Atrial fibrillation increases thrombogenicity of LVAD therapy.

LVAD atrial fibrillation heart failure hemodynamics mechanical circulatory support thrombogenic risk

Journal

The International journal of artificial organs
ISSN: 1724-6040
Titre abrégé: Int J Artif Organs
Pays: United States
ID NLM: 7802649

Informations de publication

Date de publication:
14 May 2024
Historique:
medline: 15 5 2024
pubmed: 15 5 2024
entrez: 14 5 2024
Statut: aheadofprint

Résumé

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. 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). 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. 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.

Sections du résumé

BACKGROUND UNASSIGNED
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 UNASSIGNED
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 UNASSIGNED
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 UNASSIGNED
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.

Identifiants

pubmed: 38742880
doi: 10.1177/03913988241251706
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3913988241251706

Déclaration de conflit d'intérêts

Declaration of conflicting interestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: CM is an investigator/consultant for Abbott, Abiomed, and Endotronix. VKC, JB, SL, NA, and AA have no disclosures.

Auteurs

Venkat Keshav Chivukula (V)

Department of Biomedical Engineering and Science, Florida Institute of Technology, Melbourne, FL, USA.

Jennifer Beckman (J)

Division of Cardiology, University of Washington, Seattle, WA, USA.

Song Li (S)

Division of Cardiology, University of Washington, Seattle, WA, USA.

Nazem Akoum (N)

Division of Cardiology, University of Washington, Seattle, WA, USA.

Alberto Aliseda (A)

Department of Mechanical Engineering, University of Washington, WA, USA.

Claudius Mahr (C)

Division of Cardiology, University of Washington, Seattle, WA, USA.

Classifications MeSH