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This study compared microvasculature across vascular beds in HFpEF patients and controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This prospective, case-control study included subjects\u2009\u2265\u200960years. HFpEF patients were diagnosed in an expert centre. Controls without HF were selected from the Maastricht Study, a population cohort enriched with diabetes mellitus. Microvascular assessments included central retinal venular\/arteriolar calibres (CRVE\/CRAE), flicker-light-induced retinal dilation, skin microvascular flowmotion and heat-induced hyperemia, and urinary albumin-to-creatinine ratio (UACR). Group differences were evaluated with confounder-adjustments (age, sex, blood pressure, body mass index, diabetes, haemoglobin, smoking). Interactions with sex and diabetes mellitus were tested, and stratified analyses were performed when significant interactions were present.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Microvascular assessments were performed in 138 HFpEF patients and 2140 controls. Microvascular differences were present between groups in all vascular beds. However, confounder-adjusted analyses attenuated differences. Confounder-adjusted analyses indicated that HFpEF patients versus controls still had retinal differences: narrower CRVE (\u2212\u20098.1\u00a0\u03bcm,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.008) and narrower CRAE trend (\u2212\u20093.5\u00a0\u03bcm,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.073), but similar flicker-light-induced retinal venular\/arteriolar dilation (\u2212\u20090.23%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.392; \u2212\u20090.18%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.593, respectively). Confounder-adjusted analyses showed similar skin flowmotion measures (i.e. endothelial power \u2212\u20090.09log(PU\n                      <jats:sup>2<\/jats:sup>\n                      ),\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.181), and heat-induced hyperemia (0.02log(%),\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.605) between groups. UACR remained higher in HFpEF after confounder adjustments (0.56log(g\/mol),\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009&lt;\u20090.001). Interaction analyses revealed that female patients had narrower CRVE versus controls (p\n                      <jats:sub>int<\/jats:sub>\n                      =0.023; females \u2212\u200913.8\u00a0\u03bcm,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001; males 1.2\u00a0\u03bcm,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.812). Patients had lower skin endothelial flowmotion power only when diabetes was co-occurring (p\n                      <jats:sub>int<\/jats:sub>\n                      =0.048; \u2212\u20090.36 log(PU\n                      <jats:sup>2<\/jats:sup>\n                      ),\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.014). UACR was higher in male and female patients versus controls, but was more pronounced in males (p\n                      <jats:sub>int<\/jats:sub>\n                      =0.002).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>HFpEF patients showed microvascular differences versus controls across all vascular beds studied. However, confounder-adjusted differences remained significant in eyes and kidneys. The findings across multiple organs support that MVD is likely a more systemic process than only local MVD in HFpEF, and possible sex-specific underlying pathophysiology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Registration<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"https:\/\/onderzoekmetmensen.nl\" ext-link-type=\"uri\">https:\/\/onderzoekmetmensen.nl<\/jats:ext-link>\n                      ; Unique identifier: NL7655.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1186\/s12933-025-02850-1","type":"journal-article","created":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T21:18:38Z","timestamp":1753910318000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Microvascular dysfunction across organs in heart failure with preserved ejection fraction: the PROSE-HFpEF case-control study"],"prefix":"10.1186","volume":"24","author":[{"given":"Jerremy","family":"Weerts","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blanche L. 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