The Left Ventricular Pressure-Volume Area and Stroke Work in Porcine Model of Ascending Compared to Descending Thoracic Aorta Stenosis Creating a Chronic Early Vs. Late Left Ventricular Afterload Increase

Abstract

Abstract Objective: Left ventricular hypertrophy in aortic stenosis, arterial hypertension or coarctation of the aorta is risk factor for early development of HF. In chronic late compared to early left ventricular afterload increases resulting from descending thoracic оr ascending aorta stenosis, we assess the left ventricular stroke work, pressure-volume area for О2 demand and effective work on the 4th and 8th weeks. It is suggested that reduced proximal thoracic aortic compliance presents with myocardial ischemia. However, development of adverse left ventricular hypertrophic remodeling and HF in different peak of LV afterload increase is understood poorly. Methods: Fourteen domestic male pigs (28 ± 3 kg) underwent descending thoracic or ascending aortic stenosis through posterior lateral thoracotomy, with cMRI and an invasive left ventricular pressure-volume loops’ аrea assessment (Millar 5Fr pig-tailed conductance catheter) on the 4th and 8th weeks. Left ventricular stroke work and pressure-volume area PVA, parameter for LV O2 demand, were assessed in hypertrophic left ventricular remodeling, resulting from different peaks in LV afterload (late vs. early LV afterload) increase and we thus defined early adverse LV hypertrophic remodeling in linear and nonlinear end-systolic pressure-volume regression analysis. For this we used special software. Data was compared with two-way repeated measures ANOVA. Results presented are means ± (SEM) or medians and significance is set at p < 0.05. Results: The left ventricular nonlinear PVA was not different, in LL compared to EL on the 8th week and when using the linear regression analysis. Stroke work was not different. The linear and nonlinear potential energy were not different between LL vs. the EL group. Nonlinear bLVO2 demand was not different, being higher in LL compared to EL in the 8th week. Indexed PVA parameters were not different or changed between the 4th and 8th weeks, when being normalized for body surface-area (m²) or 100 grams of LV mass. Conclusion: The left ventricular potential energy, PVA with effective work and LVO2 demands are not different in hypertrophic LV remodeling in LL vs. EL group at the 8th week. Difference is not present when end-systolic pressure-volume relation is assessed from indexed LV volumes for m² BSA or 100 grams of LV mass. EL is as important as LL in increased LV afterloads based on LV work and mechanical coupling in this hypertensive heart failure model having preserved EF.