Key result
Residual low fractional flow reserve after percutaneous coronary intervention, despite normalized hyperemic stenosis resistance, was associated with a significantly weaker (10.1 vs 15.8 10.kW.m-2.s-2) and delayed backward expansion wave.
Why the study?
A significant proportion of stenoses show abnormal FFR after angiographically successful PCI, but the mechanisms underlying residual low FFR despite normalized hyperemic stenosis resistance were not fully understood.
Does altered cardiac-coronary coupling explain residual low FFR without flow limitation after PCI in patients with stable intermediate stenoses?
Observational (n=61)
Yes
Does altered cardiac-coronary coupling explain residual low FFR without flow limitation after PCI in patients with stable intermediate stenoses?
Residual low FFR after angiographically successful PCI may be driven by altered cardiac-coronary coupling and blunted microvascular suction rather than flow limitation or microvascular dysfunction.
May indicate altered cardiac-coronary coupling in residual low FFR post-PCI; hypothesis-generating, requires prospective validation.
A significant proportion of stenoses have an abnormal fractional flow reserve (FFR) after angiographically successful percutaneous coronary intervention (PCI), which is traditionally attributed to differences in coronary flow velocity reserve (CFVR) or hyperemic microvascular resistance (hMR). This study investigated the mechanisms underlying residual low FFR despite good angiographic results and normalized hyperemic stenosis resistance (hSR) using wave‐intensity analysis (WIA), which evaluates phasic characteristics of cardiac‐coronary coupling. Sixty‐three vessels from patients who underwent PCI for stable intermediate stenoses were included. Peri‐PCI characteristics of conventional and WIA parameters were assessed. Ten (16%) vessels exhibited residual low FFR (≤0.8) despite normalized hSR (<0.8), without significant differences in hyperemic flow (velocity) (hAPV), CFVR, or hMR compared with concordant normal FFR‐hSR group ( p > 0.05). WIA revealed a significantly slower (peak‐time of backward expansion wave, tBEW peak = 20% ± 6% vs. 29% ± 17% of expansion period, p = 0.005) and weaker (BEW peak = 10.1 ± 8.9 vs. 15.8 ± 11.4 10.kW.m‐2.s‐2, p = 0.045) impact of microvascular suction responsible for diastolic coronary filling during hyperemia in the low FFR group, despite comparable pre‐PCI characteristics. Residual low FFR after PCI may reflect altered cardiac‐coronary coupling without limitation of flow or vasodilator capacity when the blunted impact of accelerating wave energy flux with delayed coronary filling fails to sustain distal pressure. The influence of cardiac‐coronary coupling on post‐PCI FFR warrants further investigation.
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Taş et al. (2025) conducted an observational in Stable intermediate coronary stenoses (n=61). Residual low fractional flow reserve (FFR ≤0.8) vs. Concordant normal FFR (>0.8) was evaluated on Peak backward expansion wave (BEWpeak) during hyperemia (p=0.045). Residual low fractional flow reserve after percutaneous coronary intervention, despite normalized hyperemic stenosis resistance, was associated with a significantly weaker (10.1 vs 15.8 10.kW.m-2.s-2) and delayed backward expansion wave.
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