The need for left ventricular mass (LVM) normalization to body size is well recognized. Currently used allometric exponents to normalize LVM may not account for the confounding effect of gender. Since gender is a strong determinant of body size and LVM, we hypothesized that these are subject to potential bias. We analyzed data from 7,528 subjects enrolled in the Asklepios study (n=2,524) and the Multiethnic Study of Atherosclerosis (MESA limited access dataset; n=5,004) in order to assess metric relationships between LVM and body size, generate normative data for indexed LVM and compare the ability of normalization methods to predict cardiovascular events. The allometric exponent that adequately described the LVM-body height relationship was 1.7 in both studies and significantly different from both the unity and 2.7, whereas the LVM-BSA relationship was approximately linear. LVM/height2.7 consistently demonstrated important residual relationships with body height and systematically misclassified subjects regarding the presence of LVH. LVH defined by LVM/height1.7 was more sensitive than LVM/BSA to identify obesity-related LVH and was most consistently associated with cardiovascular events and all-cause death. In contrast to current assumptions, LVM/height2.7 is not an adequate method to normalize LV mass for body size. We provide more appropriate normalization methods, normative data by 2-D-echocardiography and gradient-echo cardiac MRI, and cut-offs for defining LVH, along with prognostic validation data.

A fterload is recognized as an important determinant of myocardial function. Experimental animal studies demonstrate that increased afterload impacts diastolic relaxation. [1][2][3][4][5] Furthermore, studies in healthy instrumented dogs showed that, within physiological ranges, increased afterload results in differential responses in relaxation depending on its timing. In anesthetized open-chest dogs, mild-to-moderate increases in early systolic load resulted in unchanged or slightly enhanced relaxation, whereas increases in late systolic load resulted in a slow rate of diastolic ventricular pressure fall. 2,6 This, however, was not observed in conscious dogs subjected to a similar protocol.7 More recently, greater late systolic pressure assessed from a carotid pressure waveform 8 or an invasively measured aortic pressure waveform 9 has been shown to be associated with impaired early diastolic relaxation in humans. These studies implicate the loading sequence as a potential mechanistic determinant of diastolic relaxation.Whereas analyses of central arterial pressure and pressureflow relations are highly informative regarding arterial properties and ventricular-arterial interactions, they do not describe the time-varying mechanical load (stress) on the myocardium, which is determined by complex interactions between myocardial contractile elements, instantaneous leftventricular (LV) geometry and the time-varying hydraulic Abstract-Experimental studies implicate late systolic load as a determinant of impaired left-ventricular relaxation. We aimed to assess the relationship between the myocardial loading sequence and left-ventricular contraction and relaxation.

This study shows that knee size is important in the application of absolute metric cut-off values and that the posterior femur also shows a significantly different morphology.

Investigating the relationship between the shape of the trochlea and patellofemoral biomechanics can provide insight into the short-term effects (maltracking, increased pressures, and instability) and long-term effects (osteoarthritis) of different types of trochlear dysplasia. Furthermore, this investigation provides an empirical explanation for better treatment outcomes of trochleoplasty for Dejour types B and D dysplasia.

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The numerical simulation of Bileaflet Mechanical Heart Valves (BMHVs) has gained strong interest in the last years, as a design and optimization tool. In this paper, a strong coupling algorithm for the partitioned fluid-structure interaction (FSI) simulation of a BMHV is presented. The convergence of the coupling iterations between the flow solver and the leaflet motion solver is accelerated by using the Jacobian with the derivatives of the pressure and viscous moments acting on the leaflets with respect to the leaflet accelerations. This Jacobian is numerically calculated from the coupling iterations. An error analysis is performed to derive a criterion for the selection of useable coupling iterations. The algorithm is successfully tested for two 3D cases of a BMHV and a comparison is made with existing coupling schemes. It is observed that the developed coupling scheme outperforms these existing schemes in needed coupling iterations per time step and CPU time.

Abstract-Effective arterial elastance (E A ) was proposed as a lumped parameter that incorporates pulsatile and resistive afterload and is increasingly being used in clinical studies. Theoretical modeling studies suggest that E A is minimally affected by pulsatile load, but little human data are available. We assessed the relationship between E A and arterial load determined noninvasively from central pressure-flow analyses among middle-aged adults in the general population (n=2367) and a diverse clinical population of older adults (n=193). In a separate study, we investigated the sensitivity of E A to changes in pulsatile load induced by isometric exercise (n=73). The combination of systemic vascular resistance and heart rate predicted 95.6% and 97.8% of the variability in E A among middle-aged and older adults, respectively. E A demonstrated a quasi-perfect linear relationship with the ratio of systemic vascular resistance/heart period (middle-aged adults, R=0.972; older adults, R=0.99; P<0.0001). Aortic characteristic impedance, total arterial compliance, reflection magnitude, and timing accounted together for <1% of the variability in E A in either middle-aged or older adults. Despite pronounced changes in pulsatile load induced by isometric exercise, changes in E A were not independently associated with changes pulsatile load but were rather a nearly perfect linear function of the ratio of systemic vascular resistance/ heart period (R=0.99; P<0.0001). Our findings demonstrate that E A is simply a function of systemic vascular resistance and heart rate and is negligibly influenced by (and insensitive to) changes in pulsatile afterload in humans. Its current interpretation as a lumped parameter of pulsatile and resistive afterload should thus be reassessed.