title: Elevated augmentation index derived from peripheral arterial tonometry is associated with abnormal ventricular-vascular coupling.
abstract: BACKGROUND
  Although typically derived from the contour of arterial pressure waveform, augmentation index (AIx) may also be derived from the digital pulse volume waveform using finger plethysmography (peripheral arterial tonometry, PAT). Little is known regarding the physiologic correlates of AIx derived from PAT. In this study, we investigated the relation of PAT-AIx with measures of ventricular-vascular coupling.
  
  
  METHODS
  Pulse volume waves were measured via PAT and used to derive AIx. Using 2-dimensional echocardiography, effective arterial elastance index (EaI) was estimated as end-systolic pressure/stroke volume index. Left ventricular (LV) end-systolic elastance index (E(LV)I) was calculated as end-systolic pressure/end-systolic volume index. Ventricular-vascular coupling ratio was defined as EaI/E(LV)I.
  
  
  RESULTS
  Given the bi-directional nature of ventricular-vascular uncoupling as measured by echocardiography, patients were separated into three groups: low EaI/E(LV)I (<0.6, n = 21), optimal EaI/E(LV)I (mean 0.6-1.2, n = 16) and high EaI/E(LV)I (>1.2, n = 10). Adjusting for potential confounders (age, mean arterial pressure, height and heart rate), patients with optimal EaI/E(LV)I had lower AIx (1 +/- 4%, P<0.05) compared to those with low EaI/E(LV)I (13 +/- 4%) and high EaI/E(LV)I (19 +/- 5%).
  
  
  CONCLUSIONS
  Abnormal ventricular-vascular coupling, arising from either increased effective arterial elastance or increased ventricular elastance, is associated with increased AIx as measured by PAT. Additional research is needed to examine other vascular correlates of PAT-AIx.
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Kevin S
authors.initials: KS
authors.lastname: Heffernan
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Eshan A
authors.initials: EA
authors.lastname: Patvardhan
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Michael
authors.initials: M
authors.lastname: Hession
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Jenny
authors.initials: J
authors.lastname: Ruan
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Richard H
authors.initials: RH
authors.lastname: Karas
authors.affiliation: The Vascular Function Study Group, Division of Cardiology, Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
authors.forename: Jeffrey T
authors.initials: JT
authors.lastname: Kuvin
mesh_terms: D001158:Arteries / Q000503:physiopathology; D001794:Blood Pressure; D016009:Chi-Square Distribution; D003971:Diastole; D015150:Echocardiography, Doppler; D004548:Elasticity; D005260:Female; D005385:Fingers / Q000098:blood supply*; D006801:Humans; D008297:Male; D008365:Manometry; D008875:Middle Aged; D010991:Plethysmography; D011237:Predictive Value of Tests; D013318:Stroke Volume; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016277:Ventricular Function, Left; D017725:Ventricular Pressure