{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T22:31:04Z","timestamp":1761863464848,"version":"3.41.2"},"reference-count":51,"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":[[2015,8,25]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Coronary artery disease and left ventricular hypertrophy are prevalent in the chronic kidney disease (\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              ) and renal transplant (\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              ) population. Advances in cardiovascular magnetic resonance (\n              <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content>\n              ) with blood oxygen level\u2013dependent (\n              <jats:styled-content style=\"fixed-case\">BOLD<\/jats:styled-content>\n              ) technique provides capability to assess myocardial oxygenation as a measure of ischemia. We hypothesized that the myocardial oxygenation response to stress would be impaired in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              patients.\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              Fifty\u2010three subjects (23 subjects with\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              , 10\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              recipients, 10 hypertensive (\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              ) controls, and 10 normal controls without known coronary artery disease) underwent\n              <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content>\n              scanning. All groups had cine and\n              <jats:styled-content style=\"fixed-case\">BOLD CMR<\/jats:styled-content>\n              at 3\u00a0T. The\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              groups also had late gadolinium\n              <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content>\n              to assess infarction\/replacement fibrosis. The\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              group underwent 2\u2010dimensional echocardiography strain to assess fibrosis. Myocardial oxygenation was measured at rest and under stress with adenosine (140\u00a0\u03bcg\/kg per minute) using\n              <jats:styled-content style=\"fixed-case\">BOLD<\/jats:styled-content>\n              signal intensity. A total of 2898 myocardial segments (1200 segments in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              patients, 552 segments in\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              , 480 segments in\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              , and 666 segments in normal controls) were compared using linear mixed modeling. Diabetes mellitus (\n              <jats:italic>P<\/jats:italic>\n              =0.47) and hypertension (\n              <jats:italic>P<\/jats:italic>\n              =0.57) were similar between\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              ,\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              , and\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              groups. The mean\n              <jats:styled-content style=\"fixed-case\">BOLD<\/jats:styled-content>\n              signal intensity change was significantly lower in the\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              groups compared to\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              controls and normal controls (\u22120.89\u00b110.63% in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              versus 5.66\u00b17.87% in\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              versus 15.54\u00b19.58% in\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              controls versus 16.19\u00b111.11% in normal controls,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001).\n              <jats:styled-content style=\"fixed-case\">BOLD<\/jats:styled-content>\n              signal intensity change was associated with estimated glomerular filtration rate (\u03b2=0.16, 95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              =0.10 to 0.22,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001). Left ventricular mass index and left ventricular septal wall diameter were similar between the\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              predialysis,\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              , and\n              <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n              groups. None of the\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              patients had impaired global longitudinal strain and none of the\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              group had late gadolinium hyperenhancement.\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              Myocardial oxygenation response to stress is impaired in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              patients and\n              <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\n              recipients without known coronary artery disease, and unlikely to be solely accounted for by the presence of diabetes mellitus, left ventricular hypertrophy, or myocardial scarring. The impaired myocardial oxygenation in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              patients may be associated with declining renal function. Noncontrast\n              <jats:styled-content style=\"fixed-case\">BOLD CMR<\/jats:styled-content>\n              is a promising tool for detecting myocardial ischemia in the\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              population.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.115.002249","type":"journal-article","created":{"date-parts":[[2015,8,11]],"date-time":"2015-08-11T02:00:11Z","timestamp":1439258411000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":15,"title":["Impaired Myocardial Oxygenation Response to Stress in Patients With Chronic Kidney Disease"],"prefix":"10.1161","volume":"4","author":[{"given":"Susie","family":"Parnham","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"School of Medicine, Flinders University, Bedford Park, South Australia, Australia"},{"name":"South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan M.","family":"Gleadle","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"School of Medicine, Flinders University, Bedford Park, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sripal","family":"Bangalore","sequence":"additional","affiliation":[{"name":"Cardiac Catheterization Laboratory, Cardiovascular Outcomes Group, New York University School of Medicine, New York, NY"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suchi","family":"Grover","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebecca","family":"Perry","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"School of Medicine, Flinders University, Bedford Park, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard J.","family":"Woodman","sequence":"additional","affiliation":[{"name":"Flinders Centre for Epidemiology and Biostatistics, School of Medicine, Flinders University, Bedford Park, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carmine G.","family":"De Pasquale","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"School of Medicine, Flinders University, Bedford Park, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph B.","family":"Selvanayagam","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia"},{"name":"School of Medicine, Flinders University, Bedford Park, South Australia, Australia"},{"name":"South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005101085"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004030203"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000061602.03327.E2"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000235527.81917.fe"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090765"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2006.11.042"},{"key":"e_1_3_3_8_2","first-page":"S16","article-title":"Epidemiology of cardiovascular disease in chronic renal disease","volume":"9","author":"Foley RN","year":"1998","unstructured":"Foley RN, Parfrey PS, Sarnak MJ. 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