Page 163 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Time course of coronary flow capacity in STEMI
Limitations
There has been an extensive debate on the amount of adenosine needed to achieve a maximally vasodilated state. More recently, the dose–response relationship of intracoronary hyperaemia has been investigated, and no significant differences in FFR-values between low and high dose intracoronary adenosine were documented.35 In this study we used an intracoronary bolus of 40μg adenosine, which induced a sufficient state of hyperaemie to allow accurate assessment of coronary flow characteristics.
The acquisition of coronary flow velocity was performed by a sensor-equipped guidewire that assessed only coronary flow. We assessed only non-culprit vessel haemodynamics in coronary arteries without significant epicardial narrowing and assumed distal pressure to equal aortic pressure. Therefore, a potential role of subclinical atherosclerosis of the conduit artery in the absence of focal narrowing in the impairment of non-culprit vessel flow and pressure cannot be excluded. However, resting coronary flow is unlikely to be disturbed by coronary stenoses up to 85% of the vessel diameter, without interference of compensatory vasodilation of the distal vascular bed.36
Conclusion
These observations underline the impact of the coronary microcirculation both
in the culprit and non-culprit vessel in the setting of STEMI on intracoronary 9 diagnostic techniques. The coronary microcirculation recovers over time at
six-month follow-up, as shown by an improvement in CFC. Both culprit and non-culprit vessel CFC assessment in the setting of STEMI might provide
valuable insight into the recovery of the coronary circulation, emphasizing the importance of intracoronary physiology assessment following primary PCI in
AMI.
Conflict of interest
The authors have no conflicts of interest to declare.
161