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However, less is known about their characteristics and underlying (pathophysiological) hemodynamic mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>98 AS patients with reduced LVEF were included. Subgroup characteristics were analyzed by a multimodal approach using clinical and histological data, next-generation sequencing (NGS) and applying echocardiography as well as cardiovascular magnetic resonance (CMR) imaging. Biopsy samples were analyzed with respect to fibrosis and mRNA expression profiles.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      40 patients were classified as HG-AS and 58 patients as LG-AS. Severity of AS was comparable between the subgroups. Comparison of both subgroups revealed no differences in LVEF (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.1), LV mass (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.6) or end-diastolic LV diameter (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.12). Neither histological (HG: 23.2% vs. LG: 25.6%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.73) and circulating biomarker-based assessment (HG: 2.6\u2009\u00b1\u20092.2% vs. LG: 3.2\u2009\u00b1\u20093.1%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.46) of myocardial fibrosis nor global gene expression patterns differed between subgroups. Mitral regurgitation (MR), atrial fibrillation (AF) and impaired right ventricular function (MR: HG: 8% vs. LG: 24%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001; AF: HG: 30% vs. LG: 51.7%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.03; RVSVi: HG 36.7 vs. LG 31.1\u00a0ml\/m2,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.045; TAPSE: HG 20.2 vs. LG 17.3\u00a0mm,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002) were more frequent in LG-AS patients compared to HG-AS. These pathologies could explain the higher mortality of LG vs. HG-AS patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In patients with low-flow severe aortic stenosis, low transaortic gradient and cardiac output are not primarily due to LV dysfunction or global changes in gene expression, but may be attributed to other additional cardiac pathologies like mitral regurgitation, atrial fibrillation or right ventricular dysfunction. These factors should also be considered during planning of aortic valve replacement.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                    <jats:p>Comparison of patients with high-gradient (HG) and low-gradient (LG) aortic stenosis (AS) and reduced ejection fraction. Comprehensive analyses including clinical data, gene expression analyses, cardiovascular magnetic resonance (CMR) imaging as well as echocardiography were performed. AF:\u00a0Atrial fibrillation, MR:\u00a0mitral regurgitation, RVEF:\u00a0right ventricular ejection fraction, ECV%: extracellular volume.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00392-023-02372-4","type":"journal-article","created":{"date-parts":[[2024,1,18]],"date-time":"2024-01-18T06:43:09Z","timestamp":1705560189000},"page":"1455-1466","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Low-flow in aortic valve stenosis patients with reduced ejection fraction does not depend on left ventricular function"],"prefix":"10.1007","volume":"114","author":[{"given":"Svante","family":"Gersch","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Torben","family":"Lange","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bo Eric","family":"Beuthner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manar","family":"Elkenani","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Niels","family":"Paul","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Moritz","family":"Schnelle","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elisabeth","family":"Zeisberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miriam","family":"Puls","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerd","family":"Hasenfu\u00df","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andreas","family":"Schuster","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karl","family":"Toischer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,1,18]]},"reference":[{"key":"2372_CR1","doi-asserted-by":"publisher","first-page":"162","DOI":"10.1038\/nrcardio.2010.202","volume":"8","author":"B Iung","year":"2011","unstructured":"Iung B, Vahanian A (2011) Epidemiology of valvular heart disease in the adult. 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