FFR CT : Beyond FFR. Bon-Kwon Koo, MD, PhD. Seoul National University Hospital, Seoul, Korea. Seoul National University Hospital Cardiovascular Center

Transcription

1 FFR CT : Beyond FFR Bon-Kwon Koo, MD, PhD, Seoul, Korea

2 Patient-specific non-invasive coronary hemodynamic assessment Non-invasive, Pt-specific Hemodynamics Pressure Pressure difference Pressure gradient Pressure recovery FFR Flow velocity Flow rate Shear rate Shear stress average, peak, gradient Traction Oscillatory shear index Particle residence time Turbulent kinetic energy.. Static Pulsatile Resting Hyperemic Exercise mild, moderate, peak 2

3 Non-invasive hemodynamic parameter measurement using computational fluid dynamics and ccta Rest Hyperemia Pressure Velocity Hemodynamics Pressure Pressure difference Pressure gradient Pressure recovery FFR Flow velocity Flow rate Shear rate Shear stress average, peak, gradient Traction Oscillatory shear index Particle residence time Turbulent kinetic energy.. 3

4 Image-based computerised modelling of coronary circulation: Potentials Pulsatile flow - rest Static flow - hyperemic Pulsatile flow - Hyperemia Pulsatile flow - Exercise 4

5 Why Does the Plaque Rupture? Mechanistic link between Hemodynamics and Acute Coronary Syndrome 6

6 We already know. Coronary plaque rupture is a critical event that triggers the initiation of acute coronary syndrome (ACS). Risk assessment for ACS Plaque Vulnerability: cap thickness, lipid core, inflammation, neovascularization, posterior attenuation.... 6

7 Why does the plaque rupture? Durability = Vulnerability :Mechanism of material failure Rest-onset ACS Exertion-triggered ACS Tanaka, et al. Circulation 28 The broken cap was much thinner in the rest-onset group than in the exertion group (5 vs. 9 μm, P<.1) External force Information on external force in addition to vulnerability can lead to better discrimination of the risk of plaque rupture. 7

8 What kind of forces are acting on the plaque? Pressure Pressure 8

9 Low wall shear stress Proliferative, pro-inflammatory, pro-thrombotic stimulus Malek AM, JAMA

10 Very high WSS vs. Vulnerability Very Slager, et al. Nature Clin Pract 25 1

11 Circulation

12 Prototype: Total plaque force model (May 29, 213).5 WSS ROI.5 TractionForce

13 Measurement of hemodynamic parameters in a patient using ccta and computational fluid dynamics Koo BK. International Symposium on Biomechanics

14 WSS in clinically relevant lesions 8 patients Clinically driven invasive coronary angiography and CT angiography Average % diameter stenosis: 52.3±12.4% WSS (dyne/cm 2 ) WSS (dyne/cm 2 ) Koo BK. International Symposium on Biomechanics

15 Relationship between WSS and pressure gradient Koo BK. International Symposium on Biomechanics

16 Relationship between WSS and lesion characteristics Determinants β 95% CI p Pressure Gradient Blood flow <.1 Distance from LM ostium Minimal lumen area <.1 Lesion length <.1 Koo BK. International Symposium on Biomechanics

17 Regional distribution of hemodynamic forces : Pressure gradient vs. WSS Plaque Shear force vector Projection Traction force vector Koo BK. International Symposium on Biomechanics

18 Wall Shear Stress [dyne/cm 2 ] FFR FFR vs. ACS FFR 1,5 FFR External Force Pressure gradient Length [mm] Vulnerability Wall shear stress Wall Shear Stress 3 2 ACS risk Length [mm] Koo BK. International Symposium on Biomechanics

19 WSS and pressure, are they enough? Pressure, FFR and WSS are high at the upstream segment of a plaque. Therefore, these parameters cannot explain the occurrence of downstream rupture. 19

20 WSS and pressure, then what else? Traction is the total force (stress) acting on vessel wall (plaque), and can be decomposed Proximal segment Distal segment Axial plaque stress is much larger than WSS and uniquely characterizes the upstream and downstream segments of coronary stenosis. JACC imaging 215, in press 2

21 Counts Counts Counts Counts Distribution of Axial Plaque Stress 4 3 Idealized stenosis models (n=264) Axial plaque stress upstream Proximal downstream Distal 25 2 Patients lesions (n=114) Axial plaque stress upstream Proximal downstream Distal Axial Axial Plaque plaque stress Stress [dyne/cm (dyne/cm 2 ]) x 1 4 Axial plaque force Distal segment N=264 Proximal segment N=264 upstream downstream Median: dyne/cm 2 Median: dyne/cm 2 IQR: , IQR: , Axial plaque force [dyne] x Axial Plaque plaque stress Stress [dyne/cm (dyne/cm 2 ]) x 1 4 Axial plaque force Distal segment N=114 Proximal segment N=114 upstream downstream Median: dyne/cm 2 Median: dyne/cm 2 IQR: , IQR: 655.9, Axial plaque force [dyne] x 1 4 Distribution of axial plaque stress is similar between idealized models and patients lesions. JACC imaging 215, in press 21

22 Stress [dyne/cm 2 ] Stress [dyne/cm 2 ] Distribution of Axial Plaque Stress in patients 12 APS WSS FFR CT APS [dyne/cm 2 ] Proximal segment Upstream Distal segment Downstream FFR CT APS [dyne/cm 2 ] Proximal segment Upstream Distal segment Downstream JACC imaging 215, in press 22

23 Upstream-dominant lesion Downstream-dominant lesion FFR WSS (dyne/cm 2 ) APS (dyne/cm 2 ) FFR WSS (dyne/cm 2 ) APS (dyne/cm 2 ) Lesion geometry vs. Hemodynamic forces Flow , Same morphology Different severity Proximal segment Distal segment Proximal segment Distal segment Flow Upstream dominant lesion Downstream dominant lesion 2 2,5 1 1 Same severity Different morphology Proximal segment Distal segment Proximal segment Distal segment JACC imaging 215, in press 23

24 Influence of Lesion Shape on Hemodynamic Parameters (n=114) Upstream-dominant lesion (n=56) Downstream-dominant lesion (n=58) % Diameter Stenosis FFR CT Axial Plaque Stress (dyne/cm 2 ) 6% 1 15 P<.1 P<.1 4%,8,6 1 2% % 1,4,2 1 5 Proximal segment Distal segment JACC imaging 215, in press 24

25 Future perspective CT, Asymptomatic Acute MI 25

26 Future perspective CT, Asymptomatic Acute MI APS Upstream 996 dyne/cm 2 Downstream 174 dyne/cm 2 26

27 Conclusion Hemodynamic forces acting on the plaque can be measured non-invasively using coronary CT angiography and computational fluid dynamics. Very high WSS promotes plaque vulnerability and is mainly determined by pressure gradient. Therefore, WSS and pressure gradient can be the link between FFR and the risk of ACS. Axial plaque stress uniquely characterizes the stenotic segment and can provide additional information on the risk of plaque rupture. Clinical application of these non-invasive hemodynamic parameters can be helpful to assess the future risk of plaque related clinical events. 27