Left Ventricular Assist Device Inflow Cannula Insertion Depth Influences Thrombosis Risk

ASAIO J. 2020 Jul;66(7):766-773. doi: 10.1097/MAT.0000000000001068.

Abstract

Left ventricular assist device (LVAD) use has continued to grow. Despite recent advances in technology, LVAD patients continue to suffer from devastating complications, including stroke and device thrombosis. Among several variables affecting thrombogenicity, we hypothesize that insertion depth of the inflow cannula into the left ventricle (LV) influences hemodynamics and thrombosis risk. Blood flow patterns were studied in a patient-derived computational model of the LV, mitral valve (MV), and LVAD inflow cannula using unsteady computational fluid dynamics (CFD). Hundreds of thousands of platelets were tracked individually, for two inflow cannula insertion depth configurations (12 mm-reduced and 27 mm-conventional) using platelet-level (Lagrangian) metrics to quantify thrombogenicity. Particularly in patients with small LV dimensions, the deeper inflow cannula insertion resulted in much higher platelet shear stress histories (SH), consistent with markedly abnormal intraventricular hemodynamics. A larger proportion of platelets in this deeper insertion configuration was found to linger in the domain for long residence times (RT) and also accumulated much higher SH. The reduced inflow depth configuration promoted LV washout and reduced platelet SH. The increase of both SH and RT in the LV demonstrates the impact of inflow cannula depth on platelet activation and increased stroke risk in these patients. Inflow cannula depth of insertion should be considered as an opportunity to optimize surgical planning of LVAD therapy.

MeSH terms

  • Cannula / adverse effects*
  • Cardiovascular Surgical Procedures / adverse effects
  • Cardiovascular Surgical Procedures / methods
  • Catheterization / adverse effects
  • Catheterization / methods*
  • Heart Ventricles / physiopathology
  • Heart-Assist Devices / adverse effects*
  • Hemodynamics / physiology
  • Humans
  • Hydrodynamics
  • Models, Cardiovascular*
  • Stress, Mechanical
  • Thrombosis / etiology*