{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T15:27:46Z","timestamp":1790954866283,"version":"4.1.0"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2014,12,17]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Hypertension is a frequent risk factor for the development of heart failure with preserved ejection fraction (\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              ). Progressive extracellular matrix accumulation has been presumed to be the fundamental pathophysiologic mechanism that leads to the transition to impaired diastolic reserve. However, the contribution of other mechanisms affecting active and passive components of diastolic function has not been comprehensively assessed. In this study, we investigated the potential role of impaired myocardial oxygen delivery in the pathophysiology of\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              .\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              Patients with\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              , those with controlled hypertension, and healthy controls underwent simultaneous right\u2010heart catheterization, echocardiography, and paired arterial and coronary sinus blood gas sampling at rest and during supine\u2010cycle ergometry. Despite a lower workload (\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              vs control, hypertension: 43\u00b18 versus 114\u00b112, 87\u00b114\u00a0W;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001 and\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05, respectively), peak exercise pulmonary capillary wedge pressure was markedly higher in\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              patients compared with healthy and hypertensive controls (32\u00b12 versus 16\u00b11 and 17\u00b11\u00a0mm\u00a0Hg, both\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001). During exercise, the transcardiac oxygen gradient increased significantly in all groups; however, the peak transcardiac oxygen gradient was significantly lower in\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              patients (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). In addition, the left ventricular\u2013work corrected transcardiac oxygen gradient remained significantly lower in\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              patients compared with controls (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The current study provides unique data suggesting that the abnormal diastolic reserve observed during exertion in\n              <jats:styled-content style=\"fixed-case\">HFPEF<\/jats:styled-content>\n              patients may, in part, be explained by impaired myocardial oxygen delivery due possibly to microvascular dysfunction. Further studies are required to confirm the structural and functional basis of these findings and to investigate the influence of potential therapies on this abnormality.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.114.001293","type":"journal-article","created":{"date-parts":[[2014,12,3]],"date-time":"2014-12-03T06:12:20Z","timestamp":1417587140000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":63,"title":["Impaired Myocardial Oxygen Availability Contributes to Abnormal Exercise Hemodynamics in Heart Failure With Preserved Ejection Fraction"],"prefix":"10.1161","volume":"3","author":[{"given":"Vanessa P. 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