A 91-year-old woman presented with worsening exertional dyspnea. Her previous medical history included hypertension, percutaneous coronary intervention with drugeluting stent placement to the mid left anterior descending coronary artery, moderate bilateral carotid atherosclerosis, and moderate chronic obstructive pulmonary disease.Transthoracic echocardiography revealed a normal left ventricular ejection fraction with asymmetric upper septal hypertrophy (posterior wall, 1.3 cm; interventricular septum, 2.0 cm; Figure 1A) but without left ventricular outflow tract (LVOT) obstruction ( Figure 1B) at rest or with a Valsalva maneuver. There was severe aortic valve calcification and stenosis ( Figure 1A and 1C).The patient was referred for transcatheter aortic valve replacement (AVR) via the transfemoral approach. Upon crossing the stenotic aortic valve, the peak-to-peak left ventricle-aorta (LVAo) pressure gradient was recorded at 60 mm Hg (Figure 2A). After deployment of a 23-mm Edwards SAPIEN prosthesis, the patient became hypotensive and the peak-to-peak LV-Ao gradient was recorded at 120 mm Hg ( Figure 2B). Transesophageal echocardiography demonstrated a properly functioning aortic prosthesis and revealed a dynamic obstruction in the LVOT attributable to systolic anterior motion of the mitral valve ( Figure 3A), associated with severe mitral regurgitation ( Figure 3B).After review of the preprocedural coronary angiogram ( Figure 4A), the decision was made to proceed emergently to alcohol septal ablation to relieve the dynamic LVOT obstruction. Isopropyl alcohol (1.5 mL) was infused in the septal perforator, and subsequent angiography revealed occlusion of the vessel ( Figure 4B). Transesophageal echocardiography revealed marked reduction in systolic anterior motion and in the degree of LVOT obstruction and mitral regurgitation, as well ( Figure 5). Hemodynamic tracings demonstrated almostcomplete resolution of the LV-Ao gradient ( Figure 6).The patient was successfully extubated at the conclusion of the case and was discharged from the hospital 5 days later. At 1-month follow-up, transthoracic echocardiography revealed continued reduction in the LV-Ao gradient at rest (15 mm Hg) and minimal increase with provocation by a Valsalva maneuver (18 mm Hg).
DiscussionIn patients with aortic stenosis, hypertrophy of the left ventricular myocardium often occurs as a result of the increased myocardial load imposed by the valvular obstruction. In most cases, the hypertrophy is concentric, although some patients present with an asymmetric upper septal hypertrophy with or without dynamic LVOT obstruction.
1-3Our patient demonstrated severe asymmetric upper septal hypertrophy, but had no evidence of LVOT obstruction on dynamic preoperative testing. Upon implantation of the transcatheter prosthesis, however, she developed significant LVOT obstruction. This is likely the result of a number of physiological and anatomic changes. The relationship between afterload and LVOT obstruction has been elucidated by numerous investigators...