title: Pulsatile hemodynamics in patients with exertional dyspnea: potentially of value in the diagnostic evaluation of suspected heart failure with preserved ejection fraction.
abstract: OBJECTIVE
  This study sought to test whether measures of pulsatile arterial function are useful for diagnosing heart failure with preserved ejection fraction (HFPEF), in comparison with and in addition to tissue Doppler echocardiography (TDE).
  
  
  BACKGROUND
  Increased arterial stiffness and wave reflections are present in most patients with HFPEF.
  
  
  METHODS
  Patients with dyspnea as a major symptom were categorized as having HFPEF or no HFPEF, based on invasively derived filling pressures and natriuretic peptide levels. Pulse wave velocity (PWV) was measured invasively (aortic PWV). Aortic pulse pressure (aoPP) and its components (incident pressure wave height, forward wave amplitude; augmented pressure; backward wave amplitude [Pb]) were quantified noninvasively.
  
  
  RESULTS
  Seventy-one patients were classified as HFPEF and 65 as no HFPEF (223 patients had intermediate results). Patients with HFPEF were older, more often had hypertension and diabetes, and had larger left atria and higher left ventricular mass. Brachial pulse pressure (bPP), aoPP, and all measures of arterial stiffness and wave reflections were higher in HFPEF patients. Receiver-operating curve analysis-derived area under the curve (AUC) values for separating HFPEF from no HFPEF were 0.823 for E/E' at the medial annulus, the best TDE parameter; 0.816 for bPP; and 0.867, 0.851, and 0.825 for aortic PWV, aoPP, and Pb, respectively. Adding measures of pulsatile function to TDE resulted in an increase in AUC to 0.875 (bPP; p = 0.03) and 0.901 (aoPP; p = 0.005). In comparison with a TDE-based algorithm, net reclassification improvement was 32.9% (p < 0.0001).
  
  
  CONCLUSIONS
  Measures of pulsatile arterial hemodynamics may complement TDE for the diagnosis of HFPEF. (Pulsatile and Steady State Hemodynamics in Diastolic Heart Failure; NCT00720525).
authors.affiliation: Cardiology Department, Klinikum Wels-Grieskirchen, Wels, Austria. thomas.weber3@liwest.at
authors.forename: Thomas
authors.initials: T
authors.lastname: Weber
authors.forename: Siegfried
authors.initials: S
authors.lastname: Wassertheurer
authors.forename: Michael F
authors.initials: MF
authors.lastname: O'Rourke
authors.forename: Anton
authors.initials: A
authors.lastname: Haiden
authors.forename: Robert
authors.initials: R
authors.lastname: Zweiker
authors.forename: Martin
authors.initials: M
authors.lastname: Rammer
authors.forename: Bernhard
authors.initials: B
authors.lastname: Hametner
authors.forename: Bernd
authors.initials: B
authors.lastname: Eber
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D018450:Disease Progression; D004417:Dyspnea / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D015150:Echocardiography, Doppler; D005260:Female; D005500:Follow-Up Studies; D054144:Heart Failure, Diastolic / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D005082:Physical Exertion; D011379:Prognosis; D011446:Prospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume; D059289:Vascular Stiffness / Q000502:physiology*; D016277:Ventricular Function, Left