Alcohol septal ablation for hypertrophic obstructive cardiomyopathy outcomes and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nehal Eid, M.D.[2]

Outcomes and prognosis

Alcohol septal ablation (ASA) performed at experienced centers provides substantial and usually durable relief of left ventricular outflow tract obstruction (LVOTO) and symptoms in appropriately selected patients with obstructive hypertrophic cardiomyopathy. Prognosis is determined principally by age, baseline disease severity, septal thickness, residual LVOT gradient, frailty, and the need for repeat septal reduction therapy.

Periprocedural outcomes

Mortality

Contemporary procedural mortality is approximately 1% or less at experienced centers. The SHARE Registry reported 30-day mortality of 0.4% among 455 patients undergoing ASA, whereas the Euro-ASA Registry reported 30-day mortality of 1%.[1][2] A single-center series of 952 procedures reported in-hospital mortality of 0.21%.[3]

Conduction disturbances

Complete heart block requiring a permanent pacemaker (PPM) is the most frequent major complication:

  • Contemporary PPM rates are approximately 6.5%–11%.[4]
  • In the Euro-ASA cohort, PPM implantation occurred in 9.4% within 30 days, with an additional 3.1% receiving a PPM during long-term follow-up.[5]
  • Pre-existing bundle branch block, particularly left bundle branch block, prolonged baseline PR interval, bradycardia, a high baseline LVOT gradient, marked QRS prolongation during the first 48 hours, and intraprocedural third-degree atrioventricular block predict PPM requirement.[4]
  • New right bundle branch block develops in approximately 46%–60% of patients after ASA, depending on the series.[3][6]

PPM implantation after ASA has not been associated with higher long-term mortality. In Euro-ASA data, PPM recipients had greater gradient reduction and fewer subsequent reinterventions than patients who did not require pacing.[5]

In a 2025 observational study of patients who developed complete heart block after ASA, corticosteroid treatment was associated with a lower PPM implantation rate (17.1% versus 43.9%; odds ratio 0.21). This nonrandomized finding is hypothesis-generating and does not establish routine corticosteroid therapy.[7]

Other acute complications and readmission

Uncommon acute complications include coronary dissection, ethanol spillover causing unintended myocardial infarction, cardiac perforation, pericardial effusion, and ventricular septal defect.[8]

Unplanned 30-day readmission occurs in approximately 10.4%. Reported causes include atrial fibrillation, heart failure exacerbation, ventricular tachycardia, and atrioventricular block. Renal failure, previous myocardial infarction, atrial fibrillation, and a pre-existing pacemaker predict readmission.[9]

Hemodynamic and symptomatic outcomes

ASA produces clinically important reductions in LVOT gradient:

  • In the Euro-ASA Registry, mean resting LVOT gradient decreased from 67 ± 36 mm Hg to 16 ± 21 mm Hg.[2]
  • Across the SHARE septal reduction therapy cohort, 92% of patients had a maximal LVOT gradient below 50 mm Hg at 1 year.[1]
  • Using the stringent endpoint of a residual resting gradient below 10 mm Hg, procedural success has been reported in approximately 80%.[8]
  • Hemodynamic improvement may continue for 3–6 months as the infarcted septum thins and remodels.[8]

Symptomatic improvement is generally durable. In Euro-ASA, mean NYHA functional class improved from 2.9 ± 0.5 to 1.6 ± 0.7, and 89% of patients were in NYHA class I or II at last follow-up.[2] Greater residual LVOT obstruction is associated with less symptomatic improvement and worse long-term survival.[2]

Long-term survival and clinical events

In the Euro-ASA Registry, survival at 1, 5, and 10 years was 98%, 89%, and 77%, respectively, with an all-cause mortality rate of 2.42 per 100 patient-years.[2]

In the Batzner single-center series, cardiac event-free survival at 5, 10, and 15 years was 98.9%, 97.0%, and 96.5%, respectively; only 14 cardiac deaths occurred during follow-up.[3] These estimates represent cardiac event-free survival rather than all-cause survival and should be interpreted in the context of a single-center, single-operator cohort.

Follow-up extending to 25 years has demonstrated persistent symptomatic and hemodynamic benefit in surviving patients.[10]

In the SHARE Registry, which included both ASA and surgical myectomy, median follow-up was 6.8 years:

  • HCM-related death occurred in 4% of patients (0.6% per year).
  • The heart failure composite of transplantation, left ventricular assist device implantation, left ventricular ejection fraction below 35%, or NYHA class III/IV symptoms occurred in 13% (1.9% per year).
  • Ventricular arrhythmias occurred in 5% (0.7% per year).
  • Ten-year event-free survival was 83%.
  • De novo atrial fibrillation developed in 21%.[1]

Because these SHARE estimates combine both forms of septal reduction therapy, they should not be interpreted as ASA-specific event rates.

Ventricular arrhythmias and sudden cardiac death

The arrhythmogenic potential of the ASA-induced septal scar remains a concern, although contemporary data are generally reassuring:

  • Reported annual sudden cardiac death (SCD) rates after ASA range from 0.4% to 1.3%, broadly overlapping rates reported after myectomy.[11][8]
  • In a cohort of 470 patients followed for a mean of 8.4 years, 10-year SCD-free survival was 95% and the annual SCD rate was 0.5%. ASA was also associated with a reduction in the number of conventional SCD risk factors.[12]
  • The SHARE ventricular arrhythmia composite occurred at 0.7% per year after septal reduction therapy.[1]
  • Higher event rates in some early series may reflect older techniques and larger ethanol doses.[8]

The Euro-ASA-derived ASA-SCARRE score uses pre-ASA septal thickness and the residual LVOT gradient at follow-up to estimate sudden cardiac arrest risk:

  • Score 0: both residual LVOT gradient below 30 mm Hg and septal thickness below 20 mm.
  • Score 1: either residual LVOT gradient of at least 30 mm Hg or septal thickness of at least 20 mm.
  • Score 2: both residual LVOT gradient of at least 30 mm Hg and septal thickness of at least 20 mm.
  • Discrimination is modest (C-statistic 0.684).[13]

The European Society of Cardiology HCM Risk-SCD model has also been validated after ASA. In 844 patients, the model demonstrated modest discrimination for SCD events (C-statistic 0.61), supporting its use as an adjunct to clinical risk assessment after ASA.[14]

Reintervention

Residual or recurrent LVOTO requiring additional septal reduction therapy occurs in approximately 10%–20% of patients after ASA and is more frequent than after myectomy.[15][3]

Predictors of repeat septal reduction therapy include:

  • Baseline mitral regurgitation
  • Younger age
  • Incomplete ablation of proximal septal branches
  • Inadequate initial gradient reduction[16]
  • Non-anteroseptal basal left ventricular hypertrophy involving at least two segments on cardiac magnetic resonance imaging[17]

Repeat ASA can provide further gradient and symptom improvement when another suitable septal perforator is available. Patients with residual obstruction caused by muscular bundles, papillary muscle abnormalities, or other surgically correctable anatomy are more likely to require myectomy.[18]

Comparison with surgical myectomy

No randomized trial has compared ASA with surgical myectomy. Comparative studies are observational and are affected by treatment-selection bias because patients undergoing ASA are generally older and have more comorbidities.

The 2024 AHA/ACC multisociety guideline reports similar 5-year survival after ASA and myectomy but lower survival after ASA at 10 years.[19]

A multicenter study of 3,859 patients found 10-year all-cause mortality of 26.1% after ASA compared with 8.2% after myectomy, with an adjusted hazard ratio of 1.68 (95% CI 1.29–2.19; P < 0.001).[15]

A meta-analysis of 27 observational studies involving 15,968 patients found no statistically significant difference in overall all-cause mortality (hazard ratio 1.24; 95% CI 0.88–1.76). However, studies with at least 5 years of follow-up showed higher mortality after ASA (hazard ratio 1.50; 95% CI 1.04–2.15).[20]

ASA produces less complete early gradient elimination and a higher reintervention rate than myectomy. In a propensity-matched cohort, the median predischarge resting gradient was 21 mm Hg after ASA compared with 0 mm Hg after myectomy.[21]

The apparent long-term survival disadvantage of ASA may reflect residual obstruction and preferential use of ASA in older or higher-risk patients rather than a causal effect of the procedure itself.[15][20]

Predictors of adverse outcomes

Outcome Prognostic factors Evidence
All-cause mortality after ASA Older age; greater preprocedural septal thickness; worse baseline NYHA class; higher residual LVOT gradient Euro-ASA Registry[2]
Heart failure progression after septal reduction therapy Older age; female sex SHARE Registry; estimates combine ASA and myectomy[1]
HCM-related mortality after septal reduction therapy Older age SHARE Registry; estimates combine ASA and myectomy[1]
Permanent pacemaker implantation Pre-existing conduction disease; prolonged PR interval; bradycardia; higher baseline gradient; early postprocedural QRS prolongation; intraprocedural complete heart block Contemporary PPM prediction model[4]
Repeat septal reduction therapy Baseline mitral regurgitation; younger age; incomplete proximal septal ablation; inadequate initial gradient reduction; non-anteroseptal hypertrophy Observational ASA cohorts[16][17]

Outcomes in selected populations

  • Patients aged 75 years or older: ASA provides gradient and symptomatic improvement comparable to that in younger patients, but high-degree atrioventricular block is more frequent (25.5% versus 13.6%).[22] A propensity-matched comparison found similar long-term survival after ASA and myectomy in this age group.[23]
  • Frailty: Frailty is associated with higher mortality, major adverse cardiac and cerebrovascular events, ischemic stroke, major bleeding, and readmission after ASA, but was not associated with increased sudden cardiac death or acute myocardial infarction.[24]
  • Severe septal hypertrophy: Patients with septal thickness of at least 30 mm may achieve short-term gradient and symptom improvement, but Euro-ASA data demonstrate higher long-term all-cause and cardiac mortality. The 2024 guideline also identifies marked septal hypertrophy as a setting in which ASA may be less effective.[25][19]

Overall prognosis

ASA at an experienced center is associated with low early mortality, substantial improvement in LVOT gradient and functional status, and durable clinical benefit in most patients. The principal adverse prognostic marker is persistent or recurrent LVOTO. Older age, severe hypertrophy, advanced baseline symptoms, frailty, and incomplete gradient reduction identify patients at higher risk of death, heart failure progression, or repeat intervention.

Counseling should distinguish the favorable probability of symptomatic improvement from the approximately 10% risk of PPM implantation and the 10%–20% probability of repeat septal reduction therapy. Evidence remains insufficient to recommend septal reduction therapy solely to improve survival in asymptomatic patients.[19]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Maurizi N, Antiochos P, Owens A; et al. (2024). "Long-Term Outcomes After Septal Reduction Therapies in Obstructive Hypertrophic Cardiomyopathy: Insights From the SHARE Registry". Circulation. 150 (17): 1377–1390. doi:10.1161/CIRCULATIONAHA.124.069378. PMID 39355918 Check |pmid= value (help).
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Veselka J, Jensen MK, Liebregts M; et al. (2016). "Long-Term Clinical Outcome After Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy: Results From the Euro-ASA Registry". European Heart Journal. 37 (19): 1517–1523. doi:10.1093/eurheartj/ehv693. PMID 26746632.
  3. ↑ 3.0 3.1 3.2 3.3 Batzner A, Pfeiffer B, Neugebauer A; et al. (2018). "Survival After Alcohol Septal Ablation in Patients With Hypertrophic Obstructive Cardiomyopathy". Journal of the American College of Cardiology. 72 (24): 3087–3094. doi:10.1016/j.jacc.2018.09.064. PMID 30545446.
  4. ↑ 4.0 4.1 4.2 Karimianpour A, Heizer J, Leaphart D; et al. (2021). "Predicting Complete Heart Block After Alcohol Septal Ablation for Hypertrophic Cardiomyopathy Using a Risk Stratification Model and Clinical Tool". Catheterization and Cardiovascular Interventions. 98 (2): 393–400. doi:10.1002/ccd.29478.
  5. ↑ 5.0 5.1 Veselka J, Liebregts M, Cooper R; et al. (2022). "Outcomes of Patients With Hypertrophic Obstructive Cardiomyopathy and Pacemaker Implanted After Alcohol Septal Ablation". JACC: Cardiovascular Interventions. 15 (19): 1910–1917. doi:10.1016/j.jcin.2022.06.034. PMID 36202559 Check |pmid= value (help).
  6. ↑ Kusumoto FM, Schoenfeld MH, Barrett C; et al. (2019). "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay". Journal of the American College of Cardiology. 74 (7): e51–e156. doi:10.1016/j.jacc.2018.10.044.
  7. ↑ Potratz M, Mohemed K, Coppée C; et al. (2025). "Corticosteroids Reduce Pacemaker Implantation After Alcohol Septal Ablation in oHCM Patients". Clinical Research in Cardiology. doi:10.1007/s00392-025-02752-y.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Sorajja P (2017). "Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy: A Word of Balance". Journal of the American College of Cardiology. 70 (4): 489–494. doi:10.1016/j.jacc.2017.06.011. PMID 28728695.
  9. ↑ Ando T, Adegbala O, Aggarwal A; et al. (2020). "Unplanned Thirty-Day Readmission After Alcohol Septal Ablation for Hypertrophic Cardiomyopathy". The American Journal of Cardiology. 125 (12): 1890–1895. doi:10.1016/j.amjcard.2020.03.016. PMID 32305221 Check |pmid= value (help).
  10. ↑ Veselka J, Tesar D, Topalo R, Hansvenclova E, Adlova R (2023). "Follow-Up of Up to 25 Years After Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy". JACC: Cardiovascular Interventions. 16 (12): 1556–1557. doi:10.1016/j.jcin.2023.03.049. PMID 37380246 Check |pmid= value (help).
  11. ↑ Liebregts M, Vriesendorp PA, Ten Berg JM (2017). "Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy: A Word of Endorsement". Journal of the American College of Cardiology. 70 (4): 481–488. doi:10.1016/j.jacc.2017.02.080. PMID 28728694.
  12. ↑ Jensen MK, Prinz C, Horstkotte D; et al. (2013). "Alcohol Septal Ablation in Patients With Hypertrophic Obstructive Cardiomyopathy: Low Incidence of Sudden Cardiac Death and Reduced Risk Profile". Heart. 99 (14): 1012–1017. doi:10.1136/heartjnl-2012-303339.
  13. ↑ Veselka J, Liebregts M, Cooper R; et al. (2022). "Prediction of Sudden Cardiac Arrest After Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy: ASA-SCARRE Risk Score". The American Journal of Cardiology. 184: 120–126. doi:10.1016/j.amjcard.2022.08.028. PMID 36192196 Check |pmid= value (help).
  14. ↑ Liebregts M, Faber L, Jensen MK; et al. (2018). "Validation of the HCM Risk-SCD Model in Patients With Hypertrophic Cardiomyopathy Following Alcohol Septal Ablation". Europace. 20 (FI2): f198–f203. doi:10.1093/europace/eux251. PMID 29016960.
  15. ↑ 15.0 15.1 15.2 Cui H, Schaff HV, Wang S; et al. (2022). "Survival Following Alcohol Septal Ablation or Septal Myectomy for Patients With Obstructive Hypertrophic Cardiomyopathy". Journal of the American College of Cardiology. 79 (17): 1647–1655. doi:10.1016/j.jacc.2022.02.032. PMID 35483751 Check |pmid= value (help).
  16. ↑ 16.0 16.1 Hiruma T, Kitamura M, Takamisawa I; et al. (2024). "Predictors of Repeated Septal Reduction After Alcohol Septal Ablation in Patients With Hypertrophic Cardiomyopathy". Journal of the American College of Cardiology. 83 (4): 546–548. doi:10.1016/j.jacc.2023.11.013. PMID 38267115 Check |pmid= value (help).
  17. ↑ 17.0 17.1 Kitamura M, Amano Y, Takayama M; et al. (2017). "Usefulness of Non-Anteroseptal Region Left Ventricular Hypertrophy Using Cardiac Magnetic Resonance to Predict Repeat Alcohol Septal Ablation for Refractory Obstructive Hypertrophic Cardiomyopathy". The American Journal of Cardiology. 120 (1): 124–130. doi:10.1016/j.amjcard.2017.03.248. PMID 28483204.
  18. ↑ Hiruma T, Kitamura M, Takamisawa I; et al. (2026). "Outcomes After Repeat Alcohol Septal Ablation in Patients With Obstructive Hypertrophic Cardiomyopathy". JACC: Advances. 5 (3): 102595. doi:10.1016/j.jacadv.2026.102595. PMID 41689885 Check |pmid= value (help).
  19. ↑ 19.0 19.1 19.2 Ommen SR, Ho CY, Asif IM; et al. (2024). "2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy". Journal of the American College of Cardiology. 83 (23): 2324–2405. doi:10.1016/j.jacc.2024.02.014.
  20. ↑ 20.0 20.1 Yokoyama Y, Shimoda T, Shimada YJ; et al. (2023). "Alcohol Septal Ablation Versus Surgical Septal Myectomy of Obstructive Hypertrophic Cardiomyopathy: Systematic Review and Meta-Analysis". European Journal of Cardio-Thoracic Surgery. 63 (3): ezad043. doi:10.1093/ejcts/ezad043. PMID 36782361 Check |pmid= value (help).
  21. ↑ Nguyen A, Schaff HV, Hang D; et al. (2019). "Surgical Myectomy Versus Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy: A Propensity Score-Matched Cohort". The Journal of Thoracic and Cardiovascular Surgery. 157 (1): 306–315.e3. doi:10.1016/j.jtcvs.2018.08.062. PMID 30279000.
  22. ↑ Lawin D, Stellbrink C, Stellbrink E; et al. (2023). "Alcohol Septal Ablation in Patients Aged 75 Years or Older With Hypertrophic Obstructive Cardiomyopathy". Heart. 109 (23): 1778–1784. doi:10.1136/heartjnl-2023-322659. PMID 37460195 Check |pmid= value (help).
  23. ↑ Sawma T, Schaff HV, Danesh S; et al. (2026). "Outcomes of Alcohol Septal Ablation vs Transaortic Septal Myectomy in Elderly Patients With Obstructive Hypertrophic Cardiomyopathy". JACC: Advances. 5 (1): 102488. doi:10.1016/j.jacadv.2025.102488. PMID 41609286 Check |pmid= value (help).
  24. ↑ Jain H, Patel N, Jain J; et al. (2026). "Long-Term Impact of Frailty on Outcomes Following Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy". JACC: Advances. 5 (5): 102767. doi:10.1016/j.jacadv.2026.102767. PMID 42202378 Check |pmid= value (help).
  25. ↑ Veselka J, Jensen M, Liebregts M; et al. (2020). "Alcohol Septal Ablation in Patients With Severe Septal Hypertrophy". Heart. 106 (6): 462–466. doi:10.1136/heartjnl-2019-315422. PMID 31471463.
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