Since detailed knowledge about velocity fields downstream of heart valve prostheses obtained from in vitro studies has not been followed up by similar detailed studies in vivo a pig model for acute velocity field studies downstream of aortic valve prostheses was established. Two mechanical and two bioprosthetic valves were studied and a dynamic three dimensional visualisation of velocity fields one diameter downstream performed under different haemodynamic conditions in a total of 22 pigs. The Ionescu-Shiley pericardial valve had velocity fields very similar to the normal native porcine aortic valve. The Edwards-Carpentier porcine valve caused a jet type flow, and the valve design of the St Jude Medical and Björk-Shiley Monostrut valves was reflected in the velocity profile. Normalised (mean(SEM] systolic Reynolds normal stresses in the total cross sectional area were: native porcine 15(1.5) Nm-2; St Jude Medical 24(3.4) Nm-2; Björk-Shiley Monostrut 25(1.6) Nm-2; Edwards-Carpentier Supra-annular 51(6.6) Nm-2; Ionescu-Shiley Pericardial 19(2.0) Nm-2. Reynolds normal stresses were higher in areas of rapidly changing or constantly high velocity gradients.
Damage to blood corpuscles seems to be related to the magnitude and exposure time of the turbulent shear stresses (TSS). According to in vitro studies the critical TSS level for lethal erythrocyte and thrombocyte damage is 150-400 N/m2, for exposure times within physiological ranges. To study the distribution of TSS in the human ascending aorta, a hot-film anemometer needle probe was used to register blood velocities at 41 evenly distributed measuring points in the cross-sectional area 5-6 cm downstream of the aortic annulus. Measurements were made in the ascending aorta after normal aortic valves (prior to coronary bypass surgery), after stenotic aortic valves, and after implantation of either St. Jude Medical or Starr Edwards Silastic Ball valves. Three-dimensional visualization of velocity profiles were performed and Reynolds normal stresses (RNS) were calculated within 50-ms overlapping time windows in systole. By coordinating the mean RNS for each time window and for all 41 measuring points, 2-dimensional color-coded mapping of the RNS distribution was made. Based on the velocity profiles and the RNS distribution a relative blood damage index (RBDI) was calculated to incorporate the magnitude and exposure time for RNS in the entire cross-sectional area into one parameter. Turbulent shear stresses were estimated by using a previously determined correlation equation between RNS and TSS. After normal aortic valves, RNS was below 4 N/m2.(ABSTRACT TRUNCATED AT 250 WORDS)
Genome-wide association studies (GWAS) have revolutionized human genetics, allowing researchers to identify thousands of disease-related genes and possible drug targets. However, case-control status does not account for the fact that not all controls may have lived through their period of risk for the disorder of interest. This can be quantified by examining the age-of-onset distribution and the age of the controls or the age-of-onset for cases. The age-of-onset distribution may also depend on information such as sex and birth year. In addition, family history is not routinely included in the assessment of control status. Here we present LT-FH++, an extension of the liability threshold model conditioned on family history (LT-FH), that jointly accounts for age-of-onset and sex, as well as family history. Using simulations, we show that, when family history and the age-of-onset distribution are available, the proposed approach yields large power gains over both LT-FH and genome-wide association study by proxy (GWAX). We applied our method to four psychiatric disorders available in the iPSYCH data, and to mortality in the UK Biobank, finding 20 genome-wide significant associations with LT-FH++, compared to 10 for LT-FH and 8 for a standard case-control GWAS. As more genetic data with linked electronic health records become available to researchers, we expect methods that account for additional health information, such as LT-FH++, to become even more beneficial.
For practical clinical purposes, single point estimation of the mean blood velocity in the pulmonary artery should be performed centrally. The use of multiple sample volumes placed along the inferior/right to superior/left diameter improves the mean velocity estimate in healthy volunteers. Further studies should be conducted to reinforce the basis for Doppler velocity recording in the diseased human pulmonary artery as well as to investigate other important determinants of Doppler-derived CO, namely angle of insonation and assessment of the cross-sectional area.
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