title: Transfer function-derived central pressure and cardiovascular disease events: the Framingham Heart Study.
abstract: Relations between central pulse pressure (PP) or pressure amplification and major cardiovascular disease (CVD) events are controversial. Estimates of central aortic pressure derived using radial artery tonometry and a generalized transfer function may better predict CVD risk beyond the predictive value of brachial SBP.
  
  
  
  Augmentation index, central SBP, central PP, and central-to-peripheral PP amplification were evaluated using radial artery tonometry and a generalized transfer function as implemented in the SphygmoCor device (AtCor Medical, Itasca, Illinois, USA). We used proportional hazards models to examine relations between central hemodynamics and first-onset major CVD events in 2183 participants (mean age 62 years, 58% women) in the Framingham Heart Study.
  
  
  
  During median follow-up of 7.8 (limits 0.2-8.9) years, 149 participants (6.8%) had an incident event. Augmentation index (P = 0.6), central aortic systolic pressure (P = 0.20), central aortic PP (P = 0.24), and PP amplification (P = 0.15) were not related to CVD events in multivariable models that adjusted for age, sex, brachial cuff systolic pressure, use of antihypertensive therapy, total and high-density lipoprotein cholesterol concentrations, smoking, and presence of diabetes. In a model that included standard risk factors, model fit was improved (P = 0.03) when brachial systolic pressure was added after central, whereas model fit was not improved (P = 0.30) when central systolic pressure was added after brachial.
  
  
  
  After considering standard risk factors, including brachial cuff SBP, augmentation index, central PP and PP amplification derived using radial artery tonometry, and a generalized transfer function were not predictive of CVD risk.
authors.affiliation: aCardiovascular Engineering, Inc., Norwood bBoston University and NHLBI's Framingham Study, Framingham, Massachusetts cPopulation Sciences Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland dBiostatistics Department, Boston University School of Public Health eEvans Department of Medicine fWhitaker Cardiovascular Institute gSection of Preventive Medicine, Boston University School of Medicine hDepartment of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, USA *Joseph A. Vita deceased.
authors.forename: Gary F
authors.initials: GF
authors.lastname: Mitchell
authors.forename: Shih-Jen
authors.initials: SJ
authors.lastname: Hwang
authors.forename: Martin G
authors.initials: MG
authors.lastname: Larson
authors.forename: Naomi M
authors.initials: NM
authors.lastname: Hamburg
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
authors.forename: Daniel
authors.initials: D
authors.lastname: Levy
authors.forename: Joseph A
authors.initials: JA
authors.lastname: Vita
mesh_terms: D000368:Aged; D062186:Arterial Pressure; D001794:Blood Pressure; D001795:Blood Pressure Determination; D001916:Brachial Artery / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008365:Manometry; D008875:Middle Aged; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D017534:Radial Artery / Q000503:physiopathology; D012307:Risk Factors; D013599:Systole