Читать книгу Interventional Cardiology - Группа авторов - Страница 201

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)]; this is particularly important in significant stenoses with an FFR≤0.60 where the likelihood of collateral flow is high. Mathematical derivation of Pw is also possible based upon the statistical relationship between FFRcorr and FFRmyo; IMR can therefore be calculated as IMRcalc = Pa × TmnHyp × ([1.35 × Pd / Pa‐0.32) [99]. This calculation is important when coronary arteries have stenoses that will alter the distal microcirculation. However, IMR is increasingly used in patients with unobstructed vessels to determine microvascular angina.

In general, IMR values below 25 are considered normal and were consistently found in validation cohorts of healthy populations with normal valves. Values over 25 reflect elevated microvascular resistance. After STEMI, patients with high IMR values (>40) are more likely to have raised cardiac enzymes, less cardiac recovery on non‐invasive imaging and evidence of microvascular obstruction on magnetic resonance imaging. In more stable patients, values over 25 suggest microvascular dysfunction and are associated with higher rates of cardiovascular presentation and suggest a microvascular cause of patient’s angina. IMR measurement can be combined with other vasoreactivity testing for a comprehensive testing in the cardiac catheter laboratory.