Atrial fibrillation increases thrombogenicity of LVAD therapy

Int J Artif Organs. 2024 May;47(5):329-337. doi: 10.1177/03913988241251706. Epub 2024 May 14.

Abstract

Background: This study investigates the hypothesis that presence of atrial fibrillation (AF) in LVAD patients increases thrombogenicity in the left ventricle (LV) and exacerbates stroke risk.

Methods: Using an anatomical LV model implanted with an LVAD inflow cannula, we analyze thrombogenic risk and blood flow patterns in either AF or sinus rhythm (SR) using unsteady computational fluid dynamics (CFD). To analyze platelet activation and thrombogenesis in the LV, hundreds of thousands of platelets are individually tracked to quantify platelet residence time (RT) and shear stress accumulation history (SH).

Results: The irregular and chaotic mitral inflow associated with AF results in markedly different intraventricular flow patterns, with profoundly negative impact on blood flow-induced stimuli experienced by platelets as they traverse the LV. Twice as many platelets accumulated very high SH in the LVAD + AF case, resulting in a 36% increase in thrombogenic potential score, relative to the LVAD + SR case.

Conclusions: This supports the hypothesis that AF results in unfavorable blood flow patterns in the LV adding to an increased stroke risk for LVAD + AF patients. Quantification of thrombogenic risk associated with AF for LVAD patients may help guide clinical decision-making on interventions to mitigate the increased risk of thromboembolic events.

Keywords: LVAD; atrial fibrillation; heart failure; hemodynamics; mechanical circulatory support; thrombogenic risk.

MeSH terms

  • Atrial Fibrillation* / etiology
  • Atrial Fibrillation* / physiopathology
  • Blood Platelets / metabolism
  • Heart Ventricles / diagnostic imaging
  • Heart Ventricles / physiopathology
  • Heart-Assist Devices* / adverse effects
  • Hemodynamics
  • Humans
  • Hydrodynamics
  • Models, Anatomic
  • Models, Cardiovascular
  • Platelet Activation
  • Stroke / etiology
  • Thrombosis / etiology
  • Thrombosis / physiopathology
  • Ventricular Function, Left