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Hypertrophic cardiomyopathy medical therapy

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. , Caitlin J. Harrigan ; Martin S. Maron, M.D.; Barry J. Maron, M.D.; Lakshmi Gopalakrishnan, M.B.B.S. [3]

Overview

This section covers the pharmacologic management of hypertrophic cardiomyopathy (HCM) across the clinical spectrum: symptomatic obstructive HCM, nonobstructive HCM with preserved ejection fraction, atrial fibrillation management, advanced heart failure with systolic dysfunction, acute hemodynamic management, medications to avoid, and pregnancy-related considerations. The principal role of pharmacologic therapy is symptom relief; no convincing data demonstrate that pharmacologic therapy alters the natural history of HCM.[1]

The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline represents the most current comprehensive guideline and incorporates the landmark addition of cardiac myosin inhibitors as a Class I recommendation for symptomatic obstructive HCM refractory to first-line therapy. Surgical and procedural interventions (septal myectomy, alcohol septal ablation, ICD implantation) are covered in the Surgery/Procedural Therapy microchapter.

Pharmacologic Management of Symptomatic Obstructive HCM

2024 AHA/ACC Guideline Recommendations

Class I

1. In patients with obstructive HCM and symptoms attributable to LVOTO, nonvasodilating beta blockers, titrated to effectiveness or maximally tolerated doses, are recommended. (Level of Evidence: B-NR)

2. In patients with obstructive HCM and symptoms attributable to LVOTO, for whom beta blockers are ineffective or not tolerated, substitution with nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) is recommended. (Verapamil: Level of Evidence: B-NR; Diltiazem: Level of Evidence: C-LD)

3. For patients with obstructive HCM who have persistent symptoms attributable to LVOTO despite beta blockers or nondihydropyridine calcium channel blockers, adding a myosin inhibitor (adult patients only), or disopyramide (in combination with an atrioventricular nodal blocking agent), or SRT performed at experienced centers, is recommended. (Level of Evidence: B-R)

4. For patients with obstructive HCM and acute hypotension who do not respond to fluid administration, intravenous phenylephrine (or other vasoconstrictors without inotropic activity), alone or in combination with beta-blocking drugs, is recommended. (Level of Evidence: C-LD)

Class IIb

5. For patients with obstructive HCM and persistent dyspnea with clinical evidence of volume overload and high left-sided filling pressures despite other HCM GDMT, cautious use of low-dose oral diuretics may be considered. (Level of Evidence: C-EO)

6. For patients with obstructive HCM, discontinuation of vasodilators (eg, ACE inhibitors, angiotensin receptor blockers, dihydropyridine calcium channel blockers) or digoxin may be reasonable because these agents can worsen symptoms caused by dynamic outflow tract obstruction. (Level of Evidence: C-EO)

First-Line Therapy: Beta-Blockers

Nonvasodilating beta-blockers (eg, metoprolol succinate, atenolol, bisoprolol, nadolol, propranolol) are the first-line agents for symptomatic obstructive HCM (Class I, LOE B-NR). Beta-blockers reduce heart rate, decrease contractility, prolong diastolic filling, and attenuate the dynamic LVOT gradient. Key prescribing principles:

  • Titrate to symptom relief or maximally tolerated dose; failure of beta-blockade should not be declared until physiologic evidence of beta-blockade (resting heart rate suppression) is demonstrated.
  • Nonvasodilating agents are preferred; vasodilating beta-blockers (eg, carvedilol) should generally be avoided in obstructive HCM due to afterload reduction.
  • Monitor for bradycardia, hypotension, fatigue, and depression.

Second-Line Therapy: Non-Dihydropyridine Calcium Channel Blockers

For patients who do not respond to or cannot tolerate beta-blockers, substitution with verapamil (Class I, LOE B-NR) or diltiazem (Class I, LOE C-LD) is recommended. These agents improve diastolic function and reduce heart rate. Important caveats:

  • Verapamil is potentially harmful in patients with very high resting gradients (eg, >100 mmHg), severe dyspnea at rest, systemic hypotension, or in children <6 weeks of age (Class III: Harm, LOE C-LD). It should also be used with caution in patients with advanced heart failure or sinus bradycardia.
  • Combining beta-blockers with calcium channel blockers specifically for HCM-directed therapy is not supported by evidence, though this combination may be used for concomitant hypertension management.

Escalation Therapy: Cardiac Myosin Inhibitors, Disopyramide, or SRT

For patients with persistent symptoms despite beta-blockers or nondihydropyridine calcium channel blockers, the 2024 guideline provides a Class I (LOE B-R) recommendation for adding a cardiac myosin inhibitor (adult patients only), disopyramide (in combination with an AV nodal blocking agent), or referral for septal reduction therapy at experienced centers. The choice among these options should involve shared decision-making.

Cardiac Myosin Inhibitors

Cardiac myosin inhibitors represent the first disease-specific pharmacotherapy for HCM, directly targeting sarcomeric hypercontractility by reducing excessive actin-myosin cross-bridge formation.[2][3]

Mavacamten (Camzyos)

FDA-approved in 2022 for symptomatic NYHA class II–III obstructive HCM.[4]

  • Mechanism: Allosteric inhibitor of cardiac myosin ATPase; shifts myosin heads to the energy-sparing super-relaxed state, reducing hypercontractility.
  • EXPLORER-HCM (n=251, phase 3): Mavacamten was superior to placebo for the composite primary endpoint (37% vs. 17%, p=0.0005). Post-exercise LVOT gradient decreased by 36 mmHg vs. placebo. Complete response (all gradients <30 mmHg + NYHA class I) was achieved in 27% vs. <1% on placebo.[5]
  • VALOR-HCM (n=112): Among patients referred for SRT, 77% of placebo patients remained eligible for SRT at 16 weeks vs. only 18% on mavacamten, with sustained benefits at 128 weeks.
  • Dosing: Start 5 mg orally once daily; titrate in 2.5 mg increments (range 2.5–15 mg) based on LVEF and LVOT gradient assessments.
  • REMS program: Required due to risk of LVEF reduction <50% (observed in ~5.7% attributable to drug, up to 7–10% with extenuating clinical conditions). Requirements include echocardiographic monitoring every 4 weeks during the 12-week initiation phase, then every 12 weeks during maintenance; initiation not recommended if LVEF <55%; interrupt if LVEF <50%.[6]
  • Contraindications: Strong CYP2C19 inhibitors; moderate-to-strong CYP2C19 or CYP3A4 inducers; pregnancy (teratogenic).
  • Drug interactions: Significant CYP450 interactions (CYP2C19, CYP3A4); patients should report all concomitant medications including OTC proton pump inhibitors (omeprazole, esomeprazole).
Aficamten (Myqorzo)

FDA-approved in 2025 for symptomatic obstructive HCM.[7]

  • Mechanism: Allosteric inhibition of myosin ATPase at a different binding site than mavacamten, independent of the super-relaxed state mechanism.
  • SEQUOIA-HCM (n=282, phase 3): Aficamten significantly improved peak oxygen uptake vs. placebo (+1.8 mL/kg/min), with significant improvements in LVOT gradients, NYHA class, KCCQ-CSS, and NT-proBNP. Transient LVEF <50% occurred in 3.5%.[8]
  • MAPLE-HCM (phase 3, head-to-head vs. metoprolol): Aficamten as monotherapy was superior to metoprolol in improving pVO₂, NYHA functional class, quality of life, and LVOT gradient reduction, with a favorable safety profile.[9]
  • Pharmacokinetic advantages: Shorter half-life (~3 days vs. ~6–9 days for mavacamten), allowing echocardiography-based dose titration as early as 14 days and faster drug washout; fewer CYP450 drug-drug interactions.[10]
  • Safety comparison: A meta-analysis of 8 RCTs found both agents improve functional status, quality of life, and hemodynamics. Mavacamten demonstrated generally larger effect magnitudes, while aficamten showed a marginally more favorable safety profile with lower rates of treatment interruption for LVEF reduction (0.5% vs. 8.7%), lower AF incidence (4.1 vs. 11.5 per 100 patient-years), and no heart failure events (0.0 vs. 1.7 per 100 patient-years), though these comparisons are limited by shorter aficamten exposure duration.[11][12]

Disopyramide

Disopyramide is a class IA antiarrhythmic with potent negative inotropic properties that reduces LVOT gradients and improves symptoms. Key considerations:

  • Must be used in combination with an AV nodal blocking agent (beta-blocker, verapamil, or diltiazem) because disopyramide can enhance AV conduction and accelerate ventricular rate during AF.
  • Anticholinergic side effects (dry mouth, urinary retention, constipation) limit tolerability, particularly in elderly patients.
  • Typical dosing: 100–200 mg two to three times daily (immediate-release) or 200–300 mg twice daily (controlled-release); titrate based on symptom response and QTc monitoring.

Low-Dose Diuretics

For patients with persistent dyspnea and clinical evidence of volume overload despite other HCM GDMT, cautious use of low-dose oral diuretics may be considered (Class IIb, LOE C-EO). Aggressive diuresis should be avoided as volume depletion worsens LVOT obstruction.

Management of Nonobstructive HCM with Preserved EF

2024 AHA/ACC Guideline Recommendations

Class I

1. In patients with nonobstructive HCM with preserved EF and symptoms of exertional angina or dyspnea, beta blockers or nondihydropyridine calcium channel blockers are recommended. (Level of Evidence: C-LD)

Class IIa

2. In patients with nonobstructive HCM with preserved EF, it is reasonable to add oral diuretics when exertional dyspnea persists despite the use of beta blockers or nondihydropyridine calcium channel blockers. (Level of Evidence: C-EO)

Class IIb

3. In patients with nonobstructive HCM with preserved EF, the usefulness of ACE inhibitors and angiotensin receptor blockers in the treatment of symptoms (angina and dyspnea) is not well established. (Level of Evidence: C-LD)

4. In highly selected patients with apical HCM with severe dyspnea or angina (NYHA class III or class IV) despite maximal medical therapy, and with preserved EF and small LV cavity size (LV end-diastolic volume <50 mL/m2 and LV stroke volume <30 mL/m2), apical myectomy by experienced surgeons at comprehensive centers may be considered to reduce symptoms. (Level of Evidence: C-LD)

5. In asymptomatic patients with nonobstructive HCM, the benefit of beta blockers or calcium channel blockers is not well established. (Level of Evidence: C-EO)

6. For younger (eg, ≤45 years of age) patients with nonobstructive HCM due to a pathogenic or likely pathogenic cardiac sarcomere genetic variant, and a mild phenotype, valsartan may be beneficial to slow adverse cardiac remodeling. (Level of Evidence: B-R)
Mild phenotype indicates NYHA functional class I or II, maximal LV wall thickness 13 to 25 mm, no secondary prevention ICDs, no history of appropriate ICD shocks, and no AF.

Synopsis

Symptomatic nonobstructive HCM is a therapeutic challenge because there is no obvious hemodynamic target (obstruction) to treat. No trials have prospectively evaluated long-term outcomes with medications in this population.

The valsartan recommendation is based on the VANISH trial (n=178), a randomized, double-blind, placebo-controlled trial in patients aged 8–45 years with early-stage sarcomeric HCM, which demonstrated attenuation of a composite endpoint of adverse cardiac remodeling (LV wall thickness, mass, volumes, left atrial size, diastolic parameters, and biomarkers).[13]

Comorbidity management (hypertension, diabetes, obesity, obstructive sleep apnea, physical inactivity) is critical, as these are major contributors to symptoms in nonobstructive HCM.

Management of Atrial Fibrillation in HCM

2024 AHA/ACC Guideline Recommendations

Class I

1. In patients with HCM and clinical AF, anticoagulation is recommended with direct 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)

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)

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)

Class IIa

4. In patients with HCM and subclinical AF detected by internal or external device or monitor, of >5 minutes’ 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)

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 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)

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)

Synopsis

Atrial fibrillation occurs in approximately 20% to 30% of patients with HCM and carries substantial thromboembolic risk.[14] The CHA2DS2-VASc score should not be used for anticoagulation decisions in HCM; patients with HCM and AF carry stroke risk roughly equivalent to a CHA2DS2-VASc score of 3. Direct-acting oral anticoagulants (DOACs) are the first-line option. Rhythm control is often preferred due to poor tolerance of AF in HCM. Catheter ablation is effective when drug therapy fails, though repeat procedures may be necessary to maintain sinus rhythm.

Ventricular Arrhythmias in Children

2024 AHA/ACC Guideline Recommendations

Class I

1. In children with HCM and recurrent ventricular arrhythmias despite beta-blocker use, antiarrhythmic drug therapy (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)

Management of Advanced Heart Failure / Systolic Dysfunction

2024 AHA/ACC Guideline Recommendations

Class I

1. In patients with HCM who develop systolic dysfunction with an LVEF <50%, guideline-directed therapy for HF with reduced EF is recommended. (Level of Evidence: C-LD)

Class IIa

2. 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)

Synopsis

When HCM progresses to systolic dysfunction or the “burned-out” phase (LVEF <50%), the management paradigm shifts fundamentally toward standard HFrEF therapy.

  • Initiate HFrEF GDMT: Use standard HF guidelines (eg, ACE inhibitors/ARBs/ARNI, beta-blockers, mineralocorticoid receptor antagonists, and other indicated agents).
  • Discontinue Negative Inotropes: Verapamil, diltiazem, and disopyramide should be discontinued. Cardiac myosin inhibitors must be stopped if LVEF persistently remains <50%.
  • Advanced Therapies: Heart transplantation assessment is recommended for NYHA III–IV symptoms refractory to GDMT. Device therapies such as ICD or CRT may be indicated (detailed in the Surgery/Procedural Therapy microchapter).

Medications to Avoid in Obstructive HCM

The following agents can precipitate or worsen LVOT obstruction and should generally be discontinued or avoided:

  • Pure Vasodilators: Dihydropyridine calcium channel blockers (nifedipine, amlodipine), ACE inhibitors, ARBs, and nitrates reduce afterload or preload, worsening the gradient.
  • High-Dose Diuretics: Reduce preload and left ventricular filling, exacerbating obstruction.
  • Digoxin: Increases contractility (contraindicated unless used strictly for rate control in AF with nonobstructive HCM or systolic dysfunction).
  • Positive Inotropes: IV dopamine, dobutamine, norepinephrine, epinephrine, and milrinone worsen dynamic obstruction.

Pregnancy Considerations

Most women with clinically stable HCM have uncomplicated pregnancies, though expert maternal/fetal care is advised.

2024 AHA/ACC Guideline Recommendations

Class I

1. Care should be coordinated between a cardiologist and obstetrician, with high-risk patients referred to a maternal-fetal medicine specialist. (Level of Evidence: C-EO)

2. Beta-blockers should be administered for symptoms related to LVOT obstruction or arrhythmias, with monitoring of fetal growth. (Level of Evidence: C-LD)

3. Vaginal delivery is the first-choice delivery option. (Level of Evidence: C-LD)

Class IIa

4. General or epidural anesthesia is reasonable with precautions to avoid hypotension. (Level of Evidence: C-LD)

5. Cardioversion for new or recurrent atrial fibrillation during pregnancy can be beneficial. (Level of Evidence: B-NR)

Class IIb

6. Fetal echocardiography may be considered in the context of prenatal counseling. (Level of Evidence: C-LD)

Class III (Harm)

7. Mavacamten is teratogenic and absolutely contraindicated during pregnancy. (Level of Evidence: C-EO)

Synopsis

  • Beta-blockers: Preferred for symptom control, but require maternal monitoring of fetal growth.
  • Contraindicated Medications: Mavacamten requires effective contraception for females of reproductive potential. DOACs are not recommended during pregnancy; low-molecular-weight heparin or vitamin K antagonists (≤5 mg daily) should be used for AF anticoagulation.
  • Delivery & Anesthesia: Vaginal delivery is preferred. Epidural or general anesthesia is reasonable provided strict precautions are taken to avoid vasodilation and hypotension.

2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy (DO NOT EDIT)[15]

Recommendations for Pharmacologic Management of Patients With Obstructive HCM Referenced studies that support the recommendations are summarized in Online Data Supplement

Class I
1. In patients with obstructive HCM and symptoms* attributable to LVOTO, nonvasodilating beta-blockers, titrated to effectiveness or maximally tolerated doses, are recommended(Level of Evidence: B-NR)

2. In patients with obstructive HCM and symptoms* attributable to LVOTO, for whom beta-blockers are ineffective or not tolerated, substitution with non-dihydropyridine calcium channel blockers (eg, verapamil, diltiazem) is recommended.(Verapimil :Level of Evidence: B-NR) Diltiazem: (Level of Evidence: C-LD)

3. For patients with obstructive HCM who have persistent severe symptoms* attributable to LVOTO despite beta-blockers or non-dihydropyridine calcium channel blockers, either adding disopyramide in combination with 1 of the other drugs, or SRT performed at experienced centers,† is recommended(Level of Evidence: B-NR)

4. For patients with obstructive HCM and acute hypotension who do not respond to fluid administration, intravenous phenylephrine (or other vasoconstrictors without inotropic activity), alone or in combination with beta-blocking drugs, is recommended(Level of Evidence: C-LD)

Class IIb
5. For patients with obstructive HCM and persistent dyspnea with clinical evidence of volume overload and high left- sided filling pressures despite other HCM GDMT, cautious use of low-dose oral diuretics may be considered.(Level of Evidence: C-EO)

6. For patients with obstructive HCM, discontinuation of vasodilators (eg, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, dihydropyridine calcium channel blockers) or digoxin may be rea-sonable because these agents can worsen symptoms caused by dynamic outflow tract obstruction(Level of Evidence: C-EO)

Recommendations for Management of Patients With Nonobstructive HCM With Preserved EF Referenced studies that support the recommendations are summarized in Online Data Supplement

Class I
1. In patients with nonobstructive HCM with preserved EF and symptoms of exertional angina or dyspnea, beta-blockers or non-dihydropyridine calcium channel blockers are recommended.(Level of Evidence: C-LD)
Class IIa
2. In patients with nonobstructive HCM with pre-served EF, it is reasonable to add oral diuretics when exertional dyspnea persists despite the use of beta-blockers or non-dihydropyridine calcium channel blockers(Level of Evidence: C-EO)
Class IIb
3. In patients with nonobstructive HCM with preserved EF, the usefulness of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in the treatment of symptoms (angina and dyspnea) is not well established(Level of Evidence: C-LD)

4. In highly selected patients with apical HCM with severe dyspnea or angina (NYHA class III or class IV) despite maximal medical therapy, and with preserved EF and small LV cavity size (LV end-diastolic volume <50 mL/m2 and LV stroke volume <30 mL/m2), apical myectomy by experienced surgeons at comprehensive centers may be considered to reduce symptoms.(Level of Evidence: C-LD) 5. In asymptomatic patients with nonobstructive HCM, the benefit of beta-blockers or calcium channel blockers is not well established.(Level of Evidence: C-EO)

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

Class I
1. In patients with HCM and clinical AF, anticoagulation is recommended with direct-acting oral anticoagulants (DOAC) as first-line option and vitamin K antagonists as second-line option, independent of CHA2DS2-VASc score(Level of Evidence: B-NR)

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 DOAC as first-line option and vitamin K antagonists as second-line option, independent of CHA2DS2-VASc score(Level of Evidence: C-LD)

3. In patients with AF in whom rate control strategy is planned, either beta-blockers, verapamil, or diltiazem are recommended, with the choice of agents according to patient preferences and comorbid conditions(Level of Evidence: C-LD)

Class IIa
4. In patients with HCM and subclinical AF detected by internal or external device or monitor, of >5 minutes’ but <24 hours’ duration for a given episode, anticoagulation with DOAC 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)

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 sur-gical myectomy, concomitant surgical AF abla-tion 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
3. In children with HCM and recurrent ventricular arrhythmias despite beta-blocker use, antiarrhythmic drug therapy (amiodarone,3,4 mexiletine,6 sotalol3,4) 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)

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

Class I
1. In patients with HCM who develop systolic dysfunction with an LVEF <50%, guideline-directed therapy for HF with reduced EF is recommended.(Level of Evidence: C-LD)
Class IIa
5. 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)

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[16]

Pharmacologic Management in Symptomatic Patients (DO NOT EDIT)[16]

Class I
“1. Beta-blocking drugs are recommended for the treatment of symptoms (angina or dyspnea) in adult patients with obstructive or non-obstructive HCM but should be used with caution in patients with sinus bradycardia or severe conduction disease.[17][18][19][20][21][22][23][24][25][26][27][28][29] (Level of Evidence: B)”
“2. If low doses of beta-blocking drugs are ineffective for controlling symptoms (angina or dyspnea) in patients with HCM, it is useful to titrate the dose to a resting heart rate of less than 60 to 65 bpm (up to generally accepted and recommended maximum doses of these drugs).[17][18][19][22][23][24][25][26][27][28][29] (Level of Evidence: B)”
“3. Verapamil therapy (starting in low doses and titrating up to 480 mg/d) is recommended for the treatment of symptoms (angina or dyspnea) in patients with obstructive or non-obstructive HCM who do not respond to beta-blocking drugs or who have side effects or contraindications to beta-blocking drugs. However, verapamil should be used with caution in patients with high gradients, advanced heart failure, or sinus bradycardia.[18][19][20][30][31][32][33][34] (Level of Evidence: B)”
“4. Intravenous phenylephrine (or another pure vasoconstricting agent) is recommended for the treatment of acute hypotension in patients with obstructive HCM who do not respond to fluid administration.[19][35][36][37] (Level of Evidence: B)”
Class IIa
“1. It is reasonable to combine disopyramide with a beta-blocking drug or verapamil in the treatment of symptoms (angina or dyspnea) in patients with obstructive HCM who do not respond to beta-blocking drugs or verapamil alone.[18][19][20][38][39][40][41] (Level of Evidence: B)”
“2. It is reasonable to add oral diuretics in patients with non-obstructive HCM when dyspnea persists despite the use of beta blockers or verapamil or their combination.[42][21] (Level of Evidence: C)”
Class IIb
“1. Beta-blocking drugs might be useful in the treatment of symptoms (angina or dyspnea) in children or adolescents with HCM, but patients treated with these drugs should be monitored for side effects, including depression, fatigue, or impaired scholastic performance. (Level of Evidence: C)”
“2. It may be reasonable to add oral diuretics with caution to patients with obstructive HCM when congestive symptoms persist despite the use of beta-blockers or verapamil or their combination.[18][19][20](Level of Evidence: C)”
“3. The usefulness of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in the treatment of symptoms (angina or dyspnea) in patients with HCM with preserved systolic function is not well established, and these drugs should be used cautiously (if at all) in patients with resting or provocable LVOT obstruction. (Level of Evidence: C)”
“4. In patients with HCM who do not tolerate verapamil or in whom verapamil is contraindicated, diltiazem may be considered. (Level of Evidence: C)”
Class III (Harm)
“1. Nifedipine or other dihydropyridine calcium channel-blocking drugs are potentially harmful for treatment of symptoms (angina or dyspnea) in patients with HCM who have resting or provocable LVOT obstruction. (Level of Evidence: C)”
“2. Verapamil is potentially harmful in patients with obstructive HCM in the setting of systemic hypotension or severe dyspnea at rest. (Level of Evidence: C)”
“3. Digitalis is potentially harmful in the treatment of dyspnea in patients with HCM and in the absence of AF[17][18][19][43][44][45]. (Level of Evidence: B)”
“4. The use of disopyramide alone without beta blockers or verapamil is potentially harmful in the treatment of symptoms (angina or dyspnea) in patients with HCM with AF because disopyramide may enhance atrioventricular conduction and increase the ventricular rate during episodes of AF.[18][46][21][47][48][49][50][51][52] (Level of Evidence: B)”
“5. Dopamine, dobutamine, norepinephrine, and other intravenous positive inotropic drugs are potentially harmful for the treatment of acute hypotension in patients with obstructive HCM.[17][35][36][37][53][54][55][56] (Level of Evidence: B)”

Management of Atrial Fibrillation in HCM (DO NOT EDIT)[57]

Class I
“1. Anticoagulation with vitamin K antagonists (ie, warfarin, to an international normalized ratio of 2.0 to 3.0) is indicated in patients with paroxysmal, persistent, or chronic AF and HCM.[57][58][59] (Anticoagulation with direct thrombin inhibitors [ie, dabigatran] may represent another option to reduce the risk of thromboembolic events, but data for patients with HCM are not available.).[60] (Level of Evidence: C)”
“2. Ventricular rate control in patients with HCM with AF is indicated for rapid ventricular rates and can require high doses of beta antagonists and nondihydropyridine calcium channel blockers.[57][59] (Level of Evidence: C)”
Class IIa
“1. Disopyramide (with ventricular rate-controlling agents) and amiodarone are reasonable antiarrhythmic agents for AF in patients with HCM.[57][61] (Level of Evidence: B)”
“2. Radiofrequency ablation for AF can be beneficial in patients with HCM who have refractory symptoms or who are unable to take antiarrhythmic drugs.[62][63][64][65][66] (Level of Evidence: B)”
“3. Maze procedure with closure of left atrial appendage is reasonable in patients with HCM with a history of AF, either during septal myectomy or as an isolated procedure in selected patients. (Level of Evidence: C)”
Class IIb
“1. Sotalol, dofetilide, and dronedarone might be considered alternative antiarrhythmic agents in patients with HCM, especially in those with an ICD, but clinical experience is limited. (Level of Evidence: C)”

Asymptomatic Patients (DO NOT EDIT) [16]

Class I
“1. For patients with HCM, it is recommended that comorbidities that may contribute to cardiovascular disease (e.g., hypertension, diabetes, hyperlipidemia, obesity) be treated in compliance with relevant existing guidelines.[67] (Level of Evidence: C) ”
Class IIa
“1. Low-intensity aerobic exercise is reasonable as part of a healthy lifestyle for patients with HCM.[68][18] (Level of Evidence: C) ”
Class IIb
“1. The usefulness of beta blockade and calcium channel blockers to alter clinical outcome is not well established for the management of asymptomatic patients with HCM with or without obstruction.[18] (Level of Evidence: C) ”
Class III (Harm)
“1. Septal reduction therapy should not be performed for asymptomatic adult and pediatric patients with HCM with normal effort tolerance regardless of the severity of obstruction.[20][18] (Level of Evidence: C) ”
“2. In patients with HCM with resting or provocable outflow tract obstruction, regardless of symptom status, pure vasodilators and high-dose diuretics are potentially harmful.[20][17] (Level of Evidence: C) ”

Patients With LV Systolic Dysfunction (DO NOT EDIT)[16]

Class I
“1. Patients with non-obstructive HCM who develop systolic dysfunction with an EF less than or equal to 50% should be treated according to evidence-based medical therapy for adults with other forms of heart failure with reduced EF, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, and other indicated drugs[69][70]. (Level of Evidence: B) ”
“2. Other concomitant causes of systolic dysfunction (such as CAD) should be considered as potential contributors to systolic dysfunction in patients with HCM. (Level of Evidence: C) ”
Class IIb
“1. ICD therapy may be considered in adult patients with advanced (as defined by NYHA functional class III or IV heart failure) non-obstructive HCM, on maximal medical therapy, and EF less than or equal to 50%, who do not otherwise have an indication for an ICD[69]. (Level of Evidence: C) ”
“2. For patients with HCM who develop systolic dysfunction, it may be reasonable to reassess the use of negative inotropic agents previously indicated, for example, verapamil, diltiazem, or disopyramide, and to consider discontinuing those therapies. (Level of Evidence: C) ”

Pregnancy/Delivery (DO NOT EDIT)[16]

Class I
“1. In women with HCM who are asymptomatic or whose symptoms are controlled with beta-blocking drugs, the drugs should be continued during pregnancy, but increased surveillance for fetal bradycardia or other complications is warranted[71][72][73][74]. (Level of Evidence: C) ”
“2. For patients (mother or father) with HCM, genetic counseling is indicated before planned conception. (Level of Evidence: C) ”
“3. In women with HCM and resting or provocable LVOT obstruction greater than or equal to 50 mm Hg and/or cardiac symptoms not controlled by medical therapy alone, pregnancy is associated with increased risk, and these patients should be referred to a high-risk obstetrician. (Level of Evidence: C) ”
“4. The diagnosis of HCM among asymptomatic women is not considered a contraindication for pregnancy, but patients should be carefully evaluated in regard to the risk of pregnancy. (Level of Evidence: C) ”
Class IIa
“1. For women with HCM whose symptoms are controlled (mild to moderate), pregnancy is reasonable, but expert maternal/fetal medical specialist care, including cardiovascular and prenatal monitoring, is advised. (Level of Evidence: C) ”
Class III (Harm)
“1. For women with advanced heart failure symptoms and HCM, pregnancy is associated with excess morbidity/mortality. (Level of Evidence: C) ”

References

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  54. ↑ KRASNOW N, ROLETT E, HOOD WBJr, YURCHAK PM, GORLIN R (1963). “Reversible obstruction of the ventricular outflow tract”. Am. J. Cardiol. 11: 1–7. PMID 14035510. Unknown parameter |month= ignored (help)
  55. ↑ PIERCE GE, MORROW AG, BRAUNWALD E (1964). “IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS. 3. INTRAOPERATIVE STUDIES OF THE MECHANISM OF OBSTRUCTION AND ITS HEMODYNAMIC CONSEQUENCES”. Circulation. 30: SUPPL 4:152+. PMID 14227305. Unknown parameter |month= ignored (help)
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  70. ↑ Maron BJ, Spirito P (1998). “Implications of left ventricular remodeling in hypertrophic cardiomyopathy”. Am. J. Cardiol. 81 (11): 1339–44. PMID 9631972. Unknown parameter |month= ignored (help)
  71. ↑ Bos JM, Towbin JA, Ackerman MJ (2009). “Diagnostic, prognostic, and therapeutic implications of genetic testing for hypertrophic cardiomyopathy”. J. Am. Coll. Cardiol. 54 (3): 201–11. doi:10.1016/j.jacc.2009.02.075. PMID 19589432. Unknown parameter |month= ignored (help)
  72. ↑ Hershberger RE, Cowan J, Morales A, Siegfried JD (2009). “Progress with genetic cardiomyopathies: screening, counseling, and testing in dilated, hypertrophic, and arrhythmogenic right ventricular dysplasia/cardiomyopathy”. Circ Heart Fail. 2 (3): 253–61. doi:10.1161/CIRCHEARTFAILURE.108.817346. PMC 2927103. PMID 19808347. Unknown parameter |month= ignored (help)
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  74. ↑ Fitzgerald-Butt SM, Byrne L, Gerhardt CA, Vannatta K, Hoffman TM, McBride KL (2010). “Parental knowledge and attitudes toward hypertrophic cardiomyopathy genetic testing”. Pediatr Cardiol. 31 (2): 195–202. doi:10.1007/s00246-009-9583-2. PMID 19949785. Unknown parameter |month= ignored (help)

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