A Tale of Two Pressures- Medical Management Dilemmas in Post-TAVR LVOT Obstruction

Abstract

Background Systolic anterior motion (SAM) of the anterior mitral valve leaflet after transcatheter aortic valve replacement (TAVR) is an extremely rare pathophysiologic phenomenon leading to left ventricular outflow tract (LVOT) obstruction. We report a case of post-TAVR LVOT obstruction leading to pulmonary edema and respiratory failure successfully treated medically with fluid challenges. Case Presentation A 91-year-old woman with severe symptomatic aortic stenosis and New York Heart Association (NYHA) functional class III was referred to our institution for TAVR evaluation. Patient was deemed to be intermediate risk based on Society of Thoracic Surgeon (STS) score of 4.7%. The baseline transthoracic echocardiogram confirmed the presence of severe aortic stenosis with peak aortic jet velocity of 5.5 m/s, aortic valve area of 0.8 cm2and mean gradient > 40 mmHg with preserved left ventricular function and mild mitral regurgitation. No intra-ventricular gradient, septal wall hypertrophy or SAM of the anterior mitral valve leaflet was noted. Patient underwent successful transfemoral TAVR with a 29 mm Medtronic Evolut PRO valve. Angiography confirmed proper valve position and no paravalvular leak. Post-procedural echocardiogram demonstrated adequate prosthesis performance with new-onset of SAM dynamic LVOT obstruction and concomitant severe mitral regurgitation leading to systolic flow reversal in both left and right pulmonary veins and apical tethering of the anterior mitral leaflet. Postoperative course was further complicated by Enterococcus sepsis leading to atrial fibrillation with rapid ventricular response resulting in systemic hypotension, pulmonary edema and impending respiratory failure. Despite the congestion in the pulmonary vasculature, the decision was made to optimize diastolic filling and preload by titrated beta-blockade and serial fluid challenges with 250 mL boluses. Patient was able to increase forward stroke volume leading to improvements in mean arterial pressure and resolution of pulmonary congestion. Conclusions The mechanism leading to SAM and LVOT obstruction after TAVR implant is poorly elucidated and rarely reported in the literature. Chronic aortic stenosis results in increased afterload to the LV that is compensated by elevated intra-ventricular pressure to allow adequate systemic perfusion. The increased intra-ventricular pressure also prevents septal inward motion and thus keeps LVOT unobstructed. With TAVR and the relief of the fixed obstruction, intra-ventricular pressure drops simultaneously with a reduction in LVOT cross-sectional area due to an increased flow velocity. A pressure gradient is created between the left atrium and LVOT that pulls the anterior mitral leaflet toward the LVOT creating a dynamic LVOT obstruction. Every effort should be made to optimize diastolic filling and contractility through titrated beta-blockade and fluid challenge.