title: Losartan but not atenolol reduce carotid artery hypertrophy in essential hypertension. A LIFE substudy.
abstract: BACKGROUND
  We wanted to investigate whether treatment with losartan, an angiotensin II receptor blocker, induced regression of carotid artery hypertrophy as compared to the beta-receptor blocker, atenolol.
  
  
  METHODS
  In 45 patients recruited for the LIFE Study with stage II-III hypertension and ECG left ventricular (LV) hypertrophy, we measured blood pressure, intima-media thickness (IMT) and lumen in the common carotid arteries by ultrasound, and minimal forearm vascular resistance (MFVR) by plethysmography, after 2 weeks of placebo treatment and after 1, 2 and 3 years of anti-hypertensive treatment with either atenolol- or losartan-based regimens. We measured the same parameters in 26 normal subjects matched for age and gender.
  
  
  RESULTS
  The patients had as compared to normotensive controls higher IMT (0.87 vs 0.76 mm, p = 0.001) and intima-media cross-sectional area (IMA) (19.7 vs 15.5 mm2, p<0.001). Systolic and diastolic blood pressures were reduced to the same degree in patients treated with losartan as compared to atenolol. However, IMA decreased significantly only in patients treated with losartan (19.2 vs 17.6 mm2, p = 0.001) and the average relative decrease in IMA during the 3 years of treatment was significantly higher in patients treated with losartan as compared to atenolol (-7.4 vs -2.0%, p<0.05).
  
  
  CONCLUSIONS
  Patients with hypertension and LV hypertrophy had hypertrophy of the common carotid arteries. Losartan, but not atenolol, induced regression of this hypertrophy. Because carotid artery hypertrophy has been associated with strokes, our findings may explain the lower incidence of strokes in the LIFE study in patients treated with losartan as compared to atenolol.
authors.affiliation: Departemtn fo Clinical Physiology and Nuclear Medicine, Glostrup University Hospital, Copenhagen, Denmark. mho@dadlnet.dk
authors.forename: Michael H
authors.initials: MH
authors.lastname: Olsen
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Keld
authors.initials: K
authors.lastname: Neland
authors.forename: Jonathan N
authors.initials: JN
authors.lastname: Bella
authors.forename: Jens
authors.initials: J
authors.lastname: Rokkedal
authors.forename: Harriet
authors.initials: H
authors.lastname: Dige-Petersen
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
mesh_terms: D000368:Aged; D001262:Atenolol / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000473:pathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D013995:Time; D016896:Treatment Outcome; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology; D014463:Ultrasonography
chemical_list: D001262:Atenolol; D019808:Losartan