Aortic pressure-velocity loop: a potential tool for assessing risk associated with midsystolic forward compression waves in patients with chronic atherosclerotic coronary artery disease

Study objective: To evaluate whether impaired ventriculo-aretrial interaction characterizes chronic ischemic heart disease (CIHD) caused by stable chronic obstructive coronary artery disease (CAD), using wave intensity and aortic pressure–velocity (PU) loop analyses. Design: Retrospective observational study. Setting: Single-center invasive hemodynamic assessment using high-fidelity multisensor catheters. Participants: Thirty-one patients with CIHD, including 21 with chronic atherosclerotic CAD and 10 with non-CAD CIHD. Interventions: None. Main outcome measure(s): Wave intensity–derived indices of ventriculo-arterial interaction, including the initial PU-loop slope (S1), second ascending slope (S2), backward compression wave (BCW), midsystolic forward compression wave (m-FCW), and their relative magnitudes. Discriminatory ability for CAD was assessed using receiver operating characteristic (ROC) curve analysis. Results: In CAD patients, midsystolic flow was supported by a previously unreported m-FCW that emerged in response to an early-onset BCW during ventricular acceleration, reflected by higher S2 values. In contrast, midsystolic flow in non-CAD CIHD patients was primarily maintained by blood inertia and lower S1 values. S2 strongly correlated with the relative magnitude of m-FCW (r = −0.936, P < 0.001). The relative magnitude of m-FCW showed greater discriminatory ability for CAD than BCW (AUC 0.976 vs. 0.771). The S2:S1 ratio correlated closely with the relative magnitude of m-FCW and demonstrated the highest AUC (0.986). Conclusions: Chronic atherosclerotic CAD is characterized by impaired ventriculo-aortic interaction, with midsystolic flow dependent on compensatory m-FCW rather than blood inertia. Aortic PU-loop parameters, particularly the S2:S1 ratio, may provide a potential diagnostic marker for distinguishing chronic atherosclerotic CAD from other forms of CIHD.