title: Atherosclerosis and left ventricular hypertrophy: persisting problems in treated hypertensive patients.
abstract: OBJECTIVE
  First, to determine whether hypertensive patients managed in general practice have more advanced atherosclerosis and left ventricular hypertrophy than matched normotensive patients from the same practices. Second, to investigate the associations of several potentially modifiable factors with these vascular and cardiac outcomes.
  
  
  METHODS
  We performed a case-control study of 500 hypertensive cases (systolic blood pressure > or = 160 mmHg or diastolic blood pressure > or = 95 mmHg or receiving treatment) and 506 age- (mean 61 years) and sex- (54% female) matched normotensive controls recruited from general practices. Carotid artery far wall thickness (CWT), assessed by B-mode ultrasound, and left ventricular mass (LVM), assessed by M-mode echocardiography, were the main study outcome measures.
  
  
  RESULTS
  Mean systolic/diastolic blood pressure levels in the 399 treated cases (145/87 mmHg) were lower than those in untreated cases (158/94 mmHg) but higher than those in controls (133/82 mmHg, all P < 0.0001). Mean body mass index (BMI) and total triglyceride levels were higher and high-density lipoprotein cholesterol was lower in cases than in controls (all P < 0.0004). Mean CWT was 10% greater in cases than in controls and LVM was 14% greater (both P < 0.001), but both were similar in treated and untreated cases (P > 0.05). In multivariate analyses, blood pressure and BMI were both directly and independently related to CWT and LVM (both P < 0.0001).
  
  
  CONCLUSIONS
  In this study, hypertensive patients managed in general practice - whether treated with antihypertensive drugs or not - had more advanced atherosclerosis and left ventricular hypertrophy than did matched normotensive patients. Efforts to lower blood pressure further and to reduce BMI could potentially reduce these differences, and this might lead to a reduction in the risk of major cardiovascular events.
authors.affiliation: Clinical Trials Research Unit, The University of Auckland, New Zealand. gd.gamble@auckland.ac.nz
authors.forename: G
authors.initials: G
authors.lastname: Gamble
authors.forename: S
authors.initials: S
authors.lastname: MacMahon
authors.forename: A
authors.initials: A
authors.lastname: Culpan
authors.forename: C
authors.initials: C
authors.lastname: Ciobo
authors.forename: G
authors.initials: G
authors.lastname: Whalley
authors.forename: N
authors.initials: N
authors.lastname: Sharpe
mesh_terms: D000368:Aged; D001161:Arteriosclerosis / Q000209:etiology*; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D004452:Echocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D014280:Triglycerides