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In 38% of these, the pressure loss was within the stented segment, suggesting an inadequate stent result – perhaps with stent under‐expansion or stent edge complication. In the remaining 60%, there was clear focal pressure‐steps either proximal or distal to the stent, suggesting geographical miss or underappreciation of coronary disease. Further intervention could theoretically have minimized post‐PCI ischemia. As shown by other studies, angiographic appearances did not predict post‐PCI ischemia. It is hypothesized that these events would be less frequent if operators used pre‐PCI pullback data and this is the subject of an upcoming follow‐up study.

      Overall, these findings emphasize the importance of post‐PCI physiological assessment. If the purpose of intervention is to improve blood flow and relieve functional stenoses, it is imperative to ensure the procedure has been successful. The lack of symptomatic improvement after intervention in many cases could be attributed to insufficient treatment of the epicardial stenoses.

Using Physiology to Guide PCI Strategy

      There is significant practical value in mapping coronary physiology onto angiographic images as it facilitates real‐world application of physiology in treating complex coronary disease. Transtenotic pressure gradients can be overlaid onto angiography in real‐time such that Interventionalists can interact with the data to model potential physiological outcomes for a given interventional strategy. Resting physiological parameters such as iFR can readily predict the impact of removing a given stenosis, enabling a prediction of post‐PCI physiology.

      Co‐registered coronary artery mapping represents the next application of physiology in the Cardiac Catheterization laboratory and is a significant leap beyond the traditional focus on whether a pressure index is positive or negative. This has been facilitated by a quantum leap in computing power enabling real‐time tracking of pressure wire movements within a moving coronary vessel during fluoroscopy. Wire movement can be tracked in three dimensions to produce highly credible and spatially accurate co‐registered map of the pressure gradients measured by the pressure sensor on the wire. Mapping is best achieved with technologies that can track the wire position at high speed without needing a high frame rate fluoroscopy.

      Real‐time co‐registration allows for precise identification of the steps on a pressure wire pullback curve corresponding to the coronary angiogram. Whilst coronary angiography remains poor at identifying lesion significance, it remains key for guiding intervention and marking clear landmarks is essential. The same concept can be deployed for intravascular ultrasound and optical coherence tomography, and when combined with physiology, this provides the truest assessment of the coronary vessels in relation to ischemia and potential interventional approaches.

The Microcirculation

      Ischemia with non‐obstructive coronary arteries (INOCA)

      The epicardial coronary arteries represent only a small proportion of the coronary tree and it is increasingly recognized that epicardial stenoses cause angina in only a fraction of cases. Many patients with unobstructed coronary arteries are considered to have non‐cardiac causes of chest pain but data suggests many have a spectrum of conditions that are now described under the umbrella term″ ischemia with non‐obstructive coronary arteries (INOCA)” [95]. Within this group, there are those with vasospastic angina and those with coronary microvascular dysfunction. This latter condition is more common and can occur in those patients with coronary atherosclerosis. Insufficient knowledge, testing and medical therapy mean that many such patients have recurrent medical attendances at significant resource cost [95]. However, there is evidence from PET studies and those performing invasive assessment that patients with INOCA have significantly elevated rates of cardiac events and hospitalization. It is prudent to reflect upon thorough testing pathways that may facilitate novel therapeutic approaches.

Patients with recurrent chest pain that is suggestive of angina should be assessed carefully. A consensus document from the European Association of Percutaneous Cardiovascular Interventions (EAPCI) have recommended the following steps [96]:

       Those with evidence of ischemia on non‐invasive testing should be considered for invasive angiography.

       If coronary vessels appear unobstructed, an invasive physiological test should be performed to assess for unappreciated epicardial stenosis (using resting and/or hyperemic measures).

       In the absence of obstructive epicardial disease, microvascular resistance can be assessed using either thermodilution or Doppler flow velocity techniques to measure IMR, CFR or HMR. IMR typically exceeds 25 and CFR <2.0 in those with elevated microvascular resistance.

       This should be followed by vessel vasoreactivity testing with intracoronary acetylcholine bolus (more readily performed) or infusion.

      Vasoreactivity testing may trigger chest pain and electrocardiographic changes consistent with ischemia. Those with clear evidence of epicardial artery vasospasm should be treated with calcium channel antagonists such as Verapamil and/or long‐acting nitrates [96]. Aspirin and statin therapy is appropriate particularly if there is concomitant coronary disease. Those who have no clear epicardial vasospasm, may have have microvascular spasm [96]. These patients are best treated with beta‐blockers or switched to calcium channel antagonists as second line. More novel agents such as Ranolazine may be considered in addition while ACE‐inhibitors may promote recovery of endothelial dysfunction. Novel stratification of medication by use of IMR measurement and vasoreactivity testing has been shown to be useful in a small randomized study [97]. Further, larger multi‐center studies are underway.

      IMR: a clinical tool to assess microvascular function

      A greater appreciation of the value of microcirculatory testing has lead to a renewed interest of technologies that have existed for some time. Current approaches rely upon indirect assessment of the microcirculation: assessing a change in coronary flow in response to a specific agonist which evoke differential microvascular responses. Agonists are either endothelium‐dependent (requiring an intact endothelium to function, principally acetylcholine but can also include substance‐P and bradykinin) or endothelium‐independent (such as nitrate and nitroprusside) [4,16]. The level of change in coronary blood flow in response to a given agonist is inversely proportional to the functional state of the microcirculation.

IMR measures the resistance of the coronary microvasculature and is derived from an application of Ohm’s law (that the potential difference across an ideal conductor is proportional to the current through the conductor) ) (Figure 7.10) [98]. By neglecting the influence of venous pressure, IMR is determined by dividing hyperemic distal coronary pressure (Pd) by hyperemic flow. Flow is derived using thermodilution techniques which allows IMR to be calculated by the product of Pd with transit time (Tmn) during maximal adenosine‐mediated hyperemia [98]. A brisk injectant of 3 mls of room temperature saline is used to determine transit times under hyperemia. Typically, measurements are taken in triplicate and averaged. Measurements can be variable, and operators must be discerning in their technique.

Figure 7.10 IMR calculation. A combined pressure/temperature guide wire is used to obtain mean Pd and mean distal coronary blood flow (based on the principles of thermodilution in response to a 3 ml hand‐ held intra‐coronary injection of room temperature saline). IMR is derived from the ratio of mean Pd (green circle) and mean distal coronary flow at maximal hyperemia. Distal coronary flow is inversely proportional to the mean transit time (Tmn) of the injectate. Therefore IMR = Pd : 1/Tmn = Pd × Tmn.

      IMR correlates significantly with true microcirculatory resistance measured in an open‐chested pig model. In the presence of an epicardial stenosis, coronary wedge pressure should be included in the calculation (IMR = Pa x hyperemic mean transit time x [(Pd‐Pw)/(Pa‐Pw)];

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