Abstract 4367957: Transapical beating-heart septal myectomy for symptomatic nonobstructive hypertrophic cardiomyopathy: Achieving structural relief and functional recovery

Abstract

Introduction: The pathogenesis of nonobstructive hypertrophic cardiomyopathy (nHCM) involves a combination of systolic cavity obliteration with reduced stroke volume, midventricular obstruction with diastolic dysfunction, and impaired left ventricular (LV) microvascular perfusion. To date, no ideal therapy has been widely verified for symptomatic nHCM. Hypothesis: Transapical beating-heart septal myectomy (TA-BSM) could enlarge the LV cavity and relieve systolic cavity obliteration or midventricular obstruction. Methods: Patients with nHCM and without LV outflow tract obstruction were enrolled if they had drug-refractory symptoms. All patients’ perioperative symptoms and functional status were prospectively recorded. The TA-BSM procedure was performed via left mini-thoracotomy using a beating-heart myectomy device under real-time echocardiographic guidance for adequate myocardial resections aiming at enlarging the LV cavity. The primary endpoint was procedural success, defined as Kansas City Cardiomyopathy Questionnaire score improvement of ≥10 points, stroke volume increased by ≥5 mL, and diastolic function grading at normal or grade I (of III) at 6-to-12-month follow-up. [ClinicalTrials.gov Identifier: NCT05648825] Results: From January 2023 through January 2025, 97 eligible patients were enrolled. Among 96 patients who were followed up over a median of 455 days, 91.8% achieved procedural success. In a subset of 38 patients who completed cardiopulmonary exercise tests, peak oxygen uptake increased from 19.5±2.2 (mean±SD) at baseline to 21.0±4.5 mL/kg/min at 6-12 months (p<0.001). Upon follow-up, 90.5% of patients were in NYHA Class I, compared to none at baseline. Adverse events included one case of iatrogenic mitral valve injury, which was successfully repaired without sequelae. Another case of iatrogenic ventricular septal perforation, who underwent surgical repair, died on postoperative day 10 due to multiorgan failure. Myocardial perfusion imaging with N 13 -labeled ammonia positron emission tomography showed increased myocardial blood flow and coronary flow reserve after TA-BSM. Conclusions: TA-BSM can considerably restore physiological LV morphology and improve quality of life for symptomatic nHCM patients. Enhanced coronary microvascular perfusion may contribute to symptomatic relief. These findings support the use of TA-BSM as a therapeutic option for nHCM. Further validation by randomized controlled studies with long-term observation is warranted.