title: Assessment of endothelial function by non-invasive peripheral arterial tonometry predicts late cardiovascular adverse events.
abstract: OBJECTIVE
  There is growing need for the identification of novel non-invasive methodologies for the identification of individuals at risk for adverse cardiovascular (CV) events. We examined whether endothelial dysfunction, as detected by non-invasive peripheral arterial tonometry (EndoPAT), can predict late CV events.
  
  
  RESULTS
  Reactive hyperaemia (RH) was induced following upper arm occlusion of systolic blood pressure in 270 outpatients (54 +/- 12 years, 48% female). The natural logarithmic scaled RH index (L_RHI) was calculated from the ratio between the digital pulse volume during RH and at baseline. The patients were followed for CV adverse events (AE: cardiac death, myocardial infarction, revascularization or cardiac hospitalization) during a 7-year follow-up (inter-quartile range = 4.4-8). Cox models were used to estimate the association of EndoPAT results with AE adjusted for age. During the follow-up, AE occurred in 86 patients (31%). Seven-year AE rate was 48% in patients with L_RHI < 0.4 vs. 28% in those with L_RHI >or= 0.4 (P = 0.03). Additional univariate predictors of AE were advancing age (P = 0.02) and prior coronary bypass surgery (P = 0.01). The traditional Framingham risk score was not higher in patients with AE. Multivariate analysis identified L_RHI < 0.4 as an independent predictor of AE (P = 0.03).
  
  
  CONCLUSIONS
  A low RH signal detected by EndoPAT, consistent with endothelial dysfunction, was associated with higher AE rate during follow-up. L_RHI was an independent predictor of AE. Non-invasive assessment of peripheral vascular function may be useful for the identification of patients at risk for cardiac AEs.
authors.affiliation: Division of Cardiovascular Diseases, Center of Coronary Physiology and Imaging, Mayo College of Medicine, MB4 523, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Ronen
authors.initials: R
authors.lastname: Rubinshtein
authors.forename: Jeffrey T
authors.initials: JT
authors.lastname: Kuvin
authors.forename: Morgan
authors.initials: M
authors.lastname: Soffler
authors.forename: Ryan J
authors.initials: RJ
authors.lastname: Lennon
authors.forename: Shahar
authors.initials: S
authors.lastname: Lavi
authors.forename: Rebecca E
authors.initials: RE
authors.lastname: Nelson
authors.forename: Geralyn M
authors.initials: GM
authors.lastname: Pumper
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
mesh_terms: D001132:Arm / Q000098:blood supply; D001158:Arteries / Q000502:physiology; D003250:Constriction; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000175:diagnosis* / Q000503:physiopathology; D018570:Risk Assessment; D014664:Vasodilation / Q000502:physiology