{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T20:40:46Z","timestamp":1790023246959,"version":"4.0.1"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,7]]},"abstract":"\n Background<\/jats:title>\n \n Patients with type 2 diabetes mellitus and elevated urinary albumin:creatinine ratio (\n ACR<\/jats:styled-content>\n ) have increased risk of heart failure. We hypothesized this was because of cardiac tissue changes rather than silent coronary artery disease.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n In a case\u2010controlled observational study 130 subjects including 50\n ACR<\/jats:styled-content>\n +ve diabetes mellitus patients with persistent microalbuminuria (\n ACR<\/jats:styled-content>\n >2.5\u00a0mg\/mol in males and >3.5\u00a0mg\/mol in females, \u22652 measurements, no previous renin\u2013angiotensin\u2013aldosterone therapy, 50\n ACR<\/jats:styled-content>\n \u2212ve diabetes mellitus patients and 30 controls underwent cardiovascular magnetic resonance for investigation of myocardial fibrosis, ischemia and infarction, and echocardiography. Thirty\n ACR<\/jats:styled-content>\n +ve patients underwent further testing after 1\u2010year treatment with renin\u2013angiotensin\u2013aldosterone blockade. Cardiac extracellular volume fraction, a measure of diffuse fibrosis, was higher in diabetes mellitus patients than controls (26.1\u00b13.4% and 23.3\u00b13.0%\n P<\/jats:italic>\n =0.0002) and in\n ACR<\/jats:styled-content>\n +ve than\n ACR<\/jats:styled-content>\n \u2212ve diabetes mellitus patients (27.2\u00b14.1% versus 25.1\u00b12.9%,\n P<\/jats:italic>\n =0.004).\n ACR<\/jats:styled-content>\n +ve patients also had lower E\u2032 measured by echocardiography (8.2\u00b11.9\u00a0cm\/s versus 8.9\u00b11.9\u00a0cm\/s,\n P<\/jats:italic>\n =0.04) and elevated high\u2010sensitivity cardiac troponin T 18% versus 4% \u226514\u00a0ng\/L (\n P<\/jats:italic>\n =0.05). Rate of silent myocardial ischemia or infarction were not influenced by\n ACR<\/jats:styled-content>\n status. Renin\u2013angiotensin\u2013aldosterone blockade was associated with increased left ventricular ejection fraction (59.3\u00b17.8 to 61.5\u00b18.7%,\n P<\/jats:italic>\n =0.03) and decreased extracellular volume fraction (26.5\u00b13.6 to 25.2\u00b13.1,\n P<\/jats:italic>\n =0.01) but no changes in diastolic function or high\u2010sensitivity cardiac troponin T levels.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Asymptomatic diabetes mellitus patients with persistent microalbuminuria have markers of diffuse cardiac fibrosis including elevated extracellular volume fraction, high\u2010sensitivity cardiac troponin T, and diastolic dysfunction, which may in part be reversible by renin\u2013angiotensin\u2013aldosterone blockade. Increased risk in these patients may be mediated by subclinical changes in tissue structure and function.<\/jats:p>\n <\/jats:sec>\n \n Clinical Trial Registration<\/jats:title>\n \n URL<\/jats:styled-content>\n :\n https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n . Unique identifier:\n NCT<\/jats:styled-content>\n 01970319.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.005539","type":"journal-article","created":{"date-parts":[[2017,7,17]],"date-time":"2017-07-17T20:10:31Z","timestamp":1500322231000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":75,"title":["Diabetes Mellitus, Microalbuminuria, and Subclinical Cardiac Disease: Identification and Monitoring of Individuals at Risk of Heart Failure"],"prefix":"10.1161","volume":"6","author":[{"given":"Peter P.","family":"Swoboda","sequence":"first","affiliation":[{"name":"Multidisciplinary Cardiovascular Research Centre & Division of Biomedical Imaging, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam K.","family":"McDiarmid","sequence":"additional","affiliation":[{"name":"Multidisciplinary Cardiovascular Research 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Institute of Cardiovascular and Metabolic Medicine, University of Leeds, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pankaj","family":"Garg","sequence":"additional","affiliation":[{"name":"Multidisciplinary Cardiovascular Research Centre & Division of Biomedical Imaging, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tarique A.","family":"Musa","sequence":"additional","affiliation":[{"name":"Multidisciplinary Cardiovascular Research Centre & Division of Biomedical Imaging, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus K.","family":"Witte","sequence":"additional","affiliation":[{"name":"Multidisciplinary Cardiovascular Research Centre & Division of Biomedical Imaging, Leeds Institute of Cardiovascular and Metabolic Medicine, 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