Valvular Heart Disease - Cases
Miho Fukui, MD, PhD
Researcher
MHIF
Minneapolis, Minnesota, United States
Miho Fukui, MD, PhD
Researcher
MHIF
Minneapolis, Minnesota, United States
Paul Sorajja, MD
physician
Minneapolis Heart Institute Foundation, United States
Maurice Enriquez-Sarano, MD
physician
Minneapolis Heart Institute Foundation, United States
John Lesser, MD
Cardiologist
Minneapolis Heart Institute at Abbott Northwestern Hospital
Minneapolis, Minnesota, United States
Vinayak Baat, MD
surgeon
Minneapolis Heart Institute Foundation, United States
Joao Cavalcante, MD
Director, Cardiac MRI and Structural CT Labs
Minneapolis Heart Institute at Abbott Northwestern Hospital
Minneapolis, Minnesota, United States
84-year-old woman with history of surgical aortic valve replacement and symptomatic severe mixed mitral regurgitation and stenosis with severe mitral annulus calcification was considered for transcatheter mitral valve replacement (TMVR) with dedicated transapical Tendyne device (Abbott Vascular, Santa Clara, California). Baseline functional cardiac computed tomography (CT) showed small neo-LVOT area consistent with a high risk of left ventricular outflow tract (LVOT) obstruction (Figure 1). Pre-emptive alcohol septal ablation (ASA) was performed with 0.8 ml of desiccated ethanol injected into the first septal artery. Repeat CT angiography 5 weeks after ASA demonstrated increased neo-LVOT area. Patient had successful Tendyne TMVR with complete relief of mitral regurgitation and stenosis, no paravalvular regurgitation, and no LVOT obstruction. However, she experienced low cardiac output syndrome with a cardiac output index of 2.06 L/ml/m2 on right heart catheterization after TMVR, for which cardiac magnetic resonance (CMR) was performed.
Diagnostic Techniques and Their Most Important Findings:
CMR post-ASA and TMVR showed late gadolinium enhancement transmural infarction at basal to mid anteroseptum compatible with prior ASA, and small apical infarct related to transapical access for TMVR (Figure 2). Patient’s LVEF, heart rate and forward stroke volume were: 36%, 80bpm and 37ml, respectively. There was no residual MR. The hemodynamic decompensation was resulted from a combination of the large septal infarction, tensioning of the apical Tendyne pad with LV cavity reduction and problematic LV contractility and relaxation producing low forward stroke volume.
Learning Points from this Case:
TMVR with pre-emptive ASA therapy has emerged as a potential therapy for high or prohibitive surgical risk patients with severe mitral valvular disease who have the risk of LVOT obstruction, though a certain group of patients might develop post-procedure hemodynamic decompensation. CMR pre- and post-TMVR can, in addition to the evaluation of MR severity and scar burden, provide unique insights into the ventricular reserve and response after MR elimination.