Abstract
Background: Severe RV failure is common (~25%) following acute LVAD unloading. The role of IVS dysfunction in this response remains uncertain, so we studied chronic ventricular interactions with incremental LV unloading following IVS damage. Methods: Percutaneous transluminal septal myocardial ablation (PTSMA) with ethanol caused irreversible IVS damage in 6 sheep. Main septal artery catheterization was performed in 6 other sham animals, and both groups underwent hemodynamic assessment 4w later. RV volume was derived from a 3-axis ellipsoidal subtraction model using sonomicrometer dimensions. RV- ejection fraction (EF), pressure recruitable stroke work (PRSW), end-systolic elastance (Ees), 1 st derivative of maximum RV pressure (dP/dt), and Tau were derived from P/V loops during IVC occlusion and LV unloading (25/50/75/100%) using a Bio-Medicus pump. Flow-probes measured % steady-state pulmonary, aortic, and mechanical bypass flow. Results: Response to varying LV assist levels is shown in the Figure ( * =P<0.05). RV- EF, PRSW and Ees decreased in shams, but remained stable in PTSMA during high level LV unloading. DP/dt decreased in shams at 75% LV unloading and trended down at 100%. In contrast, high baseline Tau after PTSMA normalized with moderate ≥50% LV assist. Conclusions: Institution of LV unloading in a chronic IVS damaged but otherwise healthy heart protects against compromised RV function, whereas sham animals respond adversely. Chronic IVS fibrosis may confer protection by limiting changes in RV chamber geometry.
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