JACC. Advances, Volume 4, Issue 5, 18 3 2025, Pages 101728 Investigating the Anrep Effect in Hypertrophic Obstructive Cardiomyopathy With Invasive Pressure-Volume Analysis. Reil JC, Sequeira V, Reil GH, Scholtz S, Rudolph V, Maack C, Serruys P, Steendijk P
The Anrep effect, an adaptation enhancing left ventricular (LV) contractility in response to raised afterload, is hypothesized to influence hypertrophic cardiomyopathy pathophysiology. This study investigated the activation and reversibility of the Anrep effect in obstructive hypertrophic cardiomyopathy (HOCM) patients undergoing percutaneous transluminal septal myocardial ablation (PTSMA) to relieve LV outflow tract obstruction. Invasive pressure-volume (PV) analysis was performed on 14 HOCM patients before and after PTSMA. The "Anrep Triad," defined by elevated afterload (higher LV end-systolic pressure and effective arterial elastance), augmented contractility (higher end-systolic elastance and maximum LV pressure rise [dP/dtmax]), and prolonged systolic duration (dTes), was assessed via direct hemodynamic comparison preprocedure and postprocedure. Stroke work (SW), potential energy, and total PV area (PVA) quantified mechanical work and efficiency (SW/PVA). Postprocedure reversal of the Anrep effect was confirmed (pre- vs post-PTSMA), with reductions in afterload (LV end-systolic pressure: 180 vs 138 mm Hg, P = 0.0001; effective arterial elastance: 2.5 vs 1.9 mm Hg/mL, P = 0.002), contractility (end-systolic elastance: 2.0 vs 1.5 mm Hg/mL, P = 0.0001; dP/dtmax: 1,775 vs 1,560 mm Hg/s, P = 0.017), and systolic duration (dTes: 371 vs 327 ms, P = 0.002). Preprocedure, HOCM patients exhibited higher mechanical workload (SW: 8,161 vs 7,495 mm Hg·mL, P = 0.004; potential energy: 7,837 vs 4,915 mm Hg·mL, P = 0.002; PVA: 16,135 vs 11,742 mm Hg·mL, P = 0.0002) and lower efficiency (SW/PVA: 50% vs 59%, P = 0.03). The Anrep effect is an energy-demanding compensatory mechanism that maintains stroke volume under elevated afterload by increasing contractility and prolonging systole. This study confirms its chronic activation in HOCM and its immediate reversal post-PTSMA.
