Abstract 4370546: Incidence of Systolic Dysfunction After Alcohol Septal Ablation for Hypertrophic Cardiomyopathy: A Single-Center Experience

Introduction: Left ventricular systolic dysfunction (LVSD) is an uncommon late complication seen in patients with hypertrophic obstructive cardiomyopathy (HOCM). Prior studies estimated the incidence to be around 8% and reported that it is more common in patients who have undergone septal reduction therapy, which includes alcohol septal ablation (ASA). Our aim is to investigate LVSD incidence among patients who underwent ASA at our institution. Methods: We conducted a retrospective cohort study, reviewing ASAs performed at the Medical University of South Carolina from 2007 to 2024. Inclusion required sufficient echocardiographic data to compare ejection fraction (EF) from before and after each ASA and determine if LVSD (defined as EF <50%) had occurred during follow up post-ASA. Results: Out of 367 ASAs (61% male patients, average age 62 ± 13 years, 85% Caucasian, 11% Black), 186 cases (50.7%) exhibited post-procedure decline in EF (mean decrease 8 ± 6%). Median time to post-procedure echocardiogram was 16 weeks. Mean pre-ASA EF was 72 ± 6% and mean post-ASA EF was 63 ± 6%, with 3 patients (0.82%, 95% CI 0.17-2.38%) meeting criteria for LVSD (mean EF decrease of 28%, mean pre-ASA EF 70%, mean post-ASA EF 42%). Serial echocardiograms were available for 246 cases and showed that 6 more patients met LVSD criteria at some point (mean onset 8.3 ± 6.8 years post-ASA). In total, 9 of the 367 reviewed cases (2.45%, 95% CI 1.12-4.61%) appeared to meet criteria for LVSD; however, comprehensive chart reviews for these patients revealed that 4 were transient stress-induced drops, 3 were following myocardial infarction, and 1 was pacemaker-related. Only 1 case was suggestive of true HOCM-induced LVSD, for an overall incidence of 0.27% (95% CI 0.007-1.52%). Conclusion: True HOCM-induced LVSD appears to be a very rare complication following ASA, occurring in <1% of our cohort. While approximately half of the cases in our study demonstrated a decline in EF (mean 8%) after ASA, the decline was often mild and an expected physiological result of relieving left ventricular outflow tract obstruction. Rigorous chart reviews for apparent instances of LVSD (2.5%) revealed alternative explanations for the decreased EF in most cases. These findings suggest a lower incidence of LVSD post-ASA than shown in previous studies.