Flow transport and not ejection fraction determines left ventricular stasis in patients with impaired systolic function

BackgroundImpaired left ventricular (LV) systolic function is a major risk factor for mural thrombosis and embolism, but LV ejection fraction (EF) poorly predicts these events, suggesting the existence of additional sources of variability. Advances in multi-dimensional flow imaging and patient-specific simulations have sparked the derivation of diverse metrics to assess blood stasis and transit efficiency. However, simple models to interpret these metrics and their dependence on chamber function are lacking. MethodsWe introduce queue models of LV blood transit connecting two common metrics of LV efficiency: flow component analysis and residence time (RT) mapping. These models yield closed-form expressions for the average RT of blood in the LV as a function of EF, direct flow (DF) --blood entering and leaving the LV in one cardiac cycle, and residual volume (RV) -- blood persisting in the LV for >2 cycles. Models performance was tested against RT obtained from vector flow mapping in 332 subjects, including controls and patients with acute myocardial infarction (AMI), hypertrophic (HCM) and dilated (DCM) cardiomyopathy. ResultsQueue models revealed RT is increasingly sensitive to DF as EF decreases, contradicting the traditional view of large DF as a teleological advantage. Instead, RT is minimized when blood transits in a first-in-first-out (FIFO) manner, while DF short-circuits the FIFO pattern, prolonging RT for other flow components. FIFO models show a good performance to assess RT in the studied subjects, especially when accounting for patient-specific DF and RV, with R: 0.62 for the pooled data, 0.70 for control, and 0.60, 0.80 and 0.40 for AMI, DCM and HCM groups respectively. ConclusionBy developing queue models of LV blood transit, and testing them on a large clinical database, we show large DF may contribute to increased blood stasis when EF is low. These models also explain why EF is a poor thrombosis risk marker in AMI and DCM.