UC San Diego

Blood stasis in the cardiac chambers is a recognized risk factor for intracardiac thrombosis and potential cardiogenic embolic events. In patients at risk of intraventricular thrombosis, the benefits of anticoagulation therapy must be balanced with its pro-hemorrhagic effects. In the healthy heart, instead, left ventricular (LV) flow patterns have been proposed to optimize blood transport by coupling diastole and systole.

This work introduces a novel flow image-based method to assess LV blood stasis and transport by processing flow-velocity images obtained by 2D color-Doppler velocimetry or phase-contrast magnetic resonance. This approach is based on quantifying the LV blood Residence Time (TR) from time-resolved blood velocity fields by solving the advection equation for a passive scalar. This equation can be derived from statistical mechanics and the process can be further generalized to higher order moments of the time distribution to find, for example, the TR standard deviation.

We showed proof-of-concept feasibility of the method in normal hearts, patients with dilated cardiomyopathy and patients before and after the implantation of a left ventricular assist device (LVAD). We then conducted two clinical studies on two populations of patients: with acute myocardial infarction (AMI) and undergoing cardiac resynchronization therapy (CRT).

In patients with AMI we identified the biomechanical determinants of stasis and addressed the technique’s potential to predict LV thrombosis. TR was longer in the early than in the late phases of AMI and longer in AMI than in controls. The largest stagnant regions were identified in acute stage of the AMI and stasis metrics performed well to predict LV thrombosis.

To track blood transport in the LV of patients undergoing CRT we used a modified analysis with time-varying inflow boundary conditions. The device programming was varied to analyze flow transport under different atrioventricular conduction delays, and to model tachycardia. The analysis showed how CRT influences the transit of blood, contributes to conserving kinetic energy, and favors the generation of hemodynamic forces that accelerate blood in the direction of the LV outflow tract.

This work paves the way for using TR-derived measures of bloos stasis as a relevant bio-marker in the clinical setting.