The main focus of this research is on understanding the effect of changing left ventricular chamber kinematics on intraventricular flow especially diastolic vortexes. The next chapter of this thesis describes the method used to collect data which is analyzed in Chapters 3- 9 and the Appendices. It also contains information on methods used to process and analyze the different types of acquired data.
Chapter 3 describes the derivation of vortex formation time (VFT)- a dimensionless index used to quantify early diastolic filling vortex. In this work, we use a kinematic model to derive VFT and connect vortex formation to chamber kinematics. In Chapter 4, we validate the kinematic derivation of VFT using clinical data. We calculate VFT using our method from clinically measured echocardiographic data and compare it to VFT calculated by the standard method in the same dataset. We also demonstrate the advantage of using a kinematic definition of VFT by comparing the standard and kinematic definition of VFT to clinically used index of diastolic function quantification. In Chapter 5, we show the benefit of using a kinematic model based VFT in classifying subjects with normal and pseudonormal filling. Typically, these subjects are difficult to distinguish based on transmitral flow and the standard definition of VFT also can’t differentiate between them. However, the kinematic model based VFT can.
In Chapter 6, we propose a vortex based causal hypothesis for L-waves. L-waves have been observed in mid- diastole but the mechanism of formation is poorly understood. Our work using echocardiography and cardiac MRI shows that L-waves are a consequence of recirculating
flow in the vortex rings. Additionally, we predict that L-waves should form in the RV by the same mechanism. Using echocardiography in the RV and cardiac MRI we show RV L-waves which have not been previously reported.
Chapter 7 describes a method to compute directional flow impedances from clinically measured data. LV filling is anisotropic, in a normal LV, volume accommodation is primarily in a longitudinal direction rather than radial direction. However, previously there was no good way to quantify this attribute. Flow impedances allow for the interaction of pressure and flow rate and thus effectively quantify the resistance faced by filling in the longitudinal and transverse/ radial direction. Our method uses LV pressures measured from cardiac cath and flow rate measured by Doppler echocardiography to calculate longitudinal and transverse impedance. We found that consistent with previous reports, longitudinal volume accommodation is preferred over transverse and our method allowed us to quantify this property.
Chapter 8 uses LV pressure data obtained from cardiac catheterization to compute the spatiotemporal heterogeneities in isovolumic pressure decay. Previous work has focused on quantifying pressure gradients during filling. Our work shows that the pressure gradient of greater magnitude exists during isovolumic relaxation. Moreover, the rate of relaxation (as quantified by dP/dt) is also spatially heterogeneous. Our results indicate that apical relaxation is slower than mid- LV relaxation.
In Chapter 9 a new method for load independent analysis of pressures and pressure derivatives during the cardiac cycle is proposed. The values of LV pressure and pressure derivative are normalized to 0 and 1 (for pressures) and -1 and +1 (for pressure derivatives). This method of normalization revealed conserved features of the cardiac cycle. During isovolumic relaxation, the normalized pressure at which peak negative dP/dt is reached is conserved across a
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large number of beats recorded from different subjects under various loading conditions. Hence this result hints to the presence of conserved mechanisms in the relaxation process.
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