{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T08:48:40Z","timestamp":1790066920613,"version":"4.0.1"},"reference-count":58,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,2,19]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Heterogeneity in the underlying processes that contribute to heart failure with preserved ejection fraction (\n              <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n              p\n              <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>\n              ) is increasingly recognized. Diabetes mellitus is a frequent comorbidity in\n              <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n              p\n              <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>\n              , but its impact on left ventricular and arterial structure and function in\n              <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n              p\n              <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>\n              is unknown.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We assessed the impact of diabetes mellitus on left ventricular cellular and interstitial hypertrophy (assessed with cardiac magnetic resonance imaging, including T1 mapping pregadolinium and postgadolinium administration), arterial stiffness (assessed with arterial tonometry), and pulsatile arterial hemodynamics (assessed with in\u2010office pressure\u2010flow analyses and 24\u2010hour ambulatory monitoring)\u00a0among 53 subjects with\n              <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n              p\n              <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>\n              (32 diabetic and 21 nondiabetic subjects). Despite few differences in clinical characteristics, diabetic subjects with HFpEF exhibited a markedly greater left ventricular mass index (78.1 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 70.4\u201385.9] g versus 63.6 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 55.8\u201371.3] g;\n              <jats:italic>P<\/jats:italic>\n              =0.0093) and indexed extracellular volume (23.6 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 21.2\u201326.1] mL\/m\n              <jats:sup>2<\/jats:sup>\n              versus 16.2 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 13.1\u201319.4] mL\/m\n              <jats:sup>2<\/jats:sup>\n              ;\n              <jats:italic>P<\/jats:italic>\n              =0.0008). Pronounced aortic stiffening was also observed in the diabetic group (carotid\u2010femoral pulse wave velocity, 11.86 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 10.4\u201313.1] m\/s versus 8.8 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 7.5\u201310.1] m\/s;\n              <jats:italic>P<\/jats:italic>\n              =0.0027), with an adverse pulsatile hemodynamic profile characterized by increased oscillatory power (315 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 258\u2013373] mW versus 190 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 144\u2013236] mW;\n              <jats:italic>P<\/jats:italic>\n              =0.0007), aortic characteristic impedance (0.154 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 0.124\u20130.183] mm Hg\/mL per second versus 0.096 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 0.072\u20130.121] mm\u00a0Hg\/mL per second;\n              <jats:italic>P<\/jats:italic>\n              =0.0024), and forward (59.5 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 52.8\u201366.1] mm Hg versus 40.1 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 31.6\u201348.6] mm\u00a0Hg;\n              <jats:italic>P<\/jats:italic>\n              =0.0010) and backward (19.6 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 16.2\u201322.9] mm Hg versus 14.1 [95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              , 10.9\u201317.3] mm\u00a0Hg;\n              <jats:italic>P<\/jats:italic>\n              =0.0169) wave amplitude. Abnormal pulsatile hemodynamics were also evident in 24\u2010hour ambulatory monitoring, despite the absence of significant differences in 24\u2010hour systolic blood pressure between the groups.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Diabetes mellitus is a key determinant of left ventricular remodeling, arterial stiffness, adverse pulsatile hemodynamics, and ventricular\u2010arterial interactions in\n              <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n              p\n              <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Clinical Trial Registration<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">URL<\/jats:styled-content>\n              :\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n              . Unique identifier:\n              <jats:styled-content style=\"fixed-case\">NCT<\/jats:styled-content>\n              01516346.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.011457","type":"journal-article","created":{"date-parts":[[2019,2,15]],"date-time":"2019-02-15T10:01:58Z","timestamp":1550224918000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":45,"title":["Impact of Diabetes Mellitus on Ventricular Structure, Arterial Stiffness, and Pulsatile Hemodynamics in Heart Failure With Preserved Ejection Fraction"],"prefix":"10.1161","volume":"8","author":[{"given":"Julio A.","family":"Chirinos","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine Hospital of the University of Pennsylvania Philadelphia PA"},{"name":"Division of Cardiovascular Medicine University of Pennsylvania Perelman School of Medicine Philadelphia PA"},{"name":"Department of Radiology Corporal Michael J. 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