and SyncVision Co-registration."/>
Figure 7.7 Right coronary artery assessment with iFR pullback and SyncVision Co‐registration. This patient was found to have severe cardiac impairment with severe multi‐vessel disease. (a) The distal right coronary artery was assessed using minimal contrast due to renal impairment. (b) Physiological assessment provided greater spatial assessment and revealed the lesion in the distal PDA to be highly ischaemic with iFR 0.50. iFR‐Pullback demonstrated the majority of the pressure loss was localized to the PDA disease with modest pressure loss in the mid‐vessel. (c) Co‐registration could be performed without contrast to minimize the renal impact. Targeting the distal vessel would improve the intracoronary pressure loss.
Figure 7.8 Left anterior descending artery iFR pullback and SyncVision Co‐Registration. (a) This patient had an angiographically mild mid‐LAD stenosis. (b) iFR assessment demonstrated ischaemia with distal iFR 0.86. Co‐registered pullback demonstrated minor distal diffuse disease and pressure loss across the angiographic stenosis. Length measurement on co‐registration suggested a lesion of 27mm. Pullback analysis suggests that removing that lesion would yield an iFR of 0.94 in the vessel. (c) This was treated with a 3.5x26mm Drug eluting stent and this was optimized with non‐compliant balloons to ensure full expansion. (d) After intervention, the distal iFR was 0.91.
Commonly missed mistakes in Physiological Assessment
Transducer height: The transducer should be at the level of the aortic root, since when it is above the heart, the aortic pressure trace will be below that of the coronary pressure trace. This error is easily recognized. If, however, the transducer is below the heart, then the aortic pressure trace is above the distal coronary pressure to give the appearance of an apparent trans‐stenotic pressure gradient. This is more challenging to recognize and if missed can lead to erroneously positive results. However, it is readily resolved by performing normalization at the beginning of the case and checking for equalization of pressures whenever the sensor is returned to the vessel ostium.
Pressure signal drift: Iterations of pressure wire technology have reduced pressure wire drift, but it remains a recognized issue. This can be identified at the end of the distal pressure recording when the sensor is returned to the ostium. Provided there is no drift, the Pd/Pa ratio should remain at 1.0. If the value differs from 1.0, then drift has occurred – a result of electrical charge developing on the pressure sensor. Drift may also be identified when the wire is distal to a stenosis since the pressure waveform may take on the appearance of the aortic trace. Measurements should be repeated if drift exceeds 2 mmHg, especially if the measured physiology value is close to the ischemic cut‐off point. Drift is a dynamic problem as a result of electrical phenomenon and is more likely if the wire is used rapidly after activation. To avoid this, early activation of the wire with a heparinized saline flush is recommended. Allowing a longer period of inactivity between activation and clinical usage should minimize early wire drift. It is recommended that in cases in which a pressure wire is known to be needed, to have the wire activated and ready on the table, well before it is needed.
Guide catheter damping: All guiding catheters will produce a degree of ostial stenosis for the vessel. This is particularly problematic for 8 Fr and 7 Fr catheters and may be observed as damping of the aortic pressure signal with loss of the dicrotic notch. 5 Fr and 6 Fr catheters are less likely to cause significant damping, but if it occurs, the wire should be normalized in the aortic root and then the catheter should be disengaged once the wire is passed distal to the stenosis. Caution is also required during intravenous adenosine infusion since the increase in intracoronary flow and altered aortic hemodynamics mean that the guiding catheter can be drawn into the vessel: this will cause damping with a reduction of flow and under‐estimation of distal stenosis significance. Catheters with side‐holes should be avoided since they appear to generate a normal aortic pressure waveform, while the catheter pressure is not truly representative of aortic pressure.
Whipping artifact: Whipping may be observed if the pressure sensor is against the vessel wall or is repeatedly striking it. This can be overcome by withdrawing the wire slightly.
Erroneous console determination of indices: It is common for pressure wire consoles to compute FFR values when the pressure ratio is at its lowest. However, FFR should be calculated when there is stable hyperemia, and this may not be the lowest ratio. This issue is accentuated when using intracoronary adenosine injections where recording or calculation during the injection phase can give an artefactual aortic pressure trace and therefore an erroneous FFR value. Manual adjustment of the recorded ratio will resolve this. During iFR recording, ectopy or erroneous ECG tracings may affect iFR calculation. Errors can be identified by assessing when the wave‐free period has been calculated and making a repeat measure.
Large hemodynamic changes: Caution is required when there are large hemodynamic shifts in aortic pressures caused by central adenosine infusions. Large falls in proximal aortic pressure cannot account for a significant proportion of the change in distal coronary pressure and may alter the FFR results [46]. Caution should be taken to ensure ratios are calculated during stable hyperemia to match the original validation work. In some situations, the lowest FFR value can occur during the initial peak hyperemic phase causing a change in classification of stenosis significance [47,48]. Prolonged intravenous infusions of adenosine can cause paradoxical vasoconstriction of the microcirculation and the whole trace should be observed for a reliable value [49].
Pressure‐only indices to guide coronary intervention
Fractional Flow Reserve
Fractional flow reserve (FFR) is recognized as the reference standard for coronary physiology in the catheter laboratory. FFR, conceptually, is defined as the maximum myocardial blood flow in the presence of an epicardial stenosis divided by the theoretical maximum flow in the absence of a stenosis [7,50]. In reality, FFR does not measure flow, instead measuring intracoronary pressure and draws an inference to flow. Pressure and flow are not linearly related and thus a constant relationship can only be inferred if coronary microcirculatory resistance is minimal as is theoretically the case during maximal arteriolar vasodilatation during adenosine infusion. Hyperemic agents reduce microvascular resistance and increase coronary flow, thereby magnifying a trans‐stenotic pressure gradient that is often present at rest. FFR is defined as a ratio of the distal to proximal coronary pressures (Pd/Pa) during hyperemia. In common parlance, a vessel with FFR of 0.80 has 80% of the blood flow it should have if the stenosis was absent.
FFR is usually accepted as the lowest Pd/Pa during stable hyperemia; high quality traces must be assessed [51]. When using short‐lived intracoronary vasodilators, the lowest Pd/Pa ratio achieved may be used. Automated calculation may make errors as port opening, ectopy or a cardiac pause can erroneously generate a low Pd/Pa.
Consideration of right atrial pressure
The modern iteration of FFR considers the venous contribution to resistance to be minimal (zero). This simplifies the equation and obviates the need to measure the right atrial pressure [7,50]. However, typical venous pressures of 2–8 mmHg are reported during hyperemia and patients with cardiac impairment may have higher values. The implications are that stenosis severity may be underestimated, particularly if venous pressure is elevated [52]. The impact of this is unlikely to be detectible in large outcome studies where a modest number of lesions being falsely deferred would not generate a sufficient signal of MACE. For individual patients the effects and the change in categorization can be
