{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:48:14Z","timestamp":1793227694015,"version":"4.5.0"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"18","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2024,9,17]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">The process underlying Fontan pathophysiology is multifactorial and may include gut dysbiosis (GD). We investigated the presence of GD and elucidated its correlation with Fontan pathophysiology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Gut microbiomes of 155 consecutive patients with Fontan pathophysiology and 44 healthy individuals were analyzed using 16S rRNA sequencing of bacterial DNA extracted from fecal samples. GD was evaluated on the basis of \u03b1 and \u00df diversities of the gut microbiome and was compared with natural log\u2010transformed C\u2010reactive protein, hemodynamics, von Willebrand factor antigen (a bacterial translocation marker), Mac\u20102 binding protein glycosylation isomer (a liver fibrosis indicator), peak oxygen uptake, and heart failure hospitalization. Patients with Fontan exhibited GD in terms of \u03b1 and \u00df diversities as compared with controls (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01). Reduced \u03b1 diversity was associated with a failed hemodynamic phenotype, hypoxia, high natural log\u2010transformed C\u2010reactive protein levels, and elevated von Willebrand factor antigen and Mac\u20102 binding protein glycosylation isomer levels (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.05\u20130.01). In addition to elevated von Willebrand factor antigen and hypoxia, decreased \u03b1 diversity was independently correlated with a high natural log\u2010transformed C\u2010reactive protein level (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.05), which was associated with liver imaging abnormalities and a heightened risk of heart failure hospitalization (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01 for both).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Patients with Fontan pathophysiology exhibited GD compared with healthy individuals, and GD was linked to failed hemodynamics and systemic inflammation with a poor prognosis. Therefore, GD may play a pivotal role in a failing Fontan status, including Fontan\u2010associated liver disease, through GD\u2010associated systemic inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.124.034538","type":"journal-article","created":{"date-parts":[[2024,9,9]],"date-time":"2024-09-09T07:14:45Z","timestamp":1725866085000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Gut Dysbiosis in Patients With Fontan Circulation"],"prefix":"10.1161","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7092-4792","authenticated-orcid":false,"given":"Hideo","family":"Ohuchi","sequence":"first","affiliation":[{"name":"Department of Pediatric Cardiology National Cerebral and Cardiovascular Center Suita Japan"},{"name":"Adult Congenital Heart Disease Center National Cerebral and Cardiovascular Center Suita 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