Association between pre-procedural pathophysiological pattern of coronary disease and immediate hemodynamic outcome post-percutaneous coronary intervention

Background The pathophysiological pattern of coronary artery disease (CAD) pre-procedure may affect the physiological response to percutaneous coronary intervention (PCI). Purpose The aim of this study was to evaluate whether the pathophysiological pattern of CAD, derived from virtual pullbacks of angiography-based fractional flow reserve, was predictive of the immediate hemodynamic outcome post-PCI. Methods Data from 206 patients with chronic coronary syndrome enrolled in the ASET (Acetyl Salicylic Elimination Trial) JAPAN study were analyzed. The ASET JAPAN study is a multi-center, single-arm, open-label, proof-of-concept trial to demonstrate the feasibility and safety of "aspirin-free" therapy with low-dose prasugrel (3.75 mg) monotherapy following PCI, Pre-procedural pathophysiological patterns in CAD were characterized by the physiological distribution and local severity of coronary atherosclerosis using Murray law-based quantitative flow ratio (µQFR)-derived indexes acquired from pre-PCI angiograms. The physiological distribution of CAD was defined as "predominant diffuse" or "focal" according to a µQFR pullback pressure gradient (PPG) index <0.78 or ≥0.78, respectively. Physiological local severity was assessed using µQFR gradient per 1 mm (dµQFR/ds), with a value ≥ 0.025/mm defining the presence of a "major gradient". The statistical association of preprocedural pathophysiological pattern of CAD with post-PCI µQFR <0.91 was investigated. Results Out of 207 vessels, 26.6% (n=55) were classified as predominantly focal (µQFR PPG index ≥0.78) with a major gradient (dµQFR/ds ≥0.025/mm, Group 1), 1.0% (n=2) predominantly focal without a major gradient (Group 2), 53.6% (n=111) predominantly diffuse (µQFR PPG index <0.78) with a major gradient (Group 3), and 18.8% (n=39) predominantly diffuse with no major gradient (Group 4)(Figure 1). Vessels with predominantly diffuse disease and no major gradient (Group 4) had significantly higher pre-PCI µQFR (mean difference, -0.163; 95%CI, -0.211 to -0.118) and lower post-PCI µQFR (mean difference, 0.031; 95% CI, 0.014 to 0.487; by bootstrapping using 2000 replications) than those with predominantly focal disease and major gradients (Group 1). Low pre-PCI µQFR values were significantly associated with an increased risk of a post-PCI µQFR <0.91 (Figure 2A). Similarly, low µQFR PPG index showed a significantly higher risk of a post-PCI µQFR <0.91 (Figure 2B). The highest dµQFR/ds had no significant impact on the risk of a post-PCI µQFR <0.91 (Figure 2C). In multivariable analysis, low µQFR PPG index (diffuse disease) was an independent factor for predicting a post-PCI µQFR <0.91 (per 0.1 decrease of µQFR PPG index, OR:1.68, 95% CI 1.17-2.46, p=0.005). Conclusions A physiological pattern of diffuse CAD pre-procedure was an independent factor in predicting an unfavorable immediate hemodynamic outcome post-PCI.