title: Monitoring of the central pulse pressure is useful for detecting cardiac overload during antiadrenergic treatment: the Japan Morning Surge 1 study.
abstract: OBJECTIVE
  Lowering of the central pulse pressure (PP) has been shown to contribute to an improvement of the cardiac damage beyond that of lowering the brachial PP. We assessed the hypothesis that the change in the central PP is more useful than that in the brachial PP in the assessment of the change in cardiac load.
  
  
  METHODS
  We studied 434 treated hypertensive patients whose home systolic blood pressure was 135 mmHg or higher. They were followed for 6 months after allocation to either a control group or an added treatment group (doxazosin 1-4 mg and atenolol when needed). We measured the brachial and central (carotid) blood pressure simultaneously using a validated device, and the B-type natriuretic peptide at baseline and at the sixth month of treatment.
  
  
  RESULTS
  In the added treatment group, the brachial systolic blood pressure was successfully reduced, but the central PP increased significantly, whereas the other blood pressure parameters did not change from the baseline. In the added treatment group, the change in the B-type natriuretic peptide was significantly correlated with the change in the brachial PP (r = 0.18), central systolic blood pressure (r = 0.18), central PP (r = 0.26), and PP amplification (r = -0.22) even after adjusting for the confounding factors. The correlation with the central PP was stronger than with the brachial PP (P = 0.018) or central systolic blood pressure (P = 0.002), and these relationships were essentially the same even after adjustment for the use of atenolol or the change in heart rate.
  
  
  CONCLUSIONS
  This study showed that the central PP measurement may be more important to assess cardiac load than the brachial PP during antiadrenergic treatment.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medicine, Jichi Medical University School of Medicine, Tochigi, Japan. yoshio@jichi.ac.jp
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Matsui
authors.forename: Kazuo
authors.initials: K
authors.lastname: Eguchi
authors.forename: Seiichi
authors.initials: S
authors.lastname: Shibasaki
authors.forename: Joji
authors.initials: J
authors.lastname: Ishikawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hoshide
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Pickering
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shimada
authors.forename: Kazuomi
authors.initials: K
authors.lastname: Kario
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000369:Aged, 80 and over; D001262:Atenolol / Q000627:therapeutic use; D015415:Biomarkers; D001794:Blood Pressure / Q000187:drug effects; D001795:Blood Pressure Determination / Q000379:methods; D001916:Brachial Artery / Q000187:drug effects* / Q000502:physiology; D002339:Carotid Arteries / Q000187:drug effects* / Q000502:physiology; D016022:Case-Control Studies; D017292:Doxazosin / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D007564:Japan; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D015415:Biomarkers; D020097:Natriuretic Peptide, Brain; D001262:Atenolol; D017292:Doxazosin