title: Percutaneous Coronary Intervention Enhances Accelerative Wave Intensity in Coronary Arteries.
abstract: BACKGROUND
  The systolic forward travelling compression wave (sFCW) and diastolic backward travelling decompression waves (dBEW) predominantly accelerate coronary blood flow. The effect of a coronary stenosis on the intensity of these waves in the distal vessel is unknown. We investigated the relationship between established physiological indices of hyperemic coronary flow and the intensity of the two major accelerative coronary waves identified by Coronary Wave Intensity analysis (CWIA).
  Simultaneous intracoronary pressure and velocity measurement was performed during adenosine induced hyperemia in 17 patients with pressure / Doppler flow wires positioned distal to the target lesion. CWI profiles were generated from this data. Fractional Flow Reserve (FFR) and Coronary Flow Velocity Reserve (CFVR) were calculated concurrently. The intensity of the dBEW was significantly correlated with FFR (R = -0.70, P = 0.003) and CFVR (R = -0.73, P = 0.001). The intensity of the sFCW was also significantly correlated with baseline FFR (R = 0.71, p = 0.002) and CFVR (R = 0.59, P = 0.01). Stenting of the target lesion resulted in a median 178% (interquartile range 55-280%) (P<0.0001) increase in sFCW intensity and a median 117% (interquartile range 27-509%) (P = 0.001) increase in dBEW intensity. The increase in accelerative wave intensity following PCI was proportionate to the baseline FFR and CFVR, such that stenting of lesions associated with the greatest flow limitation (lowest FFR and CFVR) resulted in the largest increases in wave intensity.
  
  
  CONCLUSIONS
  Increasing ischemia severity is associated with proportionate reductions in cumulative intensity of both major accelerative coronary waves. Impaired diastolic microvascular decompression may represent a novel, important pathophysiologic mechanism driving the reduction in coronary blood flow in the setting of an epicardial stenosis.
authors.affiliation: Monash Cardiovascular Research Centre, MonashHeart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia.
authors.forename: Om
authors.initials: O
authors.lastname: Narayan
authors.affiliation: Monash Cardiovascular Research Centre, MonashHeart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia.
authors.forename: Michael C H
authors.initials: MC
authors.lastname: Leung
authors.affiliation: Monash Cardiovascular Research Centre, MonashHeart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia.
authors.forename: Dennis T L
authors.initials: DT
authors.lastname: Wong
authors.affiliation: Monash Cardiovascular Research Centre, MonashHeart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia.
authors.forename: Ian T
authors.initials: IT
authors.lastname: Meredith
authors.affiliation: Monash Cardiovascular Research Centre, MonashHeart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia.
authors.forename: James D
authors.initials: JD
authors.lastname: Cameron
mesh_terms: D000241:Adenosine; D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D015906:Angioplasty, Balloon, Coronary; D001783:Blood Flow Velocity; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D005260:Female; D053805:Fractional Flow Reserve, Myocardial; D006801:Humans; D006940:Hyperemia / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D015607:Stents
chemical_list: D000241:Adenosine