Page 173 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

non-infarct arteries affects iFR measurement. Choi et al. stated that changes in FFR and iFR for the non-culprit stenosis of myocardial infarction patients were not significantly different from those in patients with stable ischemic heart disease.15 De Waard et al. clarified in his editorial why this conclusion could be drawn.16
Two third of the analyzed patients were suffering a non-ST-segment elevation myocardial infarction (with other effects on microvascular resistance than with STEMI, partly due to the absence of deleterious effects of reperfusion), only 39% had an anterior wall infarction and both the CK-MB peak levels and the post-infarction left ventricular ejection fraction indicated small infarctions. Small infarctions will have little influence on coronary hemodynamic status whereas the coronary hemodynamic status might be disturbed after large STEMI and reperfusion effects with extensive microcirculatory dysfunction in both the culprit and the non-culprit areas.
The iSTEMI study evaluated with iFR the non-culprit stenoses during PPCI and after a median of 16 days.17 Acute iFR was 0.89 and follow-up iFR increased to 0.91. With follow-up iFR as a reference, acute iFR had a positive predictive value of 68%, and a negative predictive value of 89%. Using follow-up FFR ≤0.80 as a reference, it was 67% and 77% respectively. The potential risk to overtreatment of non-culprit lesions in the PPCI-setting is shown clearly.
The results of the ongoing iModern study, comparing iFR-guided complete revascularization with staged complete revascularization based on CMR-proved ischemia evaluated 6 weeks after STEMI (https://clinicaltrials.gov/ct2/show/ NCT03298659) and the FRAME-AMI study, comparing FFR-guided complete revascularization at the time of PPCI with angiography-only strategy (https:// clinicaltrials.gov/ct2/show/NCT02715518), will have to answer the question if acute iFR or FFR measurement can be used for decision making in the treatment strategy for non-infarct artery lesions at the time of STEMI as well as the timing of PCI for non-culprit lesions. On theoretical grounds, it is conceivable that decision-making at the time of PPCI is only possible if it concerns limited infarct sizes in true STEMI patients where the microvascular characteristics of the remote areas are not disturbed by the STEMI itself. Currently, it is not known from what infarct size affects microvascular resistance making iFR and FFR in non-culprit vessels not reliable for decision making. Also, the size of the area subtended by the non-IRA vessel plays a role. Smaller areas need a tighter
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General discussion and future perspectives
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