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About oHCM

HCM can be progressive and is often overlooked1,2

Diagnosis and prevalence

What is HCM?

Hypertrophic cardiomyopathy (HCM) is defined as left ventricular hypertrophy in the absence of another identified cause of hypertrophy3

  • It is most commonly caused by mutations in sarcomeric proteins3
  • HCM can be progressive and is characterized by excessive cardiac contractility, impaired relaxation and reduced compliance during diastole, and excess energy consumption1,4,5
    • The 2024 AHA/ACC/Multisociety* Guidelines consider HCM obstructive if LVOT gradient is ≥30 mmHg1
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Obstruction may be present at rest or upon provocation using Valsalva maneuver, squat-to-stand tests, or stress echocardiogram1,3

DEFINITION OF HYPERTROPHY1

Presence of left ventricle wall thickness

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≥15 mm

Adult patients

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≥13 mm

Patients with a known positive genotype or family history of HCM

Detecting HCM1

Triggers for HCM evaluation may include:

  • Family history of HCM
  • Symptoms of HCM
  • Cardiac event
  • Heart murmur
  • Echocardiography or ECG abnormalities

NONSPECIFIC SYMPTOMS2,3,6,7

HCM can often be overlooked, as many symptoms overlap with other conditions such as asthma, anxiety, mitral valve prolapse, and CAD.2

Chest pain iconFatigue iconHeart palpitations iconHeart murmur iconDyspnea iconDizziness and fainting iconEdema icon

oHCM is underdiagnosed in the general population

While approximately 170K people in the US are diagnosed with oHCM, approximately 60% of patients with HCM remain undiagnosed

Unmet medical need

Are your patients with oHCM still symptomatic with first-line treatments?

Beta blockers and calcium channel blockers are recommended as first-line treatments by the 2024 AHA/ACC Multisociety* Guidelines1

In oHCM, these treatments:

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May not completely address treatment goals9,10

  • Partial symptom improvement or no response
  • Inconsistent LVOT gradient reduction
  • No improvement in exercise capacity
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Have limited evidence9

  • Guideline recommendations based on small, nonrandomized studies with short follow-up
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Do not address the underlying disease pathophysiology1

  • Were not designed to reduce the underlying cardiac hypercontractility due to abnormalities in sarcomere function

Consider a treatment that addresses the underlying pathophysiology of oHCM1

START a CMI

CMIs are recommended by the 2024 AHA/ACC/Multisociety* Guidelines for patients with oHCM who need options beyond first-line treatments1

Cardiac myosin inhibitors (CMIs) are a Class I, FDA-approved treatment for oHCM1,11

For your adult patients with oHCM who remain symptomatic, is it time to start a CMI?

Learn more about MYQORZO™, a treatment that could help your patients with oHCM

How MYQORZO works

Review clinical trial results for MYQORZO

Discover the data

*Multisociety includes American Medical Society for Sports Medicine, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Cardiovascular Magnetic Resonance.1

ACC=American College of Cardiology; AHA=American Heart Association; CAD=coronary artery disease; CMI=cardiac myosin inhibitor; ECG=electrocardiogram; LVOT=left ventricular outflow tract; oHCM=obstructive hypertrophic cardiomyopathy.

References: 1. Ommen SR, Ho CY, Asif IM, et al. 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. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/cir.0000000000001250. 2. Argulian E, Sherrid MV, Messerli FH. Misconceptions and facts about hypertrophic cardiomyopathy. Am J Med. 2016;129(2):148-152. doi:10.1016/j.amjmed.2015.07.035 3. Marian AJ, Braunwald E. Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis, and therapy. Circ Res. 2017;121(7):749-770. doi:10.1161/CIRCRESAHA.117.311059 4. Garfinkel AC, Seidman JG, Seidman CE. Genetic pathogenesis of hypertrophic and dilated cardiomyopathy. Heart Fail Clin. 2018;14(2):139-146. doi:10.1016/j.hfc.2017.12.004 5. Basit H, Alahmadi MH, Rout P, Sharma S. Hypertrophic cardiomyopathy. Stat Pearls Publishing; 2024. 6. Maron BJ, Desai MY, Nishimura RA, et al. Diagnosis and evaluation of hypertrophic cardiomyopathy: JACC state-of-the-art review. J Am Coll Cardiol. 2022;79(4):372-389. doi:10.1016/j.jacc.2021.12.002 7. Zaiser E, Sehnert AJ, Duenas A, Saberi S, Brookes E, Reaney M. Patient experiences with hypertrophic cardiomyopathy: a conceptual model of symptoms and impacts on quality of life. J Patient Rep Outcomes. 2020;4(1):102. doi:10.1186/s41687-020-00269-8 8. Data on file. South San Francisco, CA. Cytokinetics Inc; 2025. 9. Zhu M, Reyes KRL, Bilgili G, et al. Medical therapies to improve left ventricular outflow obstruction and diastolic function in hypertrophic cardiomyopathy. JACC Adv. 2023;2(8):100622. doi:10.1016/j.jacadv.2023.100622 10. Dybro AM, Rasmussen TB, Nielsen RR, Andersen MJ, Jensen MK, Poulsen SH. Randomized trial of metoprolol in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2021;78(25):2505-2517. doi:10.1016/j.jacc.2021.07.065 11. Turer AT, Wang A. Cardiac myosin inhibitors: unlocking potential to improve treatment in hypertrophic cardiomyopathy. Circulation. 2023;147(9):700-702. doi:10.1161/CIRCULATIONAHA.122.061015

IMPORTANT SAFETY INFORMATION

WARNING: RISK OF HEART FAILURE

MYQORZO reduces left ventricular ejection fraction (LVEF) and can cause heart failure due to systolic dysfunction.

Echocardiogram assessments are required prior to and during treatment with MYQORZO to monitor for systolic dysfunction. Initiation of MYQORZO in patients with LVEF <55% is not recommended. Decrease the dose of MYQORZO if LVEF is <50% and ≥40%. Interrupt the dose of MYQORZO if LVEF <40% or if the patient experiences heart failure symptoms or worsening clinical status due to systolic dysfunction.

Because of the risk of heart failure due to systolic dysfunction, MYQORZO is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the MYQORZO REMS Program.

CONTRAINDICATIONS

MYQORZO is contraindicated with concomitant use of rifampin.

WARNING AND PRECAUTIONS

Heart Failure
MYQORZO reduces cardiac contractility, which can reduce LVEF and cause heart failure.

Patients who experience a serious intercurrent illness (eg, serious infection) or arrhythmia (eg, new or uncontrolled atrial fibrillation) may be at greater risk of developing systolic dysfunction and heart failure.

Assess patients’ clinical status and LVEF prior to and during treatment and adjust the MYQORZO dose accordingly. New or worsening arrhythmia, dyspnea, chest pain, fatigue, leg edema, or elevations in N-terminal pro-B-type natriuretic peptide may be signs and symptoms of heart failure.

Initiation of MYQORZO in patients with LVEF <55% is not recommended.

MYQORZO REMS Program

MYQORZO is available only through a restricted program called the MYQORZO REMS Program, because of the risk of heart failure due to systolic dysfunction.

Notable requirements of the MYQORZO REMS Program include:

  • Prescribers must be certified by enrolling in the MYQORZO REMS Program
  • Patients must enroll in the MYQORZO REMS Program and comply with ongoing monitoring requirements
  • Pharmacies must be certified by enrolling in the MYQORZO REMS Program and must only dispense to patients who are authorized to receive MYQORZO
  • Wholesalers and distributors must only distribute to certified pharmacies

Further information is available at www.MYQORZOREMS.com, or at 1-844-285-7367.

Cytochrome P450 Interactions Leading to Heart Failure or Loss of Effectiveness
MYQORZO is metabolized primarily by CYP2C9, and to a lesser extent by CYP3A, CYP2D6, and CYP2C19 enzymes. Initiation of medications that inhibit multiple P450 pathways of MYQORZO elimination (eg, fluconazole, voriconazole, or fluvoxamine) or strong CYP2C9 inhibitors, and discontinuation of moderate-to-strong CYP3A inducers may lead to increased blood concentrations of aficamten and increase the risk of heart failure due to systolic dysfunction. Conversely, initiation of medications that induce P450 pathways of MYQORZO (eg, rifampin, moderate-to-strong CYP3A inducers) may lead to decreased blood concentrations of aficamten and potential loss of effectiveness. Assess LVEF 2 to 8 weeks after initiation of such inhibitors or after discontinuation of such inducers and adjust the dose of MYQORZO accordingly.

Advise patients of the potential for drug interactions. Advise patients to inform their healthcare provider of all concomitant medications prior to and during MYQORZO treatment.

ADVERSE REACTIONS

Hypertension (8% vs 2%) was the only adverse reaction occurring in >5% of patients and more commonly on MYQORZO than on placebo in the pivotal trial.

INDICATIONS AND USAGE

MYQORZO is indicated for the treatment of adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM) to improve functional capacity and symptoms.

Please see full Prescribing Information, including Boxed WARNING.