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Fig. 6. Multiple variables determine flow at 90 min, and they are often related to each other. For instance, LAD location, the percent of the vessel distal to the stenosis, and the presence of a pulsatile flow pattern were all related to each other as well as the 90-min CTFC. In particular, there was a greater percent of the culprit vessel distal to the stenosis in patients with an LAD lesion (76.6 ± 11.1% [n = 252] vs 61.4 ± 22.9% [n = 422],p < 0.0001); LAD lesions predominated in patients with pulsatile flow (61.1% LAD [n = 66 out of 108] vs 38.9% non-LAD [n = 42 out of 108], p < 0.001); and finally patients with a pulsatile flow pattern also had a greater percent of the vessel distal to the stenosis (72.9 ± 16.2% [n = 97] vs 65.8 ± 21.3% [n = 548],p = 0.002). Patients with pulsatile flow had less severe percent stenoses (68.6 ± 18.8% [n = 106] vs 73.0 ± 18.9% [n = 733], p = 0.02), and pulsatile lesions tended to be collateralized less frequently (pulsatile lesions collateralized in 9.5% [n = 10 out of 105] of cases, and nonpulsatile lesions collateralized in 16% [n = 116 out of 723] of cases, p = 0.08). Patients who were patent for less than 30 min also had a higher incidence of thrombus (50.0% [n = 24 out of 48] vs 21.4% [n = 119 out of 555], p < 0.001).

Fig. 6. Multiple variables determine flow at 90 min, and they are often related to each other. For instance, LAD location, the percent of the vessel distal to the stenosis, and the presence of a pulsatile flow pattern were all related to each other as well as the 90-min CTFC. In particular, there was a greater percent of the culprit vessel distal to the stenosis in patients with an LAD lesion (76.6 ± 11.1% [n = 252] vs 61.4 ± 22.9% [n = 422],p < 0.0001); LAD lesions predominated in patients with pulsatile flow (61.1% LAD [n = 66 out of 108] vs 38.9% non-LAD [n = 42 out of 108], p < 0.001); and finally patients with a pulsatile flow pattern also had a greater percent of the vessel distal to the stenosis (72.9 ± 16.2% [n = 97] vs 65.8 ± 21.3% [n = 548],p = 0.002). Patients with pulsatile flow had less severe percent stenoses (68.6 ± 18.8% [n = 106] vs 73.0 ± 18.9% [n = 733], p = 0.02), and pulsatile lesions tended to be collateralized less frequently (pulsatile lesions collateralized in 9.5% [n = 10 out of 105] of cases, and nonpulsatile lesions collateralized in 16% [n = 116 out of 723] of cases, p = 0.08). Patients who were patent for less than 30 min also had a higher incidence of thrombus (50.0% [n = 24 out of 48] vs 21.4% [n = 119 out of 555], p < 0.001).

After PTCA, the guidewire tip is placed at the coronary landmark, and a Kelly clamp is placed on the guidewire where it exits the Y-Adapter. The guidewire tip is then withdrawn to the catheter tip, and a second Kelly clamp is placed on the wire where it exits the Y-Adapter. The distance between the 2 Kelly clamps outside the body is the distance between the catheter tip and the anatomic landmark inside the body. Velocity (cm/s) may be calculated as this distance [(cm) TFC (frames)] X film frame speed (frames/s). Flow (cm3/s) may be calculated by multiplying this velocity (cm/s) and the mean cross-sectional lumen area (cm2) along the length of the artery to the TIMI landmark (37). In 30 patients, velocity increased from 13.9 ± 8.5 cm/s pre-PTCA to 22.8 ± 9.3 cm/s post-PTCA (p < 0.001). Despite TIMI grade 3 flow, both before and after PTCA in 18 patients, velocity actually increased 38% from 17.0 ± 5.4 cm/s to 23.5 ± 9.0 cm/sec (p = 0.01). For all 30 patients, flow doubled from 0.6 ± 0.4 cm3/s pre-PTCA to 1.2 ± 0.6 cm3/s post-PTCA (p < 0.001). In the 18 patients with TIMI grade 3 glow both before and after PTCA, flow increased 86% from 0.7 ± 0.3 cm3/s to 1.3 ± 0.6 cm3/s (p = 0.001) (37). These data illustrate the wide range of velocities associated with TIMI grade 3 flow and the potential that TIMI grade 3 flow can be improved upon and made faster. A range of velocities that constitutes different TFGs has also been described using the Doppler velocity wires (39-41). We have also planimetered the length of arteries from the angiogram and combined this with the frame count to calculate what is called the quantitative coronary angiography (QCA) velocity, and we have shown that the QCA velocity proximal and distal to the lesion is almost identical to that reported using Doppler velocity wires (42,43).

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