title: Does the instantaneous wave-free ratio approximate the fractional flow reserve?
abstract: OBJECTIVE
  This study sought to examine the clinical performance of and theoretical basis for the instantaneous wave-free ratio (iFR) approximation to the fractional flow reserve (FFR).
  
  
  BACKGROUND
  Recent work has proposed iFR as a vasodilation-free alternative to FFR for making mechanical revascularization decisions. Its fundamental basis is the assumption that diastolic resting myocardial resistance equals mean hyperemic resistance.
  
  
  METHODS
  Pressure-only and combined pressure-flow clinical data from several centers were studied both empirically and by using pressure-flow physiology. A Monte Carlo simulation was performed by repeatedly selecting random parameters as if drawing from a cohort of hypothetical patients, using the reported ranges of these physiologic variables.
  
  
  RESULTS
  We aggregated observations of 1,129 patients, including 120 with combined pressure-flow data. Separately, we performed 1,000 Monte Carlo simulations. Clinical data showed that iFR was +0.09 higher than FFR on average, with ±0.17 limits of agreement. Diastolic resting resistance was 2.5 ± 1.0 times higher than mean hyperemic resistance in patients. Without invoking wave mechanics, classic pressure-flow physiology explained clinical observations well, with a coefficient of determination of >0.9. Nearly identical scatter of iFR versus FFR was seen between simulation and patient observations, thereby supporting our model.
  
  
  CONCLUSIONS
  iFR provides both a biased estimate of FFR, on average, and an uncertain estimate of FFR in individual cases. Diastolic resting myocardial resistance does not equal mean hyperemic resistance, thereby contravening the most basic condition on which iFR depends. Fundamental relationships of coronary pressure and flow explain the iFR approximation without invoking wave mechanics.
authors: Weatherhead PET Center For Preventing and Reversing Atherosclerosis, Division of Cardiology, Department of Medicine, University of Texas Medical School and Memorial Hermann Hospital, Houston, Texas.
authors: Nils P
authors: NP
authors: Johnson
authors: Richard L
authors: RL
authors: Kirkeeide
authors: Kaleab N
authors: KN
authors: Asrress
authors: William F
authors: WF
authors: Fearon
authors: Timothy
authors: T
authors: Lockie
authors: Koen M J
authors: KM
authors: Marques
authors: Stylianos A
authors: SA
authors: Pyxaras
authors: M Cristina
authors: MC
authors: Rolandi
authors: Marcel
authors: M
authors: van 't Veer
authors: Bernard
authors: B
authors: De Bruyne
authors: Jan J
authors: JJ
authors: Piek
authors: Nico H J
authors: NH
authors: Pijls
authors: Simon
authors: S
authors: Redwood
authors: Maria
authors: M
authors: Siebes
authors: Jos A E
authors: JA
authors: Spaan
authors: K Lance
authors: KL
authors: Gould
mesh_terms: D000241:Adenosine / Q000008:administration & dosage; D001783:Blood Flow Velocity / Q000502:physiology*; D023921:Coronary Stenosis / Q000175:diagnosis* / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology; D053805:Fractional Flow Reserve, Myocardial / Q000502:physiology*; D006801:Humans; D006940:Hyperemia / Q000175:diagnosis; D008955:Models, Cardiovascular; D009010:Monte Carlo Method; D009200:Myocardial Contraction / Q000502:physiology*; D009204:Myocardial Revascularization; D014655:Vascular Resistance / Q000502:physiology; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine