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Interventional Cardiology


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micro‐vasospastic changes of the epicardial vessel which are triggered by the passage of the intracoronary wire. Such spam can artificially escalate the significance of a given stenosis. Prolonged pressure wire cases should have repeated doses of intracoronary nitrates. This is facilitated by using a manifold with ports readily available for intracoronary injections. Nitrates should also be given again for any physiological measurements made after PCI.

      Performing physiological measurement

      The pressure wire should be positioned distal to the coronary stenosis being investigated under fluoroscopic guidance. The sensor should be at least two to three vessel diameters away from the stenosis to reduce the impact of pressure recovery phenomena. Fluroscopic documentation of wire position is recommended and can be done without contrast. If contrast is used, then the catheter should be thoroughly flushed and time should be allowed for the effect on the pressure trace to subside.

      Before any measurement is made, a long saline flush should be performed to clear the guiding catheter of contrast. Contrast is viscous and can impact pressure tracing. If the vessel had been challenging to wire, a repeat dose of intracoronary nitrates can alleviate any epicardial spasm. Measurements should be made with the needle‐introducer fully removed and the port closed to avoid minor pressure drift. Resting indices can be repeated readily until a steady value has been achieved. If there is marked variability, then the wire position should be adjusted. For optimal resting assessment, additional contrast injections should be avoided just prior to measurement of the index. If a contrast injection is necessary, it would be appropriate to wait 20 seconds to allow the impact of submaximal hyperemia to subside.,

      If using hyperemic measures, this can be used induced either with intravenous infusion or with intracoronary boluses. Hyperemic measurements should be made during a steady and a careful review of the pressure traces is required to ensure validity of the measurement. It is best practice to avoid handling the wire during recording static readings.

      Non‐specific agents such as adenosine and papaverine are commonly used to induce maximal hyperemia for assessment of indices such as Coronary Flow Reserve (CFR), FFR and index of microcirculatory resistance (IMR). The dose of adenosine is usually 140 mcg/kg/min when given as a central venous infusion; ATP can be given as an alternative. The hyperemic effect is typically observed after 30 seconds and infusions should continue for 1–2 minutes to observe for stable hyperemia. Side‐effects include relative hypotension, a central chest discomfort or burning, dyspnea, and bronchospasm. Adenosine should be avoided in patients with severe brittle asthma. However, it has been used relatively safely in those with milder variants of asthma, albeit with full resuscitation facilities available. Other lung conditions such as chronic obstructive pulmonary disease can generally tolerate an adenosine infusion. Short‐lived atrio‐ventricular conduction delay is frequent; caution should be considered in those with established conduction disease.

      For intracoronary dosing, clinical practice remains variable. Early validation work was all performed using considerably lower doses than found in clinical practice today. Accepted intracoronary doses of adenosine or ATP are 80–120 mcg in the left coronary system and 40 mcg in right coronary artery. Intracoronary adenosine typically achieves hyperemia lasting 5 to 10 seconds. Papaverine is an alternative intracoronary agent that achieves a longer lasting hyperemia between 30–60 seconds which may permit pullback assessments at the cost of transient QT prolongation and rare trigger ventricular tachycardia or torsarde de pointes. It is typically used where adenosine is not available (15–20mg in the left coronary artery; 10–12 mg in the right coronary artery).

      Newer alternatives include Regadenoson, a selective A2A receptor agonist which has been approved for use in myocardial perfusion imaging. Given as a single bolus into a peripheral vein using a weight‐unadjusted dose (400 mcg over 10 seconds), regadenoson achieves a peak flow velocity after a minute and declines thereafter. The duration of hyperemia is variable between patients making pullback and multi‐vessel assessment unreliable. Side‐effects include adenosine‐like effects with hypotension, chest discomfort and flushing. Third‐degree heart block has also occurred.

      Maximal hyperemia is believed to occur in two stages. Agents primarily achieve maximal hyperemia through their vasodilator action on microvascular smooth muscle cells (an endothelium‐independent response). The resultant increase in blood flow is thought to stimulate shear stress‐induced endothelial nitric oxide release, which promotes further vasodilatation of the microcirculation (flow‐mediated dilatation) and increase in blood flow (an endothelium‐dependent response). Therefore, the response to hyperemic agents will integrate a change in coronary blood flow and microvascular function but alone cannot distinguish between both components.

      Pullback and drift check

      Once measurements have been made, a pullback is recommended to understand if the coronary artery disease has a diffuse, focal, or mixed pattern. This is readily performed by moving the pressure wire backwards by applying gentle traction to bring the sensor to the vessel osmium. The port on the manifold should remain closed while doing this. Pullback can be done using a NHPR or FFR. If measuring FFR, pullback is most easily done when using an intravenous infusion of adenosine. An alternative is to use intracoronary papaverine which achieves a prolonged hyperemic state; however, this agent has become less common in practice and is associated with torsades de pointes. Regadenoson has also proved to be helpful for single vessel assessment. It is less practical for pullback or multi‐vessel assessment, as the dose can be administered only once, and the duration of hyperemia is extremely variable between patients (30 to 120 seconds). In some cases, the hyperemic effect can be diminishing during the pullback, making the interpretation challenging.

      The sensor should always be returned to the vessel ostium after assessment to exclude the presence of significant pressure‐wire or hemodynamic system drift which would make the measurement unreliable. Values of drift over 2 mmHg suggest the measurement should be repeated.

      Pressure wire measurement after intervention provides additional information to inform the operator on the hemodynamic gain of the intervention. This data has been shown to alter further interventional decisions, and in many cases, where an optimal physiological result, further stents and optimization may be necessary. In cases where the intervention has been performed using the pressure wire as the principle primary wire, then a measurement can be readily made by reconnecting the pressure wire to the console system. Further intracoronary nitrates should be administered, and the guiding catheter should be flushed. In the post‐PCI state, resting flow states have typically resumed by the time the balloon is withdrawn and the catheters have been flushed. In practical terms, no additional delay over and above what would occur during intervention is required to make a repeat resting measurement. Once measurements have been made, the pressure wire should be withdrawn to the guiding catheter to assess for pressure drift. In long interventional cases, there may be significant drift, which would mandate repeat measurement. In cases where the intervention was performed on another guiding wire, the pressure wire should be re‐introduced as described above. The sensor location should be maintained where possible.

      There have been concerns that there is no such thing as a resting state in the cardiac catheter laboratory. The majority of interventionists will find that their patients are calm and comfortable during their procedures without significant changes in hemodynamics. Patient anxiety or conscious state affecting resting