BACKGROUND: Pulmonary vascular resistance (PVR) is the current standard for evaluating reactivity in children with pulmonary arterial hypertension (PAH). However, PVR measures only the mean component of right ventricular afterload and neglects pulsatile effects. We recently developed and validated a method to measure pulmonary vascular input impedance, which revealed excellent correlation between the zero harmonic impedance value and PVR and suggested a correlation between higher-harmonic impedance values and pulmonary vascular stiffness. Here we show that input impedance can be measured routinely and easily in the catheterization laboratory, that impedance provides PVR and pulmonary vascular stiffness from a single measurement, and that impedance is a better predictor of disease outcomes compared with PVR. METHODS: Pressure and velocity waveforms within the main pulmonary artery were measured during right heart catheterization of patients with normal pulmonary artery hemodynamics (n = 14) and those with PAH undergoing reactivity evaluation (49 subjects, 95 conditions). A correction factor needed to transform velocity into flow was obtained by calibrating against cardiac output. Input impedance was obtained off-line by dividing Fourier-transformed pressure and flow waveforms. RESULTS: Exceptional correlation was found between the indexed zero harmonic of impedance and indexed PVR (y = 1.095x + 1.381, R2 = 0.9620). In addition, the modulus sum of the first 2 harmonics of impedance was found to best correlate with indexed pulse pressure over stroke volume (y = 13.39x - 0.8058, R2 = 0.7962). Among a subset of patients with PAH (n = 25), cumulative logistic regression between outcomes to total indexed impedance was better (R(L)2 = 0.4012) than between outcomes and indexed PVR (R(L)2 = 0.3131). CONCLUSIONS: Input impedance can be consistently and easily obtained from pulse-wave Doppler and a single catheter pressure measurement, provides comprehensive characterization of the main components of RV afterload, and better predicts patient outcomes compared with PVR alone.
BACKGROUND: Pulmonary vascular resistance (PVR) is the current standard for evaluating reactivity in children with pulmonary arterial hypertension (PAH). However, PVR measures only the mean component of right ventricular afterload and neglects pulsatile effects. We recently developed and validated a method to measure pulmonary vascular input impedance, which revealed excellent correlation between the zero harmonic impedance value and PVR and suggested a correlation between higher-harmonic impedance values and pulmonary vascular stiffness. Here we show that input impedance can be measured routinely and easily in the catheterization laboratory, that impedance provides PVR and pulmonary vascular stiffness from a single measurement, and that impedance is a better predictor of disease outcomes compared with PVR. METHODS: Pressure and velocity waveforms within the main pulmonary artery were measured during right heart catheterization of patients with normal pulmonary artery hemodynamics (n = 14) and those with PAH undergoing reactivity evaluation (49 subjects, 95 conditions). A correction factor needed to transform velocity into flow was obtained by calibrating against cardiac output. Input impedance was obtained off-line by dividing Fourier-transformed pressure and flow waveforms. RESULTS: Exceptional correlation was found between the indexed zero harmonic of impedance and indexed PVR (y = 1.095x + 1.381, R2 = 0.9620). In addition, the modulus sum of the first 2 harmonics of impedance was found to best correlate with indexed pulse pressure over stroke volume (y = 13.39x - 0.8058, R2 = 0.7962). Among a subset of patients with PAH (n = 25), cumulative logistic regression between outcomes to total indexed impedance was better (R(L)2 = 0.4012) than between outcomes and indexed PVR (R(L)2 = 0.3131). CONCLUSIONS: Input impedance can be consistently and easily obtained from pulse-wave Doppler and a single catheter pressure measurement, provides comprehensive characterization of the main components of RV afterload, and better predicts patient outcomes compared with PVR alone.
Authors: C Stefanadis; J Dernellis; C Vlachopoulos; C Tsioufis; E Tsiamis; K Toutouzas; C Pitsavos; P Toutouzas Journal: Circulation Date: 1997-09-16 Impact factor: 29.690
Authors: C Stefanadis; J Dernellis; E Tsiamis; C Stratos; L Diamantopoulos; A Michaelides; P Toutouzas Journal: Eur Heart J Date: 2000-03 Impact factor: 29.983
Authors: G F Mitchell; L A Moyé; E Braunwald; J L Rouleau; V Bernstein; E M Geltman; G C Flaker; M A Pfeffer Journal: Circulation Date: 1997-12-16 Impact factor: 29.690
Authors: Craig E Weinberg; Jean R Hertzberg; D Dunbar Ivy; K Scott Kirby; K Chen Chan; Lilliam Valdes-Cruz; Robin Shandas Journal: Circulation Date: 2004-10-18 Impact factor: 29.690
Authors: Michal Schäfer; Cynthia Myers; R Dale Brown; Maria G Frid; Wei Tan; Kendall Hunter; Kurt R Stenmark Journal: Curr Hypertens Rep Date: 2016-01 Impact factor: 5.369
Authors: Steven R Lammers; Phil H Kao; H Jerry Qi; Kendall Hunter; Craig Lanning; Joseph Albietz; Stephen Hofmeister; Robert Mecham; Kurt R Stenmark; Robin Shandas Journal: Am J Physiol Heart Circ Physiol Date: 2008-07-25 Impact factor: 4.733
Authors: Michal Schäfer; D Dunbar Ivy; Steven H Abman; Alex J Barker; Lorna P Browne; Brian Fonseca; Vitaly Kheyfets; Kendall S Hunter; Uyen Truong Journal: Circ Cardiovasc Imaging Date: 2017-02 Impact factor: 7.792
Authors: Corey E Ventetuolo; Nicole B Gabler; Jason S Fritz; K Akaya Smith; Harold I Palevsky; James R Klinger; Scott D Halpern; Steven M Kawut Journal: Circulation Date: 2014-06-20 Impact factor: 29.690
Authors: A Bellofiore; J Henningsen; C G Lepak; L Tian; A Roldan-Alzate; H B Kellihan; D W Consigny; C J Francois; N C Chesler Journal: J Biomech Eng Date: 2015-02-05 Impact factor: 2.097
Authors: Kendall S Hunter; Justin K Gross; Craig J Lanning; K Scott Kirby; Karrie L Dyer; D Dunbar Ivy; Robin Shandas Journal: Congenit Heart Dis Date: 2008 Mar-Apr Impact factor: 2.007