Читать книгу Interventional Cardiology - Группа авторов - Страница 198

IFR can detect the pressure change achieved by coronary intervention but there is no clear established cut‐point that predicts later MACE [49]. During routine PCI, there is detectible change in pressure gradients without a significant change in resting coronary blood flow; this is true for the majority of moderate or severe stenoses [45]. As resting flow does not change significantly, residual pressure gradients do not change significantly. This means that changes in coronary pressure can be predicted before coronary intervention is undertaken and this has been shown in both small [22] and large studies [23]. The level of prediction is good but there are limits and this becomes evident when very severe stenoses are involved; those lesions in which the potential gain is greater than 0.40 iFR units, there can be change in resting flow conditions such that there is change to the pressure‐flow relationships within the vessel which alters the residual pressure gradients. In this situation, the pre‐PCI prediction may be less accurate. [45]. However, for the majority of lesions in which pressure wires are used, this is less of an issue.

In this context, the DEFINE‐PCI study [91] assessed the physiological success of coronary intervention in a blinded manner, after expert operators had deemed the procedure a technical success. Angiography was used to judge procedural success with intravascular imaging being optional. Angiographically evident residual stenosis was infrequent. Post‐PCI iFR demonstrated that almost one quarter of the included PCI were still ischemic based on a post‐PCI iFR ≤0.89. This is notable because, on average, 20–30% of patients with apparently successful PCI have ongoing angina and this is consistent across multiple major studies, including COURAGE [92], SYNTAX [93], FREEDOM [94] and FAME [14].

In DEFINE‐PCI, iFR‐pullback was performed after PCI with core‐lab analysis, enabling identification of the points of failure for physiological success. In 80% of these cases, the residual pressure drop was focal such that it could be have been improved with further intervention. 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.