{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,9]],"date-time":"2026-08-09T05:41:33Z","timestamp":1786254093799,"version":"build-2736575974"},"reference-count":27,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T00:00:00Z","timestamp":1779321600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T00:00:00Z","timestamp":1779321600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100018853","name":"Common Good","doi-asserted-by":"publisher","award":["TPCH INN2022\u201017"],"award-info":[{"award-number":["TPCH INN2022\u201017"]}],"id":[{"id":"10.13039\/501100018853","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Artificial Organs"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The hemodynamic consequence of increasing veno\u2010arterial extracorporeal membrane oxygenator (V\u2010A ECMO) flow on left ventricular (LV) loading is controversial, with in\u00a0vivo studies reporting conflicting results on left ventricular distension. We investigated increased V\u2010A ECMO flow on LV pressure\u2010volume characteristics under varying cardiac and volume conditions using a repeatable in\u00a0vitro mock circulation loop (MCL).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A MCL was configured with V\u2010A ECMO system to simulate four cardiogenic shock patients due to decompensated chronic heart failure patient: (1) LV failure with healthy right ventricle (RV) at normal volume (mean circulatory filling pressure, MCFP: 7\u2009mmHg), (2) combined LV and RV failure at normal volume, (3) LV failure with healthy RV and volume overload (MCFP: 12\u2009mmHg), and (4) combined LV and RV failure with volume overload. For each condition, ECMO flow was increased from 2\u2009L\/min to 4\u2009L\/min, and systemic vascular resistance (SVR) was adjusted to evaluate effects on LV pressure\u2010volume loops.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In LV failure with preserved RV function with normal volume, increased ECMO flow at constant SVR led to LV distension (&gt;\u200930 mL increase in end\u2010diastolic volume). Reducing SVR mitigated this effect but resulted in hypotension (MAP &lt;\u200965\u2009mmHg). In combined LV and RV failure at normal volume, LV distension was less pronounced and manageable with SVR reduction while maintaining adequate MAP. Under volume overload, ECMO flow increases caused marked LV dilation and elevated central venous pressure, risking venous congestion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We demonstrated that LV distension during V\u2010A ECMO flow is influenced by ventricular function, volume status, and SVR. Judicious volume management and afterload control are essential, and patients with preserved RV function may require adjunct LV unloading strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aor.70163","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T03:44:49Z","timestamp":1779421489000},"page":"1190-1196","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Comparison of Left Ventricular Pressure\u2010Volume Loops With Veno\u2010Arterial Extracorporeal Membrane Oxygenator Support: In Vitro Investigation"],"prefix":"10.1111","volume":"50","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9023-2638","authenticated-orcid":false,"given":"Eric L.","family":"Wu","sequence":"first","affiliation":[{"name":"Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group The Prince Charles Hospital  Chermside Australia"},{"name":"Institute of Molecular Bioscience The University of Queensland  Brisbane Australia"},{"name":"School of Mechanical and Mining Engineering The University of Queensland  Brisbane Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Boesch","sequence":"additional","affiliation":[{"name":"Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group The Prince Charles Hospital  Chermside Australia"},{"name":"Institute of Molecular Bioscience The University of Queensland  Brisbane Australia"},{"name":"Department of Anaesthesia and Intensive Care Medicine Medical University Innsbruck  Innsbruck Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideaki","family":"Nonaka","sequence":"additional","affiliation":[{"name":"Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group The Prince Charles Hospital  Chermside 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Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group The Prince Charles Hospital  Chermside Australia"},{"name":"Institute of Molecular Bioscience The University of Queensland  Brisbane Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John F.","family":"Fraser","sequence":"additional","affiliation":[{"name":"Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group The Prince Charles Hospital  Chermside Australia"},{"name":"Institute of Molecular Bioscience The University of Queensland  Brisbane 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