{
    "abstract": "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.\nUsing 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).\nThe 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\u2009+\u2009AF case, resulting in a 36% increase in thrombogenic potential score, relative to the LVAD\u2009+\u2009SR case.\nThis supports the hypothesis that AF results in unfavorable blood flow patterns in the LV adding to an increased stroke risk for LVAD\u2009+\u2009AF 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.",
    "authors": [
        {
            "affiliation": "Department of Biomedical Engineering and Science, Florida Institute of Technology, Melbourne, FL, USA.",
            "firstname": "Venkat",
            "initials": "V",
            "lastname": "Keshav Chivukula"
        },
        {
            "affiliation": "Division of Cardiology, University of Washington, Seattle, WA, USA.",
            "firstname": "Jennifer",
            "initials": "J",
            "lastname": "Beckman"
        },
        {
            "affiliation": "Division of Cardiology, University of Washington, Seattle, WA, USA.",
            "firstname": "Song",
            "initials": "S",
            "lastname": "Li"
        },
        {
            "affiliation": "Division of Cardiology, University of Washington, Seattle, WA, USA.",
            "firstname": "Nazem",
            "initials": "N",
            "lastname": "Akoum"
        },
        {
            "affiliation": "Department of Mechanical Engineering, University of Washington, WA, USA.",
            "firstname": "Alberto",
            "initials": "A",
            "lastname": "Aliseda"
        },
        {
            "affiliation": "Division of Cardiology, University of Washington, Seattle, WA, USA.",
            "firstname": "Claudius",
            "initials": "C",
            "lastname": "Mahr"
        }
    ],
    "conclusions": null,
    "copyrights": null,
    "doi": "10.1177/03913988241251706",
    "journal": "The International journal of artificial organs",
    "keywords": [
        "LVAD",
        "atrial fibrillation",
        "heart failure",
        "hemodynamics",
        "mechanical circulatory support",
        "thrombogenic risk"
    ],
    "methods": null,
    "publication_date": "2024-05-15",
    "pubmed_id": "38742880",
    "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\u2009+\u2009AF case, resulting in a 36% increase in thrombogenic potential score, relative to the LVAD\u2009+\u2009SR case.",
    "title": "Atrial fibrillation increases thrombogenicity of LVAD therapy.",
    "xml": "<Element 'PubmedArticle' at 0x7885045883b0>"
}