming the velocity profile in arteries to be parabolic, which is generally not the case. Wall shear stress has been calculated, because of the lack of techniques to assess wall shear stress in vivo. In recent years, techniques have been developed to accurately assess velocity profiles in arterioles, using fluorescently labeled particles as flow tracers, and non-invasively in large arteries by means of ultrasound or magnetic resonance imaging. Wall shear rate is derived from the in vivo recorded velocity profiles and wall shear stress is estimated as the product of wall shear rate and plasma viscosity in arterioles and whole blood viscosity in large arteries. In this review, we will discuss wall shear stress in vivo, paying attention to its assessment and especially to the results obtained in both arterioles and large arteries. The limitations of the methods currently in use are discussed as well. The data obtained in the arterial system in vivo are compared with the theoretically predicted ones, and the consequences of values deviating from theory for in vitro studies are considered. Applications of wall shear stress as in flow-mediated arterial dilation, clinically in use to assess endothelial cell (dys)function, are also addressed. This review starts with some background considerations and some theoretical aspects.

Redistribution of myocardial fiber strain and blood flow by asynchronous activation.

Abstract: Hearts of 11 anesthetized open-chest dogs were paced from the right atrium (RA), right ventricular outflow tract (RVOT), and left ventricular apex (LVA). Maps of the sequence of electrical activati...

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

Abstract: 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 ...

Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion

Abstract: Aims Left ventricular (LV) dilatation, hypertrophy, and septal perfusion defects are frequently observed in patients with left bundle branch block (LBBB). We investigated whether isolated LBBB causes these abnormalities. Methods and results In eight dogs, LBBB was induced by radio frequency ablation. Two-dimensional echocardiography showed that 16 weeks of LBBB decreased LV ejection fraction (by 23±14%) and increased LV cavity volume (by 25±19%) and wall mass (by 17±16%). The LV septal-to-lateral wall mass ratio decreased by 6±9%, indicating asymmetric hypertrophy. After onset of LBBB, myocardial blood flow (MBF, fluorescent microspheres) and systolic circumferential shortening [CSsys, magnetic resonance (MR) tagging] decreased in the septum to 83±16% and −11±20% of baseline, respectively, and increased in LV lateral wall to 118±12% and 180±90% of baseline, respectively. MBF and CSsys values did not change over 16 weeks of LBBB. Changes in external mechanical work paralleled those in CSsys. Glycogen content was not significantly different between septum and LV lateral wall of LBBB hearts (16 weeks) and control samples, indicating absence of hibernation. Conclusions The asynchronous ventricular activation during LBBB leads to redistribution of circumferential shortening and myocardial blood flow and, in the long run, LV remodelling. Septal hypoperfusion during LBBB appears to be primarily determined by reduced septal workload.

A model of the mechanics of the left ventricle

Abstract: The relation between cardiac muscle mechanics and left ventricular (LV) pump function is simulated by a mathematical model. In the following article special attention is paid to the relation between LV pressure and LV volume on the one hand and the transmural distribution of sarcomere length and fiber stress on the other. The LV is simulated by a thick-walled cylinder composed of 8 concentric shells. The myocardial material is assumed to be anisotropic. The orientation and sequential activation of the muscle fibers across the LV wall are considered per shell. Twisting of the base with respect to the apex around the axis of the LV is simulated by rotation of the upper cross-sectional surface of the cylinder with respect to the lower one aroud the axis of the cylinder.

A new constitutive framework for arterial wall mechanics and a comparative study of material models

Abstract: In this paper we develop a new constitutive law for the description of the (passive) mechanical response of arterial tissue. The artery is modeled as a thick-walled nonlinearly elastic circular cylindrical tube consisting of two layers corresponding to the media and adventitia (the solid mechanically relevant layers in healthy tissue). Each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component of the material and symmetrically disposed with respect to the cylinder axis. The resulting constitutive law is orthotropic in each layer. Fiber orientations obtained from a statistical analysis of histological sections from each arterial layer are used. A specific form of the law, which requires only three material parameters for each layer, is used to study the response of an artery under combined axial extension, inflation and torsion. The characteristic and very important residual stress in an artery in vitro is accounted for by assuming that the natural (unstressed and unstrained) configuration of the material corresponds to an open sector of a tube, which is then closed by an initial bending to form a load-free, but stressed, circular cylindrical configuration prior to application of the extension, inflation and torsion. The effect of residual stress on the stress distribution through the deformed arterial wall in the physiological state is examined. The model is fitted to available data on arteries and its predictions are assessed for the considered combined loadings. It is explained how the new model is designed to avoid certain mechanical, mathematical and computational deficiencies evident in currently available phenomenological models. A critical review of these models is provided by way of background to the development of the new model.

Platelets in atherothrombosis

Abstract: The participation of platelets in atherogenesis and the subsequent formation of occlusive thrombi depend on platelets' adhesive properties and the inability to respond to stimuli with rapid activation. By understanding the multifaceted mechanisms involved in platelet interactions with vascular surfaces and aggregation, new approaches can be tailored to selectively inhibit the pathways most relevant to the pathological aspects of atherothrombosis.

2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society.

Abstract: Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons Andrew E. Epstein, MD, FACC, FAHA, FHRS, Chair ; John P. DiMarco, MD, PhD, FACC, FHRS; Kenneth A. Ellenbogen. MD, FACC, FAHA, FHRS; N.A. Mark Estes III, MD, FACC, FAHA, FHRS; Roger A.