Impact of leftward septal shift and potential role of ischemia in its production during experimental right ventricular pressure overload

Abstract

To determine whether leftward septal shifting mediates primary changes in left ventricular (LV) preload and diastolic function, seven animals were studied after instrumentation with right ventricular (RV) and LV Millar microtip pressure transducers and RV and LV segment length crystals. This allowed assessment of LV preload and LV diastolic pressure segment length relationships before and after the pulmonary artery pressure was first doubled, then tripled by embolizing the pulmonary circulation with glass beads, and then after an additional injection of glass beads reduced the cardiac output by 30%. Echocardiographic images were also acquired to assess LV size and septal configuration. To determine whether reversal of the transseptal pressure gradient and leftward septal shifting during acute pulmonary hypertension is associated with RV ischemia, transmural biopsies of the right ventricle for adenosine triphosphate and creatine phosphate analysis were performed at each stage. We determined that doubling and tripling of the pulmonary artery pressure was not associated with RV ischemia or alteration in septal configuration or diastolic function of the left ventricle. However, LV preload, measured by both segment length crystals and echo-derived areas and circumferences, was decreased when the pulmonary artery was tripled. When cardiac output was decreased 30% there was depletion of adenosine triphosphate and creatine phosphate, a reversal of the transseptal pressure gradient, and reduction of the LV shape and eccentricity indices consistent with leftward septal shift. The LV diastolic pressure/ segment length relationships were not consistently altered. We conclude that (1) LV preload decreases before the transseptal pressure gradient decreases and the septum shifts leftward, (2) LV distensibility does not appear to be altered by leftward septal shift when it occurs provided the pericardium is opened, and (3) RV ischemia likely contributes to the reversal of the transseptal pressure gradient and shifting of the septum leftward.