Hypertrophic cardiomyopathy interventions

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]Cafer Zorkun, M.D. [3]; Caitlin J. Harrigan [4]; Martin S. Maron, M.D.; Barry J. Maron, M.D.; Lakshmi Gopalakrishnan, M.B.B.S. [5]

Overview

This microchapter covers procedural and device-based interventions for hypertrophic cardiomyopathy (HCM), including septal reduction therapy (surgical myectomy and alcohol septal ablation), implantable cardioverter-defibrillator (ICD) placement for sudden cardiac death (SCD) prevention, catheter ablation for atrial fibrillation (AF) and ventricular tachycardia (VT), cardiac pacing, cardiac resynchronization therapy (CRT), mechanical circulatory support, and cardiac transplantation. The role of cardiac myosin inhibitors in reducing the need for septal reduction therapy is addressed as context for procedural decision-making.[1]

Septal Reduction Therapy (SRT)

General Principles

SRT is recommended for patients with obstructive HCM who remain symptomatic despite guideline-directed medical therapy (GDMT), performed at experienced HCM centers (Class I).[1] The 2024 AHA/ACC guideline defines general eligibility criteria for SRT across three domains:[1]

  • Clinical: Severe dyspnea or chest pain (usually NYHA class III–IV), or other exertional symptoms (syncope, near-syncope) attributable to LVOT obstruction that interfere with everyday activity despite optimal medical therapy.
  • Hemodynamic: Dynamic LVOT gradient ≥50 mm Hg at rest or with physiologic provocation, associated with septal hypertrophy and systolic anterior motion (SAM) of the mitral valve.
  • Anatomic: Targeted anterior septal thickness sufficient to perform the procedure safely and effectively.

SRT is not recommended for asymptomatic patients with normal exercise capacity (Class III: Harm). Mitral valve replacement should not be performed solely for relief of LVOT obstruction when SRT is an option (Class III: Harm).[1]

2024 AHA/ACC Guideline Recommendations for Invasive Treatment

Class I
1. In patients with obstructive HCM who remain symptomatic despite GDMT, SRT in eligible patients, performed at experienced HCM centers,† is recommended for relieving LVOTO. (Level of Evidence: B-NR)[1]
2. In symptomatic patients with obstructive HCM who have associated cardiac disease requiring surgical treatment (eg, associated anomalous papillary muscle, markedly elongated anterior mitral leaflet, intrinsic mitral valve disease, multivessel CAD, valvular aortic stenosis), surgical myectomy, performed at experienced HCM centers,† is recommended. (Level of Evidence: B-NR)[1]
3. In adult patients with obstructive HCM who remain severely symptomatic, despite GDMT and in whom surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age, alcohol septal ablation in eligible patients, performed at experienced HCM centers,† is recommended. (Level of Evidence: C-LD)[1]
Class IIb
4. In patients with obstructive HCM, earlier (NYHA class II) surgical myectomy performed at comprehensive HCM centers may be reasonable in the presence of additional clinical factors, including: (Level of Evidence: B-NR)[1]
a. Severe and progressive pulmonary hypertension thought to be attributable to LVOTO or associated MR;
b. Left atrial enlargement with ≥1 episodes of symptomatic AF;
c. Poor functional capacity attributable to LVOTO as documented on treadmill exercise testing;
d. Children and young adults with very high resting LVOT gradients (>100 mm Hg).
5. For symptomatic patients with obstructive HCM, SRT in eligible patients, performed at experienced HCM centers,† may be considered as an alternative to escalation of medical therapy after shared decision-making including risks and benefits of all treatment options. (Level of Evidence: C-LD)[1]

Impact of Cardiac Myosin Inhibitors on SRT Decision-Making

The 2024 guideline includes cardiac myosin inhibitors (mavacamten, aficamten) as a Class I second-line option for patients who fail first-line beta-blockers or nondihydropyridine calcium channel blockers, positioned alongside disopyramide and SRT as escalation options.[1]

In the VALOR-HCM trial, among 112 patients with severely symptomatic obstructive HCM referred for SRT, only 17.9% of mavacamten-treated patients met guideline criteria for SRT or proceeded with the procedure at 16 weeks, compared with 76.8% of placebo patients (difference 58.9%; P < 0.001).[2] At 128 weeks, sustained freedom from SRT was observed, with only 15.7% meeting the composite endpoint and approximately 88% of patients transitioning to commercial mavacamten.[3] Notably, 13.8% of patients (5.41 per 100 patient-years) experienced LVEF <50% during the 128-week follow-up, including 2 patients with LVEF ≤30% and 1 death; 80% of those with reduced LVEF continued treatment after dose adjustment. New-onset atrial fibrillation occurred in 10.2% (4.55 per 100 patient-years).[3] SRT may be considered as an alternative to escalation of medical therapy after shared decision-making (Class IIb).[1] Aficamten, a next-in-class cardiac myosin inhibitor, received FDA approval in December 2025 for symptomatic obstructive HCM. In the phase 3 SEQUOIA-HCM trial (n=282), aficamten improved peak oxygen uptake by 1.7 mL/kg/min versus placebo (P<0.001), with significant improvements in all 10 prespecified secondary endpoints including NYHA class, KCCQ-CSS, and LVOT gradients.[4] The MAPLE-HCM trial subsequently demonstrated superiority of aficamten monotherapy over metoprolol monotherapy (between-group pVO₂ difference 2.3 mL/kg/min; P<0.001).[5]


Extended Septal Myectomy (ESM)

Technique and Indications: Transaortic ESM is the most broadly applicable SRT, allowing gradient relief at any level within the ventricle.[1] It is the preferred approach when concomitant cardiac pathology requires surgical correction (anomalous papillary muscles, markedly elongated anterior mitral leaflet, intrinsic mitral valve disease, multivessel CAD, valvular aortic stenosis) — Class I.[1]

Outcomes: Operative mortality is <1% at experienced centers, with clinical success rates of >90–95%.[1][6] Successful ESM eliminates or reduces SAM-mediated mitral regurgitation and its consequences.[1] Long-term survival after ESM is similar to an age-matched general population, and recurrent outflow tract obstruction is rare.[1]

Earlier Myectomy Considerations: The 2024 guideline allows consideration of earlier surgical myectomy (NYHA class II) at comprehensive HCM centers in the presence of (Class IIb):[1]

  • Severe and progressive pulmonary hypertension attributable to LVOT obstruction or associated MR
  • Left atrial enlargement with ≥1 episodes of symptomatic AF
  • Poor functional capacity documented on exercise testing
  • Children and young adults with very high resting LVOT gradients (>100 mm Hg)

Alcohol Septal Ablation (ASA)

Technique and Patient Selection: ASA is a percutaneous catheter-based procedure involving injection of absolute alcohol into a septal perforator artery supplying the area of SAM-septal contact, producing a controlled septal infarction. It requires appropriate coronary anatomy and is performed under echocardiographic guidance.[1][6]

Indications: ASA is recommended (Class I) for adult patients with obstructive HCM who remain severely symptomatic despite GDMT and in whom surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age.[1] ASA avoids sternotomy, has a shorter hospital stay, and is advantageous when frailty or comorbidities increase the risk of ESM.[1]

Limitations: ASA is less effective with gradients ≥100 mm Hg and septal thickness ≥30 mm.[1][6] It is associated with a greater risk of permanent pacemaker (approximately 10–20%, or 4- to 5-fold higher than myectomy) and a greater need for repeat intervention for residual obstruction (7–20% of patients).[1][6]

Myectomy vs. ASA Selection: No randomized controlled trials comparing the two procedures exist. The choice involves shared decision-making at experienced centers, considering patient age, anatomy, comorbidities, and preferences.[1] Patients who fail one modality may still be candidates for the other.[6] In a multicenter observational study, 10-year survival was lower with ASA compared with ESM, though unmeasured confounding by indication may contribute to this finding.[7]

Implantable Cardioverter-Defibrillator (ICD)

Secondary Prevention

ICD placement is recommended (Class I) for patients with HCM and prior documented cardiac arrest or sustained VT.[1]

Primary Prevention

For adult patients with ≥1 major risk factors for SCD, it is reasonable to offer an ICD (Class IIa). The 2024 guideline identifies the following major risk factors:[1]

  • Sudden death attributable to HCM in ≥1 first-degree or close relatives ≤50 years of age
  • Massive LVH ≥30 mm in any LV segment
  • ≥1 recent episodes of syncope suspected to be arrhythmic
  • LV apical aneurysm with transmural scar or LGE
  • LV systolic dysfunction (EF <50%)

For patients without major risk factors but with extensive LGE on CMR or non-sustained ventricular tachycardia (NSVT) on ambulatory monitoring, an ICD may be considered (Class IIb). Discussion of estimated 5-year SCD risk can be useful during shared decision-making (Class IIa).[1]

Populations with Special Considerations:

  • Children: ICD is reasonable for those with ≥1 conventional risk factors (unexplained syncope, massive LVH, NSVT, family history of early SCD), balanced against higher long-term complication rates (Class IIa).[1]
  • Older adults (>60 years): Given the very low SCD event rate, the risk stratification strategy with major markers is most applicable to younger and middle-aged patients; ICD is discouraged as routine in clinically stable patients >60 years but may be considered case-by-case.[1][8]
  • End-stage HCM (LVEF <50%): ICD placement can be beneficial (Class IIa).[1]

ICD should NOT be placed in patients without risk factors (Class III: Harm) or solely to permit competitive athletics (Class III: Harm). Note: The 2011 guideline Class III (Harm) recommendation against ICD in genotype-positive/phenotype-negative individuals was not carried forward in the 2024 guideline, though ICD remains inappropriate in this population given the absence of clinical disease.[1]

2024 AHA/ACC Guideline Recommendations for ICD Placement

Class I
1. In patients with HCM, application of individual clinical judgment is recommended when assessing the prognostic strength of conventional risk marker(s) within the clinical profile of the individual patient, as well as a thorough and balanced discussion of the evidence, benefits, and estimated risks to engage the fully informed patient's active participation in ICD decision-making. (Level of Evidence: C-EO)[1]
2. For patients with HCM and previous documented cardiac arrest or sustained VT, ICD placement is recommended. (Level of Evidence: B-NR)[1]
Class IIa
3. For adult patients with HCM with ≥1 major risk factors for SCD, it is reasonable to offer an ICD. These major risk factors include: (Level of Evidence: B-NR)[1]
a. Sudden death judged definitively or likely attributable to HCM in ≥1 first-degree or close relatives who are ≤50 years of age;
b. Massive LVH ≥30 mm in any LV segment;
c. ≥1 recent episodes of syncope suspected by clinical history to be arrhythmic (ie, unlikely to be of neurocardiogenic [vasovagal] etiology, or related to LVOTO);
d. LV apical aneurysm with transmural scar or LGE;
e. LV systolic dysfunction (EF <50%).
4. For children with HCM who have ≥1 conventional risk factors, including unexplained syncope, massive LVH, NSVT, or family history of early HCM-related SCD, ICD placement is reasonable after considering the relatively high complication rates of long-term ICD placement in younger patients. (Level of Evidence: B-NR)[1]
5. For patients with HCM with ≥1 major SCD risk factors, discussion of the estimated 5-year sudden death risk and mortality rates can be useful during the shared decision-making process for ICD placement. (Level of Evidence: B-NR)[1]
Class IIb
6. In select adult patients with HCM and without major SCD risk factors after clinical assessment, or in whom the decision to proceed with ICD placement remains otherwise uncertain, ICD may be considered in patients with extensive LGE by contrast-enhanced CMR imaging or NSVT present on ambulatory monitoring. (Level of Evidence: B-NR)[1]
7. In pediatric patients with HCM, it can be useful to consider additional factors such as extensive LGE on contrast-enhanced CMR imaging and systolic dysfunction in risk stratification for ICD shared decision-making. (Level of Evidence: B-NR)[1]

Device Selection

Either single-chamber transvenous ICD or subcutaneous ICD (S-ICD) is recommended after shared decision-making (Class I).[1] S-ICDs are particularly suitable for younger patients when antitachycardia pacing and antibradycardia pacing are unlikely to be needed.[1][8] Single-coil leads are preferred over dual-coil leads (Class I).[1] Dual-chamber ICDs are reasonable for patients with bradycardia/conduction abnormalities or as an attempt to relieve obstruction in patients >65 years (Class IIa).[1]

2024 AHA/ACC Guideline Recommendations for ICD Device Selection

Class I
1. In patients with HCM who are receiving an ICD, either a single-chamber transvenous ICD or a subcutaneous ICD is recommended after a shared decision-making discussion that takes into consideration patient preferences, age, lifestyle, and potential need for pacing for bradycardia or VT termination. (Level of Evidence: B-NR)[1]
2. In patients with HCM who are receiving a transvenous ICD, single-coil ICD leads are recommended in preference to dual-coil leads, if defibrillation threshold is deemed adequate. (Level of Evidence: B-NR)[1]
Class IIa
3. In patients with HCM who are receiving an ICD, dual-chamber ICDs are reasonable for patients with a need for atrial or atrioventricular sequential pacing for bradycardia/conduction abnormalities, or as an attempt to relieve symptoms of obstructive HCM (most commonly in patients >65 years of age). (Level of Evidence: B-NR)[1]
4. In selected adult patients with nonobstructive HCM receiving an ICD who have NYHA class II to ambulatory class IV HF, left bundle branch block (LBBB), and LVEF <50%, cardiac resynchronization therapy (CRT) for symptom reduction is reasonable. (Level of Evidence: C-LD)[1]
Class IIb
5. In patients with HCM in whom a decision has been made for ICD implantation and who have paroxysmal atrial tachycardias or AF, dual-chamber ICDs may be reasonable, but this decision must be balanced against higher complication rates of dual-chamber devices. (Level of Evidence: C-LD)[1]

Ventricular Arrhythmia Management

Antiarrhythmic drug therapy is recommended (Class I) for adults with HCM and symptomatic ventricular arrhythmias or recurrent ICD shocks despite beta-blocker use, with the choice of agent (amiodarone [LOE: B-NR], dofetilide, mexiletine, or sotalol [each LOE: C-LD]) guided by age, comorbidities, severity, and patient preferences.[1] Programming antitachycardia pacing in pacing-capable ICDs is recommended (Class I) to minimize shocks, as monomorphic VT and ventricular flutter are amenable to pacing termination in approximately 74% of episodes.[1]

Catheter ablation for VT (Class IIa) can be useful for recurrent symptomatic sustained monomorphic VT or recurrent ICD shocks when antiarrhythmic therapy is ineffective, not tolerated, or not preferred.[1] Combined epicardial and endocardial ablation achieves a ~73% success rate; apical aneurysms are a common source of monomorphic VT. Surgical aneurysmectomy and left cardiac sympathetic denervation are additional options for refractory cases.[1] For patients with apical aneurysms who are not undergoing surgery, anticoagulation can also be considered given the increased risk of thromboembolic events.[1]

For life-threatening ventricular tachyarrhythmias refractory to maximal antiarrhythmic therapy and ablation, heart transplantation assessment is indicated (Class I).[1]

2024 AHA/ACC Guideline Recommendations for Ventricular Arrhythmia Management

Class I
1. In patients with HCM and recurrent, poorly tolerated life-threatening ventricular tachyarrhythmias refractory to maximal antiarrhythmic drug therapy and ablation, heart transplantation assessment is indicated in accordance with current listing criteria. (Level of Evidence: B-NR)[1]
2. In adults with HCM and symptomatic ventricular arrhythmias or recurrent ICD shocks despite beta-blocker use, antiarrhythmic drug therapy (eg, amiodarone, dofetilide,† mexiletine,† or sotalol†) is recommended, with the choice of agent guided by age, underlying comorbidities, severity of disease, patient preferences, and balance between efficacy and safety. (LOE: B-NR; †LOE: C-LD)[1]
3. In children with HCM and recurrent ventricular arrhythmias despite beta-blocker use, antiarrhythmic drug therapy (eg, amiodarone, mexiletine, sotalol) is recommended, with the choice of agent guided by age, underlying comorbidities, severity of disease, patient preferences, and balance of efficacy and safety. (Level of Evidence: C-LD)[1]
4. In patients with HCM and pacing-capable ICDs, programming antitachycardia pacing is recommended to minimize risk of shocks. (Level of Evidence: C-LD)[1]
Class IIa
5. In patients with HCM and recurrent symptomatic sustained monomorphic VT, or recurrent ICD shocks despite optimal device programming, and in whom antiarrhythmic drug therapy is either ineffective, not tolerated, or not preferred, catheter ablation can be useful for reducing arrhythmia burden. (Level of Evidence: C-LD)[1]

Atrial Fibrillation Management: Procedural Interventions

Anticoagulation

All patients with HCM and clinical AF should receive anticoagulation (DOACs first-line, vitamin K antagonists second-line), independent of CHA₂DS₂-VASc score (Class I).[1][9] This also applies to subclinical AF >24 hours detected by devices (Class I) and may be beneficial for episodes >5 minutes but <24 hours (Class IIa).[1]

Catheter and Surgical Ablation for AF

As part of a rhythm-control strategy, catheter ablation for AF can be effective when drug therapy is ineffective, contraindicated, or not preferred (Class IIa).[1] However, outcomes are less favorable than in patients without HCM, with a 2-fold higher risk of relapse, more frequent need for repeat procedures, and higher use of concomitant antiarrhythmic drugs.[1][10]

Concomitant surgical AF ablation (Cox-Maze IV) during myectomy can be beneficial for AF rhythm control (Class IIa), with approximately 70% of patients free from AF at 5 years.[1][10]

2024 AHA/ACC Guideline Recommendations for Management of Atrial Fibrillation

Class I
1. In patients with HCM and clinical AF, anticoagulation is recommended with direct-acting oral anticoagulants (DOACs) as first-line option and vitamin K antagonists as second-line option, independent of CHA₂DS₂-VASc score. (Level of Evidence: B-NR)[1]
2. In patients with HCM and subclinical AF detected by internal or external cardiac device or monitor of >24 hours' duration for a given episode, anticoagulation is recommended with DOACs as first-line option and vitamin K antagonists as second-line option, independent of CHA₂DS₂-VASc score. (Level of Evidence: C-LD)[1]
3. In patients with AF in whom rate control strategy is planned, beta blockers, verapamil, or diltiazem are recommended, with the choice of agents according to patient preferences and comorbid conditions. (Level of Evidence: C-LD)[1]
Class IIa
4. In patients with HCM and subclinical AF detected by internal or external device or monitor, of >5 minutes' duration but <24 hours' duration for a given episode, anticoagulation with DOACs as first-line option and vitamin K antagonists as second-line option can be beneficial, taking into consideration duration of AF episodes, total AF burden, underlying risk factors, and bleeding risk. (Level of Evidence: C-LD)[1]
5. In patients with HCM and poorly tolerated AF, a rhythm-control strategy with cardioversion or antiarrhythmic drugs can be beneficial with the choice of an agent according to AF symptom severity, patient preferences, and comorbid conditions. (Level of Evidence: B-NR)[1]
6. In patients with HCM and symptomatic AF, as part of an AF rhythm-control strategy, catheter ablation for AF can be effective when drug therapy is ineffective, contraindicated, or not the patient's preference. (Level of Evidence: B-NR)[1]
7. In patients with HCM and AF who require surgical myectomy, concomitant surgical AF ablation procedure can be beneficial for AF rhythm control. (Level of Evidence: B-NR)[1]

Cardiac Pacing and Resynchronization Therapy

Cardiac Pacing

Dual-chamber pacing is not recommended as first-line therapy for symptomatic obstructive HCM in patients who are candidates for SRT.[1][6] While RV apical pacing acutely reduces the LVOT gradient, long-term clinical benefits have not been consistently demonstrated. Pacing may be considered in medically refractory patients who are suboptimal candidates for SRT (Class IIb). Permanent pacing remains indicated for standard bradycardia indications (sinus node dysfunction, AV block) in patients with HCM.[6]

Cardiac Resynchronization Therapy (CRT)

CRT may be beneficial (Class IIa, LOE: C-LD) in selected patients with nonobstructive HCM receiving an ICD who have NYHA class II to ambulatory class IV HF, LBBB, and LVEF <50%. The strongest evidence supports CRT for LVEF ≤35% with LBBB and QRS ≥150 ms; extension to LVEF 35–50% is extrapolated from the bradycardia guideline for patients expected to be paced >40% of the time.[1]

Advanced Heart Failure Management

For patients with nonobstructive HCM and advanced HF (NYHA class III–IV despite GDMT), assessment for heart transplantation is recommended (Class I).[1] Continuous-flow LVAD therapy is reasonable as a bridge to transplantation (Class IIa). Cardiopulmonary exercise testing (CPET) should be performed to quantify functional limitation and aid in transplant candidacy assessment (Class I).[1]

When LVEF falls below 50%, cardiac myosin inhibitors should be discontinued (Class I), and previously indicated negative inotropic agents (verapamil, diltiazem, disopyramide) should be reconsidered (Class IIa). GDMT for HFrEF should be initiated.[1]

2024 AHA/ACC Guideline Recommendations for Advanced Heart Failure Management

Class I
1. In patients with HCM who develop systolic dysfunction with an LVEF <50%, GDMT for HF with reduced EF is recommended. (Level of Evidence: C-LD)[1]
2. In patients with HCM and systolic dysfunction, diagnostic testing to assess for concomitant causes of systolic dysfunction (eg, CAD) is recommended. (Level of Evidence: C-LD)[1]
3. In patients with nonobstructive HCM and advanced HF (NYHA functional class III to class IV despite GDMT), CPET should be performed to quantify the degree of functional limitation and aid in selection of patients for heart transplantation or mechanical circulatory support. (Level of Evidence: B-NR)[1]
4. In patients with nonobstructive HCM and advanced HF (NYHA functional class III to class IV despite GDMT) or with life-threatening ventricular arrhythmias refractory to maximal GDMT, assessment for heart transplantation in accordance with current listing criteria is recommended. (Level of Evidence: B-NR)[1]
5. In patients with HCM who develop persistent systolic dysfunction (LVEF <50%), cardiac myosin inhibitors should be discontinued. (Level of Evidence: B-R)[1]
Class IIa
6. For patients with HCM who develop systolic dysfunction (LVEF <50%), it is reasonable to discontinue previously indicated negative inotropic agents (specifically, verapamil, diltiazem, or disopyramide). (Level of Evidence: C-EO)[1]
7. In patients with nonobstructive HCM and advanced HF (NYHA functional class III to class IV despite GDMT) who are candidates for heart transplantation, continuous-flow LVAD therapy is reasonable as a bridge to heart transplantation. (Level of Evidence: B-NR)[1]
8. In patients with HCM and persistent LVEF <50%, ICD placement can be beneficial. (Level of Evidence: C-LD)[1]
9. In patients with HCM and LVEF <50%, NYHA functional class II to class IV symptoms despite GDMT, and LBBB, CRT can be beneficial to improve symptoms. (Level of Evidence: C-LD)[1]

High-Yield Clinical Pearls

  • SRT eligibility requires all three criteria: symptoms despite GDMT, gradient ≥50 mm Hg, and adequate septal thickness — missing any one disqualifies the patient.[1]
  • Volume-outcome relationship: Myectomy mortality is <1% and success >90–95% at experienced centers; referral to comprehensive HCM centers is essential.[1]
  • Anticoagulation in HCM-associated AF is independent of the CHA₂DS₂-VASc score. All patients with clinical AF require anticoagulation.[1][9]
  • LVEF <50% in HCM triggers a management pivot: Discontinue myosin inhibitors and negative inotropes, initiate HFrEF GDMT, consider ICD and transplant evaluation.[1]

Common Pitfalls

  • Declaring medical therapy failure prematurely: Beta-blockers should be titrated to physiologic evidence of beta-blockade (resting heart rate suppression) before escalation.[1]
  • Using CHA₂DS₂-VASc to guide anticoagulation in HCM: This score is not applicable; HCM itself confers stroke risk equivalent to a CHA₂DS₂-VASc of ~3.[9][10]
  • Selecting ASA in patients with septal thickness ≥30 mm or gradients ≥100 mm Hg: These patients are less likely to benefit from ASA and are better served by myectomy.[1][6]
  • Implanting ICDs in genotype-positive/phenotype-negative individuals or solely for athletic participation (Class III Harm).[1]
  • Overlooking apical aneurysms: These are a source of monomorphic VT and thromboembolic events and represent a major SCD risk factor warranting ICD consideration.[1]

2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines[11]

Recommendations for Invasive Treatment of Symptomatic Patients With Obstructive HCM Referenced studies that support the recommendations are summarized in the Online Data Supplement

Class I
1. 1. In patients with obstructive HCM who remain severely symptomatic despite GDMT, SRT in eligible patients,* performed at experienced centers,† is recommended for relieving LVOTO(Level of Evidence: B-NR )

2. In symptomatic patients with obstructive HCM who have associated cardiac disease requiring surgical treatment (eg, associated anomalous papillary muscle, markedly elongated anterior mitral leaflet, intrinsic mitral valve disease, multivessel CAD, valvular aortic stenosis), surgical myectomy, performed at experienced centers,† is recommended(Level of Evidence: B-NR ) 3. In adult patients with obstructive HCM who remain severely symptomatic, despite GDMT and in whom surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age, alcohol septal ablation in eligible patients,* performed at experienced centers,† is recommended(Level of Evidence: C-LD)

Class IIb
4. In patients with obstructive HCM, earlier (NYHA class II) surgical myectomy performed at comprehensive HCM centers (Table 3 and Table 4) may be reasonable in the presence of additional clinical factors, including3,11–22(Level of Evidence: B-NR ):

a. Severe and progressive pulmonary hypertension thought to be attributable to LVOTO or associated MR

b. Left atrial enlargement with ≥1 episodes of symptomatic AF

c. Poor functional capacity attributable to LVOTO as documented on treadmill exercise testing.

d. Children and young adults with very high resting LVOT gradients (>100 mm Hg).

5. For severely symptomatic patients with obstructive HCM, SRT in eligible patients,* performed at experienced centers† (Table 3 and Table 4), may be considered as an alter-native to escalation of medical therapy after shared decision-making including risks and benefits of all treatment options(Level of Evidence: C-LD)

Recommendations for Management of Atrial Fibrillation Referenced studies that support the recommendations are summarized in the Online Data Supplement

Class IIa
5. In patients with HCM and poorly tolerated AF, a rhythm control strategy with cardioversion or antiarrhythmic drugs can be beneficial with the choice of an agent according to AF symptom severity, patient preferences, and comorbid conditions(Level of Evidence: B-NR )

6. In patients with HCM and symptomatic AF, as part of a AF rhythm control strategy, catheter ablation for AF can be effective when drug therapy is ineffective, contraindicated, or not the patient’s preference(Level of Evidence: B-NR ) 7. In patients with HCM and AF who require surgical myectomy, concomitant surgical AF ablation procedure can be beneficial for AF rhythm control.(Level of Evidence: B-NR )

Recommendations for the Management of Patients With HCM and Ventricular Arrhythmias Referenced studies that support the recommendations are summarized in the Online Data Supplement

Class I
4. In patients with HCM and pacing-capable ICDs, programming antitachycardia pacing is recommended to minimize risk of shocks.(Level of Evidence: C-LD)
Class IIa
5. In patients with HCM and recurrent symptomatic sustained monomorphic VT, or recurrent ICD shocks despite optimal device programming, and in whom anti-arrhythmic drug therapy is either inef-fective, not tolerated, or not preferred, catheter ablation can be useful for reducing arrhythmia burden(Level of Evidence: C-LD)

Recommendations for Patients With HCM and Advanced HF Referenced studies that support the recommendations are summarized in the Online Data Supplement

Class IIa
6. In patients with nonobstructive HCM and advanced HF (NYHA functional class III to class IV despite GDMT) who are candidates for heart transplantation, continuous-flow LVAD therapy is reasonable as a bridge to heart transplantation(Level of Evidence: B-NR )

7. In patients with HCM and LVEF <50%, ICD placement can be beneficial(Level of Evidence: C-LD) 8. In patients with HCM and LVEF <50%, NYHA functional class II to class IV symptoms despite guideline-directed therapy, and LBBB, CRT can be beneficial to improve symptoms(Level of Evidence: C-LD)

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[12]

Alcohol Septal Ablation (DO NOT EDIT)[12]

Class IIa
"1. Consultation with centers experienced in performing both surgical septal myectomy and alcohol septal ablation is reasonable when discussing treatment options for eligible patients with HCM with severe drug-refractory symptoms and LVOT obstruction. (Level of Evidence: C)"
"2. When surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age, alcohol septal ablation, when performed in experienced centers, can be beneficial in eligible adult patients with HCM with LVOT obstruction and severe drug-refractory symptoms (usually NYHA functional classes III or IV).[13][14][15][16][17][18][19] (Level of Evidence: B)"
Class IIb
"1. Alcohol septal ablation, when performed in experienced centers, may be considered as an alternative to surgical myectomy for eligible adult patients with HCM with severe drug-refractory symptoms and LVOT obstruction when, after a balanced and thorough discussion, the patient expresses a preference for septal ablation.[14] [20][16][18][19] (Level of Evidence: B)"
"2. The effectiveness of alcohol septal ablation is uncertain in patients with HCM with marked (i.e., >30 mm) septal hypertrophy, and therefore the procedure is generally discouraged in such patients. (Level of Evidence: C)"
Class III (Harm)
"1. Alcohol septal ablation should not be done in patients with HCM with concomitant disease that independently warrants surgical correction (e.g., coronary artery bypass grafting for CAD, mitral valve repair for ruptured chordae) in whom surgical myectomy can be performed as part of the operation. (Level of Evidence: C)"
"2. Alcohol septal ablation should not be done in patients with HCM who are less than 21 years of age and is discouraged in adults less than 40 years of age if myectomy is a viable option. (Level of Evidence: C)"

Sources

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy[12] and 2012 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities (DO NOT EDIT)[24][25]

Pacing (DO NOT EDIT)[12][25]

Class I
"1. Permanent pacing is indicated for SND or AV block in patients with hypertrophic cardiomyopathy as described in permanent pacing in sinus node dysfunction and acquired atrioventricular block in adults. (Level of Evidence: C)"
Class IIa
"1. In patients with HCM who have had a dual-chamber device implanted for non-HCM indications, it is reasonable to consider a trial of dual-chamber atrial-ventricular pacing (from the right ventricular apex) for the relief of symptoms attributable to LVOT obstruction.[26][27][28][29] (Level of Evidence: B)"
"2. Permanent pacing may be considered in medically refractory symptomatic patients with hypertrophic cardiomyopathy and significant resting or provoked LV outflow tract obstruction. (Level of Evidence: A)"
Class IIb
"1. Permanent pacing may be considered in medically refractory symptomatic patients with obstructive HCM who are suboptimal candidates for septal reduction therapy.[26][27][28][29][30] (Level of Evidence: B)"
Class III (No Benefit)
"1. Permanent pacemaker implantation is not indicated for patients who are asymptomatic or whose symptoms are medically controlled.[30][31][32] (Level of Evidence: C)"
"2. Permanent pacemaker implantation should not be performed as a first-line therapy to relieve symptoms in medically refractory symptomatic patients with HCM and LVOT obstruction who are candidates for septal reduction.[30][31][32] (Level of Evidence: B)"
"3. Permanent pacemaker implantation is not indicated for symptomatic patients without evidence of LV outflow tract obstruction. (Level of Evidence: C)"

2007 ESC Guidelines for Cardiac Pacing and Cardiac Resynchronization Therapy (DO NOT EDIT)[22]

Cardiac Pacing in HCM[22]

Class III
"1. Asymptomatic patients. (Level of Evidence: C)"
"2. Symptomatic patients who do not have LVOT obstruction. (Level of Evidence: C)"
Class IIa
"1. Symptomatic bradycardia due to beta-blockade when alternative therapies are unacceptable. (Level of Evidence: C)"
Class IIb
"1. Patients with drug-refractory hypertrophic cardiomyopathy with significant resting or provoked LVOT gradient and contraindications for septal ablation or myectomy. (Level of Evidence: A)"[33][34][32]

Sources

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[35]

Selection of Patients for ICDs (DO NOT EDIT)[35]

Class I
"1. The decision to place an ICD in patients with HCM should include the application of individual clinical judgment, as well as a thorough discussion of the strength of evidence, benefits, and risks to allow the informed patient's active participation in decision making.[36][37][38][39] (Level of Evidence: C) "
"2. ICD placement is recommended for patients with HCM with prior documented cardiac arrest, ventricular fibrillation, or hemodynamically significant VT[40][41][42][37]. (Level of Evidence: B) "
Class IIa
"1. It is reasonable to recommend an ICD for patients with HCM with:
a. Sudden death presumably caused by HCM in 1 or more first-degree relatives.[43] (Level of Evidence: C)

b. A maximum LV wall thickness greater than or equal to 30 mm.[44][45][46][47] (Level of Evidence: C)
c. One or more recent, unexplained syncopal episodes.[48] (Level of Evidence: C) ''

"2. An ICD can be useful in select patients with NSVT (particularly those <30 years of age) in the presence of other SCD risk factors or modifiers.[49][36] (Level of Evidence: C) "
"3. An ICD can be useful in select patients with HCM with an abnormal blood pressure response with exercise in the presence of other SCD risk factors or modifiers.[50][51][52] (Level of Evidence: C) "
"4. It is reasonable to recommend an ICD for high-risk children with HCM, based on unexplained syncope, massive LV hypertrophy, or family history of SCD, after taking into account the relatively high complication rate of long-term ICD implantation. (Level of Evidence: C) "
Class IIb
"1. The usefulness of an ICD is uncertain in patients with HCM with isolated bursts of NSVT when in the absence of any other SCD risk factors or modifiers[36]. (Level of Evidence: C) "
"2. The usefulness of an ICD is uncertain in patients with HCM with an abnormal blood pressure response with exercise when in the absence of any other SCD risk factors or modifiers, particularly in the presence of significant outflow obstruction.[50][51][52] (Level of Evidence: C) "
Class III (Harm)
"1. ICD placement as a routine strategy in patients with HCM without an indication of increased risk is potentially harmful. (Level of Evidence: C)"
"2. ICD placement as a strategy to permit patients with HCM to participate in competitive athletics is potentially harmful. (Level of Evidence: C)"
"3. ICD placement in patients who have an identified HCM genotype in the absence of clinical manifestations of HCM is potentially harmful. (Level of Evidence: C)"

Selection of ICD Device Type (DO NOT EDIT)[35]

Class IIa
"1. In patients with HCM who meet indications for ICD implantation, single-chamber devices are reasonable in younger patients without a need for atrial or ventricular pacing.[53][54][55][56] (Level of Evidence: B)"
"2. In patients with HCM who meet indications for ICD implantation, dual-chamber ICDs are reasonable for patients with sinus bradycardia and/or paroxysmal AF.[53] (Level of Evidence: C)"
"3. In patients with HCM who meet indications for ICD implantation, dual-chamber ICDs are reasonable for patients with elevated resting outflow gradients greater than 50 mm Hg and significant heart failure symptoms who may benefit from right ventricular pacing (most commonly, but not limited to, patients >65 years of age).[30][31][32][53] (Level of Evidence: B) "

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death - Hypertrophic Cardiomyopathy (DO NOT EDIT)[57]

Class I
"1. ICD therapy should be used for treatment in patients with hypertrophic cardiomyopathy (HCM) who have sustained VT and/or VF and who are receiving chronic optimal medical therapy and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B) "
Class IIa
"1. ICD implantation can be effective for primary prophylaxis against SCD in patients with HCM who have one or more major risk factor for SCD and who are receiving chronic optimal medical therapy and in patients who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)"
"2. Amiodarone therapy can be effective for treatment in patients with HCM with a history of sustained VT and/or VF when ICD is not feasible. (Level of Evidence: C)"
Class IIb
"1. EP testing may be considered for risk assessment for SCD in patients with HCM. (Level of Evidence: C) "
"2. Amiodarone may be considered for primary prophylaxis against SCD in patients with HCM who have one or more major risk factor for SCD, if ICD implantation is not feasible. (Level of Evidence: C) "

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 1.43 1.44 1.45 1.46 1.47 1.48 1.49 1.50 1.51 1.52 1.53 1.54 1.55 1.56 1.57 1.58 1.59 1.60 1.61 1.62 1.63 1.64 1.65 1.66 1.67 1.68 1.69 1.70 1.71 1.72 1.73 1.74 1.75 1.76 1.77 1.78 1.79 1.80 1.81 1.82 1.83 1.84 1.85 1.86 1.87 1.88 1.89 1.90 Ommen SR, Ho CY, Asif IM; et al. (2024). "2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines". Journal of the American College of Cardiology. 83 (23): 2324–2405. doi:10.1016/j.jacc.2024.02.014.
  2. ↑ Desai MY, Owens A, Geske JB; et al. (2022). "Myosin Inhibition in Patients With Obstructive Hypertrophic Cardiomyopathy Referred for Septal Reduction Therapy". Journal of the American College of Cardiology. 80 (2): 95–108. doi:10.1016/j.jacc.2022.04.048.
  3. ↑ 3.0 3.1 Desai MY, Wolski K, Owens A; et al. (2025). "Mavacamten in Patients With Hypertrophic Cardiomyopathy Referred for Septal Reduction: Week 128 Results From VALOR-HCM". Circulation. 151 (19): 1378–1390. doi:10.1161/CIRCULATIONAHA.124.072445.
  4. ↑ Maron MS, Masri A, Nassif ME; et al. (2024). "Aficamten for Symptomatic Obstructive Hypertrophic Cardiomyopathy". The New England Journal of Medicine. 390 (20): 1849–1861. doi:10.1056/NEJMoa2401424.
  5. ↑ Garcia-Pavia P, Maron MS, Masri A; et al. (2025). "Aficamten or Metoprolol Monotherapy for Obstructive Hypertrophic Cardiomyopathy". The New England Journal of Medicine. 393 (10): 949–960. doi:10.1056/NEJMoa2504654.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 Ommen SR, Mital S, Burke MA; et al. (2020). "2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Journal of the American College of Cardiology. 76 (25): e159–e240. doi:10.1016/j.jacc.2020.08.045.
  7. ↑ 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.
  8. ↑ 8.0 8.1 Maron BJ, Desai MY, Nishimura RA; et al. (2022). "Management of Hypertrophic Cardiomyopathy: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 79 (4): 390–414. doi:10.1016/j.jacc.2021.11.021.
  9. ↑ 9.0 9.1 9.2 Writing Committee Members, Joglar JA, Chung MK; et al. (2024). "2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Journal of the American College of Cardiology. 83 (1): 109–279. doi:10.1016/j.jacc.2023.08.017.
  10. ↑ 10.0 10.1 10.2 Rowin EJ, Link MS, Maron MS, Maron BJ (2023). "Evolving Contemporary Management of Atrial Fibrillation in Hypertrophic Cardiomyopathy". Circulation. 148 (22): 1797–1811. doi:10.1161/CIRCULATIONAHA.123.065037.
  11. ↑ Ommen SR, Mital S, Burke MA, Day SM, Deswal A, Elliott P; et al. (2020). "2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 142 (25): e558–e631. doi:10.1161/CIR.0000000000000937. PMID 33215931 Check |pmid= value (help).
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, Naidu SS, Nishimura RA, Ommen SR, Rakowski H, Seidman CE, Towbin JA, Udelson JE, Yancy CW (2011). "2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Journal of the American College of Cardiology. 58 (25): e212–60. doi:10.1016/j.jacc.2011.06.011. PMID 22075469. Retrieved 2011-12-19. Unknown parameter |month= ignored (help)
  13. ↑ Sorajja P, Valeti U, Nishimura RA; et al. (2008). "Outcome of alcohol septal ablation for obstructive hypertrophic cardiomyopathy". Circulation. 118 (2): 131–9. doi:10.1161/CIRCULATIONAHA.107.738740. PMID 18591440. Unknown parameter |month= ignored (help)
  14. ↑ 14.0 14.1 Fernandes VL, Nielsen C, Nagueh SF; et al. (2008). "Follow-up of alcohol septal ablation for symptomatic hypertrophic obstructive cardiomyopathy the Baylor and Medical University of South Carolina experience 1996 to 2007". JACC Cardiovasc Interv. 1 (5): 561–70. doi:10.1016/j.jcin.2008.07.005. PMID 19463359. Unknown parameter |month= ignored (help)
  15. ↑ Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H (2004). "Transcoronary ablation of septal hypertrophy for hypertrophic obstructive cardiomyopathy: feasibility, clinical benefit, and short term results in elderly patients". Heart. 90 (6): 638–44. PMC 1768263. PMID 15145866. Unknown parameter |month= ignored (help)
  16. ↑ 16.0 16.1 Kuhn H, Lawrenz T, Lieder F; et al. (2008). "Survival after transcoronary ablation of septal hypertrophy in hypertrophic obstructive cardiomyopathy (TASH): a 10 year experience". Clin Res Cardiol. 97 (4): 234–43. doi:10.1007/s00392-007-0616-7. PMID 18071624. Unknown parameter |month= ignored (help)
  17. ↑ Kwon DH, Kapadia SR, Tuzcu EM; et al. (2008). "Long-term outcomes in high-risk symptomatic patients with hypertrophic cardiomyopathy undergoing alcohol septal ablation". JACC Cardiovasc Interv. 1 (4): 432–8. doi:10.1016/j.jcin.2008.05.009. PMID 19463341. Unknown parameter |month= ignored (help)
  18. ↑ 18.0 18.1 Nagueh SF, Ommen SR, Lakkis NM; et al. (2001). "Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy". J. Am. Coll. Cardiol. 38 (6): 1701–6. PMID 11704383. Unknown parameter |month= ignored (help)
  19. ↑ 19.0 19.1 Qin JX, Shiota T, Lever HM; et al. (2001). "Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery". J. Am. Coll. Cardiol. 38 (7): 1994–2000. PMID 11738306. Unknown parameter |month= ignored (help)
  20. ↑ Firoozi S, Elliott PM, Sharma S; et al. (2002). "Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy. A comparison of clinical, haemodynamic and exercise outcomes". Eur. Heart J. 23 (20): 1617–24. PMID 12323162. Unknown parameter |month= ignored (help)
  21. ↑ Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207
  22. ↑ 22.0 22.1 22.2 22.3 Vardas PE, Auricchio A, Blanc JJ, Daubert JC, Drexler H, Ector H; et al. (2007). "Guidelines for cardiac pacing and cardiac resynchronization therapy. The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association". Europace. 9 (10): 959–98. doi:10.1093/europace/eum189. PMID 17726043.
  23. ↑ 23.0 23.1 Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, Naidu SS, Nishimura RA, Ommen SR, Rakowski H, Seidman CE, Towbin JA, Udelson JE, Yancy CW (2011). "2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: Executive Summary A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Journal of the American College of Cardiology. 58 (25): 2703–38. doi:10.1016/j.jacc.2011.10.825. PMID 22075468. Retrieved 2011-12-19. Unknown parameter |month= ignored (help)
  24. ↑ Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD (2013). "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 61 (3): e6–75. doi:10.1016/j.jacc.2012.11.007. PMID 23265327.
  25. ↑ 25.0 25.1 25.2 Epstein AE, Dimarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS; et al. (2008). "ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary". Heart Rhythm. 5 (6): 934–55. doi:10.1016/j.hrthm.2008.04.015. PMID 18534377.
  26. ↑ 26.0 26.1 Erwin JP, Nishimura RA, Lloyd MA, Tajik AJ (2000). "Dual chamber pacing for patients with hypertrophic obstructive cardiomyopathy: a clinical perspective in 2000". Mayo Clin. Proc. 75 (2): 173–80. doi:10.4065/75.2.173. PMID 10683657. Unknown parameter |month= ignored (help)
  27. ↑ 27.0 27.1 Gadler F, Linde C, Daubert C; et al. (1999). "Significant improvement of quality of life following atrioventricular synchronous pacing in patients with hypertrophic obstructive cardiomyopathy. Data from 1 year of follow-up. PIC study group. Pacing In Cardiomyopathy". Eur. Heart J. 20 (14): 1044–50. doi:10.1053/euhj.1998.1331. PMID 10381856. Unknown parameter |month= ignored (help)
  28. ↑ 28.0 28.1 Slade AK, Sadoul N, Shapiro L; et al. (1996). "DDD pacing in hypertrophic cardiomyopathy: a multicentre clinical experience". Heart. 75 (1): 44–9. PMC 484221. PMID 8624871. Unknown parameter |month= ignored (help)
  29. ↑ 29.0 29.1 Ommen SR, Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ (1999). "Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy: a comparison of objective hemodynamic and exercise end points". J. Am. Coll. Cardiol. 34 (1): 191–6. PMID 10400010. Unknown parameter |month= ignored (help)
  30. ↑ 30.0 30.1 30.2 30.3 Maron BJ, Nishimura RA, McKenna WJ, Rakowski H, Josephson ME, Kieval RS (1999). "Assessment of permanent dual-chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy. A randomized, double-blind, crossover study (M-PATHY)". Circulation. 99 (22): 2927–33. PMID 10359738. Unknown parameter |month= ignored (help)
  31. ↑ 31.0 31.1 31.2 Nishimura RA, Trusty JM, Hayes DL; et al. (1997). "Dual-chamber pacing for hypertrophic cardiomyopathy: a randomized, double-blind, crossover trial". J. Am. Coll. Cardiol. 29 (2): 435–41. PMID 9015001. Unknown parameter |month= ignored (help)
  32. ↑ 32.0 32.1 32.2 32.3 Kappenberger L, Linde C, Daubert C; et al. (1997). "Pacing in hypertrophic obstructive cardiomyopathy. A randomized crossover study. PIC Study Group". Eur. Heart J. 18 (8): 1249–56. PMID 9458416. Unknown parameter |month= ignored (help)
  33. ↑ Fananapazir L, Cannon RO, Tripodi D, Panza JA (1992). "Impact of dual-chamber permanent pacing in patients with obstructive hypertrophic cardiomyopathy with symptoms refractory to verapamil and beta-adrenergic blocker therapy". Circulation. 85 (6): 2149–61. PMID 1350522.
  34. ↑ Fananapazir L, Epstein ND, Curiel RV, Panza JA, Tripodi D, McAreavey D (1994). "Long-term results of dual-chamber (DDD) pacing in obstructive hypertrophic cardiomyopathy. Evidence for progressive symptomatic and hemodynamic improvement and reduction of left ventricular hypertrophy". Circulation. 90 (6): 2731–42. PMID 7994815.
  35. ↑ 35.0 35.1 35.2 Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS; et al. (2011). "2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 124 (24): 2761–96. doi:10.1161/CIR.0b013e318223e230. PMID 22068435.
  36. ↑ 36.0 36.1 36.2 Maron BJ (2010). "Contemporary insights and strategies for risk stratification and prevention of sudden death in hypertrophic cardiomyopathy". Circulation. 121 (3): 445–56. doi:10.1161/CIRCULATIONAHA.109.878579. PMID 20100987. Unknown parameter |month= ignored (help)
  37. ↑ 37.0 37.1 Maron BJ, Spirito P, Shen WK; et al. (2007). "Implantable cardioverter-defibrillators and prevention of sudden cardiac death in hypertrophic cardiomyopathy". JAMA. 298 (4): 405–12. doi:10.1001/jama.298.4.405. PMID 17652294. Unknown parameter |month= ignored (help)
  38. ↑ Maron BJ, Shen WK, Link MS; et al. (2000). "Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy". N. Engl. J. Med. 342 (6): 365–73. doi:10.1056/NEJM200002103420601. PMID 10666426. Unknown parameter |month= ignored (help)
  39. ↑ Maron BJ, Spirito P (2008). "Implantable defibrillators and prevention of sudden death in hypertrophic cardiomyopathy". J. Cardiovasc. Electrophysiol. 19 (10): 1118–26. doi:10.1111/j.1540-8167.2008.01147.x. PMID 18384577. Unknown parameter |month= ignored (help)
  40. ↑ Cecchi F, Maron BJ, Epstein SE (1989). "Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest". J. Am. Coll. Cardiol. 13 (6): 1283–8. PMID 2703610. Unknown parameter |month= ignored (help)
  41. ↑ Elliott PM, Sharma S, Varnava A, Poloniecki J, Rowland E, McKenna WJ (1999). "Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy". J. Am. Coll. Cardiol. 33 (6): 1596–601. PMID 10334430. Unknown parameter |month= ignored (help)
  42. ↑ Fananapazir L, Chang AC, Epstein SE, McAreavey D (1992). "Prognostic determinants in hypertrophic cardiomyopathy. Prospective evaluation of a therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings". Circulation. 86 (3): 730–40. PMID 1516184. Unknown parameter |month= ignored (help)
  43. ↑ Bos JM, Maron BJ, Ackerman MJ; et al. (2010). "Role of family history of sudden death in risk stratification and prevention of sudden death with implantable defibrillators in hypertrophic cardiomyopathy". Am. J. Cardiol. 106 (10): 1481–6. doi:10.1016/j.amjcard.2010.06.077. PMID 21059440. Unknown parameter |month= ignored (help)
  44. ↑ Elliott PM, Poloniecki J, Dickie S; et al. (2000). "Sudden death in hypertrophic cardiomyopathy: identification of high risk patients". J. Am. Coll. Cardiol. 36 (7): 2212–8. PMID 11127463. Unknown parameter |month= ignored (help)
  45. ↑ Elliott PM, Gimeno Blanes JR, Mahon NG, Poloniecki JD, McKenna WJ (2001). "Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy". Lancet. 357 (9254): 420–4. doi:10.1016/S0140-6736(00)04005-8. PMID 11273061. Unknown parameter |month= ignored (help)
  46. ↑ Sorajja P, Nishimura RA, Ommen SR, Ackerman MJ, Tajik AJ, Gersh BJ (2006). "Use of echocardiography in patients with hypertrophic cardiomyopathy: clinical implications of massive hypertrophy". J Am Soc Echocardiogr. 19 (6): 788–95. doi:10.1016/j.echo.2006.01.005. PMID 16762758. Unknown parameter |month= ignored (help)
  47. ↑ Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ (2000). "Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy". N. Engl. J. Med. 342 (24): 1778–85. doi:10.1056/NEJM200006153422403. PMID 10853000. Unknown parameter |month= ignored (help)
  48. ↑ Spirito P, Autore C, Rapezzi C; et al. (2009). "Syncope and risk of sudden death in hypertrophic cardiomyopathy". Circulation. 119 (13): 1703–10. doi:10.1161/CIRCULATIONAHA.108.798314. PMID 19307481. Unknown parameter |month= ignored (help)
  49. ↑ Monserrat L, Elliott PM, Gimeno JR, Sharma S, Penas-Lado M, McKenna WJ (2003). "Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients". J. Am. Coll. Cardiol. 42 (5): 873–9. PMID 12957435. Unknown parameter |month= ignored (help)
  50. ↑ 50.0 50.1 Olivotto I, Maron BJ, Montereggi A, Mazzuoli F, Dolara A, Cecchi F (1999). "Prognostic value of systemic blood pressure response during exercise in a community-based patient population with hypertrophic cardiomyopathy". J. Am. Coll. Cardiol. 33 (7): 2044–51. PMID 10362212. Unknown parameter |month= ignored (help)
  51. ↑ 51.0 51.1 Sadoul N, Prasad K, Elliott PM, Bannerjee S, Frenneaux MP, McKenna WJ (1997). "Prospective prognostic assessment of blood pressure response during exercise in patients with hypertrophic cardiomyopathy". Circulation. 96 (9): 2987–91. PMID 9386166. Unknown parameter |month= ignored (help)
  52. ↑ 52.0 52.1 Maki S, Ikeda H, Muro A; et al. (1998). "Predictors of sudden cardiac death in hypertrophic cardiomyopathy". Am. J. Cardiol. 82 (6): 774–8. PMID 9761089. Unknown parameter |month= ignored (help)
  53. ↑ 53.0 53.1 53.2 Boriani G, Maron BJ, Shen WK, Spirito P (2004). "Prevention of sudden death in hypertrophic cardiomyopathy: but which defibrillator for which patient?". Circulation. 110 (15): e438–42. doi:10.1161/01.CIR.0000144463.65977.C9. PMID 15477422. Unknown parameter |month= ignored (help)
  54. ↑ Hauser RG, Maron BJ, Marine JE; et al. (2008). "Safety and efficacy of transvenous high-voltage implantable cardioverter-defibrillator leads in high-risk hypertrophic cardiomyopathy patients". Heart Rhythm. 5 (11): 1517–22. doi:10.1016/j.hrthm.2008.08.021. PMID 18984525. Unknown parameter |month= ignored (help)
  55. ↑ Kleemann T, Becker T, Doenges K; et al. (2007). "Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of >10 years". Circulation. 115 (19): 2474–80. doi:10.1161/CIRCULATIONAHA.106.663807. PMID 17470696. Unknown parameter |month= ignored (help)
  56. ↑ Maisel WH, Sweeney MO, Stevenson WG, Ellison KE, Epstein LM (2001). "Recalls and safety alerts involving pacemakers and implantable cardioverter-defibrillator generators". JAMA. 286 (7): 793–9. PMID 11497532. Unknown parameter |month= ignored (help)
  57. ↑ Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.
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