{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T11:27:22Z","timestamp":1788607642437,"version":"build-2803163510"},"reference-count":37,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,12,2]],"date-time":"2018-12-02T00:00:00Z","timestamp":1543708800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004359","name":"Vetenskapsr\u00e5det","doi-asserted-by":"publisher","award":["2016\u201001617"],"award-info":[{"award-number":["2016\u201001617"]}],"id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007308","name":"Sveriges L\u00e4karf\u00f6rbund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100007308","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010794","name":"Medicinska fakulteten, Ume\u00e5 Universitet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100010794","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003252","name":"Lunds Universitet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003252","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Physio Funct Imaging"],"published-print":{"date-parts":[[2019,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Total heart volume (<jats:styled-content style=\"fixed-case\">THV<\/jats:styled-content>) within the pericardium is not constant throughout the cardiac cycle and <jats:styled-content style=\"fixed-case\">THV<\/jats:styled-content> would intuitively be lowest at end systole. We have, however, observed a phase shift between ventricular outflow and atrial inflow which causes the minimum <jats:styled-content style=\"fixed-case\">THV<\/jats:styled-content> to occur before end systole. The aims were to explain the mechanism of the late\u2010systolic net inflow to the heart and determine whether this net inflow is affected by increased cardiac output or systolic heart failure.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and Results<\/jats:title><jats:p>Healthy controls (<jats:italic>n<\/jats:italic>\u00a0=\u00a021) and patients with <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>&lt;35% (<jats:italic>n<\/jats:italic>\u00a0=\u00a014) underwent magnetic resonance imaging with flow measurements in vessels to and from the heart, and this was repeated in nine controls during 140 \u03bcgram kg<jats:sup>\u22121<\/jats:sup>\u00a0min<jats:sup>\u22121<\/jats:sup> adenosine infusion. Minimum <jats:styled-content style=\"fixed-case\">THV<\/jats:styled-content> occurred 78\u00a0\u00b1\u00a06\u00a0ms before end of systolic ejection (8\u00a0\u00b1\u00a01% of the cardiac cycle) in controls. The late\u2010systolic net inflow was 12\u00b73\u00a0\u00b1\u00a01\u00b71\u00a0ml or 6\u00b70\u00a0\u00b1\u00a00\u00b75% of total stroke volume (<jats:styled-content style=\"fixed-case\">TSV<\/jats:styled-content>). Cardiac output increased 66\u00a0\u00b1\u00a08% during adenosine but late\u2010systolic net inflow to the heart did not change (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b773). In patients with heart failure, late\u2010systolic net inflow of the heart\u2032s left side was lower (3\u00b74\u00a0\u00b1\u00a00\u00b75%) compared to healthy subjects (5\u00b73\u00a0\u00b1\u00a00\u00b76%, <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b703).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Heart size increases before end systole due to a late\u2010systolic net inflow which is unaffected by increased cardiac output. This may be explained by inertia of blood that flows into the atria generated by ventricular systole. The lower late\u2010systolic net inflow in patients with systolic heart failure may be a measure of decreased ventricular filling due to decreased systolic function, thus linking systolic to diastolic dysfunction.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cpf.12555","type":"journal-article","created":{"date-parts":[[2018,12,3]],"date-time":"2018-12-03T03:34:30Z","timestamp":1543808070000},"page":"192-200","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Heart filling exceeds emptying during late ventricular systole in patients with systolic heart failure and healthy subjects \u2013 a cardiac <scp>MRI<\/scp> study"],"prefix":"10.1111","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9480-5250","authenticated-orcid":false,"given":"Marcus","family":"Carlsson","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences, Clinical Physiology Skane University Hospital Lund University Lund 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