The Effects of Left Ventricle Contractility on Aortic-Brain Hemodynamic Coupling

Abnormal aortic wave dynamics can impact the brain through two mechanisms: 1) reducing blood flow to the brain and 2) increasing pulsatile energy transmission to the brain. Clinical studies have shown that decreased flow affects lacunes, microinfarcts, white matter hyperintensities (WMH), (sub)cortical atrophy, and white/gray matter integrity. On the other hand, increased pulsatility affects Virchow−Robin spaces and microbleeds. Aortic arch stiffening leads to the loss of constructive wave dynamics that normally limit transmission of harmful pulsatile energy into the brain. Furthermore, clinical studies have shown that patients with heart failure (HF) who suffer from impaired left ventricle (LV) function have worse degrees of cognitive impairment than age-matched individuals without HF. Although previous studies have attempted to elucidate the complex relationship between aortic arch stiffness and pulsatility transmission to the brain, these studies have not adequately addressed the effect of interactions between aortic arch stiffness and LV contractility on such energy transmission nor on brain perfusion. To investigate these phenomena, we employ a computational approach using a high-order FC-based solver for coupled LV-arterial hemodynamic wave propagation.