Sukhjinder S Nijjer1, Ricardo Petraco1, Tim P van de Hoef1, Sayan Sen1, Martijn A van Lavieren1, Rodney A Foale1, Martijn Meuwissen1, Christopher Broyd1, Mauro Echavarria-Pinto1, Rasha Al-Lamee1, Nicolas Foin1, Amarjit Sethi1, Iqbal S Malik1, Ghada W Mikhail1, Alun D Hughes1, Jamil Mayet1, Darrel P Francis1, Carlo Di Mario1, Javier Escaned1, Jan J Piek1, Justin E Davies2. 1. From the National Heart and Lung Institute, Imperial College London, London, United Kingdom (S.S.N., R.P., S.S., R.A.F., C.B., R.A.-L., N.F., A.S., I.S.M., G.W.M., A.D.H., J.M., D.P.F., C.D.M., J.E.D.); AMC Heart Centre, Amsterdam Medical Centre, Amsterdam, The Netherlands (T.P.v.d.H., M.A.v.L., J.J.P.); Cardiovascular Institute, Hospital Clínico San Carlos, Madrid, Spain (M.E.-P., J.E.); Department of Cardiology, Amphia Hospital, Breda, The Netherlands (M.M.); and Cardiovascular National Institute of Health Research Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom (C.D.M.). 2. From the National Heart and Lung Institute, Imperial College London, London, United Kingdom (S.S.N., R.P., S.S., R.A.F., C.B., R.A.-L., N.F., A.S., I.S.M., G.W.M., A.D.H., J.M., D.P.F., C.D.M., J.E.D.); AMC Heart Centre, Amsterdam Medical Centre, Amsterdam, The Netherlands (T.P.v.d.H., M.A.v.L., J.J.P.); Cardiovascular Institute, Hospital Clínico San Carlos, Madrid, Spain (M.E.-P., J.E.); Department of Cardiology, Amphia Hospital, Breda, The Netherlands (M.M.); and Cardiovascular National Institute of Health Research Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom (C.D.M.). Justin.Davies@imperial.ac.uk.
Abstract
BACKGROUND: Percutaneous coronary intervention (PCI) aims to increase coronary blood flow by relieving epicardial obstruction. However, no study has objectively confirmed this and assessed changes in flow over different phases of the cardiac cycle. We quantified the change in resting and hyperemic flow velocity after PCI in stenoses defined physiologically by fractional flow reserve and other parameters. METHODS AND RESULTS: Seventy-five stenoses (67 patients) underwent paired flow velocity assessment before and after PCI. Flow velocity was measured over the whole cardiac cycle and the wave-free period. Mean fractional flow reserve was 0.68±0.02. Pre-PCI, hyperemic flow velocity is diminished in stenoses classed as physiologically significant compared with those classed nonsignificant (P<0.001). In significant stenoses, flow velocity over the resting wave-free period and hyperemic flow velocity did not differ statistically. After PCI, resting flow velocity over the wave-free period increased little (5.6±1.6 cm/s) and significantly less than hyperemic flow velocity (21.2±3 cm/s; P<0.01). The greatest increase in hyperemic flow velocity was observed when treating stenoses below physiological cut points; treating stenoses with fractional flow reserve ≤0.80 gained Δ28.5±3.8 cm/s, whereas those fractional flow reserve >0.80 had a significantly smaller gain (Δ4.6±2.3 cm/s; P<0.001). The change in pressure-only physiological indices demonstrated a curvilinear relationship to the change in hyperemic flow velocity but was flat for resting flow velocity. CONCLUSIONS: Pre-PCI physiology is strongly associated with post-PCI increase in hyperemic coronary flow velocity. Hyperemic flow velocity increases 6-fold more when stenoses classed as physiologically significant undergo PCI than when nonsignificant stenoses are treated. Resting flow velocity measured over the wave-free period changes at least 4-fold less than hyperemic flow velocity after PCI.
BACKGROUND: Percutaneous coronary intervention (PCI) aims to increase coronary blood flow by relieving epicardial obstruction. However, no study has objectively confirmed this and assessed changes in flow over different phases of the cardiac cycle. We quantified the change in resting and hyperemic flow velocity after PCI in stenoses defined physiologically by fractional flow reserve and other parameters. METHODS AND RESULTS: Seventy-five stenoses (67 patients) underwent paired flow velocity assessment before and after PCI. Flow velocity was measured over the whole cardiac cycle and the wave-free period. Mean fractional flow reserve was 0.68±0.02. Pre-PCI, hyperemic flow velocity is diminished in stenoses classed as physiologically significant compared with those classed nonsignificant (P<0.001). In significant stenoses, flow velocity over the resting wave-free period and hyperemic flow velocity did not differ statistically. After PCI, resting flow velocity over the wave-free period increased little (5.6±1.6 cm/s) and significantly less than hyperemic flow velocity (21.2±3 cm/s; P<0.01). The greatest increase in hyperemic flow velocity was observed when treating stenoses below physiological cut points; treating stenoses with fractional flow reserve ≤0.80 gained Δ28.5±3.8 cm/s, whereas those fractional flow reserve >0.80 had a significantly smaller gain (Δ4.6±2.3 cm/s; P<0.001). The change in pressure-only physiological indices demonstrated a curvilinear relationship to the change in hyperemic flow velocity but was flat for resting flow velocity. CONCLUSIONS: Pre-PCI physiology is strongly associated with post-PCI increase in hyperemic coronary flow velocity. Hyperemic flow velocity increases 6-fold more when stenoses classed as physiologically significant undergo PCI than when nonsignificant stenoses are treated. Resting flow velocity measured over the wave-free period changes at least 4-fold less than hyperemic flow velocity after PCI.
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