Microvascular resistance increases after angioplasty in NSTEMI patients


Cansu Akdeniz, Department of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey, and others reported in EuroIntervention that when collateral flow is considered, microvascular resistance after percutaneous coronary intervention (PCI) in patients with non-ST-elevation myocardial infarction (NSTEMI) increases.

Akdeniz et al wrote that previous studies have shown microvascular resistance to significantly decrease after PCI and that it is increased by increasing severity of epicardial stenosis. However the authors reported that these studies did not take collateral flow into account when calculating microvascular resistance and added that further studies that did take collateral flow into account excluded patients with unstable lesions or patients who developed periprocedural myocardial infarction. Akdeniz et al commented: “Therefore, the impact of periprocedural myonecrosis on microvascular resistance and the relationship between unstable epicardial lesions and the microcirculation remain to be elucidated.” They added: “In this study, we hypothesised that unstable epicardial lesions possess different features which may lead to different responses in the distal microcirculation after PCI.”

The authors enrolled 43 patients presenting with NSTEMI and undergoing PCI (with bare metal stents) for a single lesion within 48 hours of admission. A Doppler and pressure-sensor equipped guidewire (ComboWire XT, Volcano Therapuetics), advanced across the stenosis, was used to measure epicardial and microvascular haemodynamics. They stated: “Reliable calculation of microvascular resistance in the presence of an epicardial stenosis requires incorporation of the collateral flow, as measurable by the coronary wedge pressure.” Therefore, pre-PCI microvascular resistance was calculated at maximum hyperaemia by taking coronary wedge pressure into account. Akdeniz et al added: “Since myocardial flow is equal to coronary flow in the absence of epicardial stenosis, post-PCI microvascular resistance was calculated during maximum hyperaemia simply as distal coronary pressure divided by average peak flow velocity.”

Stable and reliable intracoronary Doppler and pressure signals were only available for 38 of the 43 patients in the study. In these 38 patients, overall, microvascular resistance significantly increased by 20% after the removal of epicardial stenosis through PCI. Akdeniz et al reported, unlike previous studies, that this increase was not influenced by the haemodynamic significance of the epicardial stenosis. They also noted that 19 (50%) patients developed periprocedural myocardial infarction and that the increase in microvascular resistance was significantly higher in these patients compared with patients without periprocedural myocardial infarction. They commented: “Removal of the epicardial lesion did not change microvascular resistance in the group of patients in whom periprocedural myocardial infarction did not occur. On the other hand, microvascular resistance increased significantly after PCI in patients who developed periprocedural myocardial infarction.”

Additionally, the authors calculated the pre-PCI microvascular resistance without taking collateral flow into account and found that it was “substantially overestimated (by 50%)” compared with the microvascular resistance that was calculated by taking collateral flow into account. They wrote: “Because of this initial overestimation, it would appear that removing an epicardial stenosis may decrease post-PCI microvascular resistance. This paradoxical decrease in uncorrected microvascular resistance (which did not incorporate collateral flow) following PCI was also observed in our study.”

Akdeniz et al concluded: “Since increased microvascular resistance after PCI indicates further microvascular dysfunction, any preventive measures or therapeutic approach to avoid microvascular damage should be considered in the NSTEMI population.” They added that this might involve identifying patients with NSTEMI with lesions that have the potential to embolise distally, which may “facilitate tailoring of interventional therapy, such as using distal protection devices or avoiding predilation.”