{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T23:14:54Z","timestamp":1769210094874,"version":"3.49.0"},"reference-count":40,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2016,4,13]],"date-time":"2016-04-13T00:00:00Z","timestamp":1460505600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>BACKGROUND<\/jats:title>\n                  <jats:p>The average of multiple blood pressure (BP) readings (mean BP) independently predicts target organ damage (TOD). Observational studies have also shown an independent relationship between BP variability (BPV) and TOD, but there is limited longitudinal data. This study aimed to determine the effects of changes in mean BP levels compared with BPV on left ventricular mass index (LVMI) and aortic pulse wave velocity (aPWV).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>Mean BP levels (research-protocol clinic BP (clinic BP), 24-hour ambulatory BP, and 7-day home BP) and BPV were assessed in 286 patients with uncomplicated hypertension (mean age 64\u00b18 SD years, 53% women) over 12 months. Reading-to-reading BPV (from 24-hour ambulatory BP) and day-to-day BPV (from 7-day home BP) were assessed at baseline and 12 months, and visit-to-visit BPV (clinic BP) was assessed from 5 visits over 12 months. LVMI was measured by 3D echocardiography and aPWV with applanation tonometry.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>The strongest predictors of the changes in LVMI (\u0394LVMI) were the changes in mean 24-hour systolic BPs (SBPs) ( P &amp;lt; 0.02). Similarly, the strongest predictors of the changes in aPWV (\u0394aPWV) were the changes in mean 24-hour ambulatory SBPs ( P &amp;lt; 0.01) and the changes in mean clinic SBP ( P &amp;lt; 0.001). However, none of the changes in BPV were independently associated with \u0394LVMI or \u0394aPWV ( P &amp;gt; 0.05 for all).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Changes in mean BP levels, but not BPV, were most relevant to changes in TOD in patients with uncomplicated hypertension. Thus, from this point of view, BPV appears to have limited clinical utility in this patient population.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ajh\/hpw037","type":"journal-article","created":{"date-parts":[[2016,4,14]],"date-time":"2016-04-14T03:54:24Z","timestamp":1460606064000},"page":"1046-1054","source":"Crossref","is-referenced-by-count":25,"title":["Blood Pressure Variability and Prediction of Target Organ Damage in Patients With Uncomplicated Hypertension"],"prefix":"10.1093","volume":"29","author":[{"given":"Panagiota","family":"Veloudi","sequence":"first","affiliation":[{"name":"Menzies Institute for Medical Research, University of Tasmania 1 , Hobart, Tasmania , Australia ;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher L.","family":"Blizzard","sequence":"additional","affiliation":[{"name":"Menzies Institute for Medical Research, University of Tasmania 1 , Hobart, Tasmania , Australia ;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Geoffrey A.","family":"Head","sequence":"additional","affiliation":[{"name":"Baker IDI Heart and Diabetes Institute 2 , Melbourne, Victoria , Australia ;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Walter P.","family":"Abhayaratna","sequence":"additional","affiliation":[{"name":"Canberra Hospital, College of Medicine, Biology and Environment, Australian National University 3 , Garran, Canberra , Australia ;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Stowasser","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, School of Medicine, University of Queensland 4 , Brisbane, Queensland , Australia ."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James E.","family":"Sharman","sequence":"additional","affiliation":[{"name":"Menzies Institute for Medical Research, University of Tasmania 1 , Hobart, Tasmania , 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