{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T16:10:17Z","timestamp":1778343017103,"version":"3.51.4"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,4,21]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Severe aortic stenosis (AS) is associated with ischemic stroke independently of atrial fibrillation or other causes. Even after aortic valve replacement (AVR), patients remain affected by a 6% 5\u2010year stroke rate with knowledge gaps in the underlying pathophysiology. We hypothesize that severe AS is associated with prothrombotic left atrial (LA) flow changes that do not normalize after AVR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Seventy\u2010seven participants without atrial fibrillation were recruited: 40 with severe AS (median age, 73\u2009years; CHA\n                      <jats:sub>2<\/jats:sub>\n                      DS\n                      <jats:sub>2<\/jats:sub>\n                      VASc score, 3) and 37 controls with similar risk profile (median age, 71\u2009years; CHA\n                      <jats:sub>2<\/jats:sub>\n                      DS\n                      <jats:sub>2<\/jats:sub>\n                      VASc score, 3). All underwent baseline cardiac magnetic resonance imaging. Among the 40 patients with AS, 23 (58%) underwent AVR and repeat cardiac magnetic resonance imaging \u22486\u2009months after surgery.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Compared with controls, patients with severe AS displayed significantly higher left ventricular (LV) mass (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.04), smaller LV volumes (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.01), and reduced global longitudinal strain (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.001). Although LA volume was within the normal range and LA emptying fraction was not different from controls, severe AS was associated with lower LA peak flow velocity (mean, 0.25 versus 0.28\u2009m\/s, respectively;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.02) and lower LA flow vorticity (mean, 16.6 versus 21.1\u2009radians;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.001) compared with controls.\n                    <\/jats:p>\n                    <jats:p xml:lang=\"en\">\n                      AVR led to regression of LV hypertrophy with LV mass that was no longer different from controls (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.32). Nevertheless, post\u2010AVR patients displayed a persistent adverse morpho\u2010functional phenotype characterized by persistently lower velocity (mean, 0.24 versus 0.28\u2009m\/s;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.003) and vorticity (17.1 versus 21.1 radians;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.001) compared with controls.\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 severe AS display adverse prothrombotic LA flow characteristics that persist after successful AVR despite general regression of LV hypertrophy.<\/jats:p>\n                  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