2020 Guideline for the Diagnosis and

Treatment of Patients with Hypertrophic

Cardiomyopathy
GUIDELINES MADE SIMPLE
A Selection of Tables and Figures

ACC.org/GMSHCM
2020 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

Writing Committee:
Steve R. Ommen, MD, FACC, FAHA, Chair
Seema Mital, MD, FACC, FAHA, FRCPC, Vice Chair
Michael A. Burke, MD
Sharlene M. Day, MD
Anita Deswal, MD, MPH, FACC, FAHA
Perry Elliott, MD, FACC
Lauren L. Evanovich, PhD
Judy Hung, MD, FACC
José A. Joglar, MD, FACC, FAHA
Paul Kantor, MBBCh, MSc
Carey Kimmelstiel, MD, FACC
Michelle Kittleson, MD, PhD, FACC
Mark S. Link, MD, FACC
Martin S. Maron, MD
Matthew W. Martinez, MD, FACC
Christina Y. Miyake, MD, MS
Hartzell V. Schaff, MD, FACC
Christopher Semsarian, MBBS, PhD, MPH, FAHA
Paul Sorajja, MD, FACC, FAHA

The ACC/AHA Joint Committee on Clinical Practice Guidelines has commissioned this guideline
to address comprehensive evaluation and management of adults and children with hypertrophic
cardiomyopathy (HCM). Diagnostic modalities such as electrocardiography, imaging and genetic
testing, and management of patients include medical therapies, septal reduction therapies,
sudden cardiac death (SCD) risk assessment/prevention, and lifestyle considerations such as
participation in activities/sports, occupation, and pregnancy.

The following resource contains tables and figures from the 2020 Guideline for the Diagnosis and
Treatment of Patients with Hypertrophic Cardiomyopathy. The resource is only an excerpt from
the Guideline and the full publication should be reviewed for more tables and figures as well as
important context.

CITATION: J AM Coll Cardiol. Nov 2020; DOI: 10.1016/j.jacc.2020.08.045.

 2020 Guideline for the Diagnosis and Treatment of Patients
with Hypertrophic Cardiomyopathy
Table of Contents Page
Class of Recommendation (COR)/ Level of Evidence (LOE) Table…………………………………………… 4

Master Abbreviation List………………………………………………………………………………………… 5

Top 10 Take-Home Messages (1 of 2)…………………………………………………………………………… 6

Genetic Testing and Evaluation…………………………………………………………………………………… 8

Figure 1. Recommended Evaluation and Testing for HCM……………………………………………… 8
Table 6. Screening With Electrocardiography and 2D Echocardiography
in Asymptomatic Family Members……………………………………………………………… 9
Figure 2. Genetic Testing Process in HCM…………………………………………………………………10

Diagnosis………………………………………………………………………………………………………… 11
Table 5. Clinical Features in Patients With “HCM Phenocopies (Mimics)”………………………………11

Sudden Cardiac Death Risk Assessment…………………………………………………………………… 12

Table 7. Established Clinical Risk Factors for HCM Sudden Death Risk Stratification…………………12
Figure 3. ICD Patient Selection………………………………………………………………………………13

Management of Symptoms……………………………………………………………………………………… 14
Figure 4. Management of Symptoms in Patients With HCM………………………………………………14

Recommendations for Pharmacologic Management of Patients With Obstructive HCM……………… 15

Table 3. Suggested Competencies of Comprehensive and Primary HCM Centers………………………16
Table 4. Example Targets for Invasive Septal Reduction Therapies Outcomes…………………………17

Sports Participation…………………………………………………………………………………………… 18

Recommendations for Sports and Activity…………………………………………………………………18

Heart Failure Symptoms in Patients with HCM……………………………………………………………… 19

Figure 5. Heart Failure Algorithm……………………………………………………………………………19
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GUIDELINES MADE SIMPLE
HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Class of Recommendation (COR)/ Level of Evidence (LOE) Table

(Updated May 2019)

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Master Abbreviation List

Abbreviation Meaning/Phrase Abbreviation Meaning/Phrase
AF atrial fibrillation LVOT left ventricular outflow tract
CAD coronary artery disease left ventricular outflow tract
LVOTO
obstruction
cardiovascular magnetic
CMR
resonance MET metabolic equivalent
CPET cardiopulmonary exercise test MR mitral regurgitation
CRT cardiac resynchronization therapy nonsustained ventricular
NSVT
tachycardia
DOAC direct-acting oral anticoagulants
NYHA New York Heart Association
EF ejection fraction
RCT randomized controlled trial
guideline-directed management
GDMT
and therapy RV right ventricular
HCM hypertrophic cardiomyopathy SAM systolic anterior motion
HF heart failure SCAF subclinical AF
implantable cardioverter- SCD sudden cardiac death
ICD
defibrillator
SRT septal reduction therapy
lysosome-associated membrane
LAMP2
protein-2 TEE trans-esophageal
LBBB left bundle branch block echocardiogram
TTE transthoracic
LGE late gadolinium enhancement
echocardiogram
LV left ventricular VF ventricular fibrillation
LVAD left ventricular assist device VT ventricular tachycardia
LVEF left ventricular ejection fraction
LVH left ventricular hypertrophy

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Top 10 Take-Home Messages (1 of 2)

1 Shared decision-making, a dialogue between patients and their care team that includes full
disclosure of all testing and treatment options, discussion of the risks and benefits of those
options and, importantly, engagement of the patient to express their own goals, is particularly relevant in the
management of conditions such as hypertrophic cardiomyopathy (HCM).

2 Athough the primary cardiology team can initiate evaluation, treatment, and longitudinal care, referral
to multidisciplinary HCM centers with graduated levels of expertise can be important to optimizing
care for patients with HCM. Challenging treatment decisions—where reasonable alternatives exist, where the
strength of recommendation is weak (e.g., any Class 2b decision) or is particularly nuanced, and for invasive
procedures that are specific to patients with HCM—represent crucial opportunities to refer patients to these HCM
centers.

3 Counseling patients with HCM regarding the potential for genetic transmission of HCM is one of the
cornerstones of care. Screening first-degree family members of patients with HCM, using either genetic
testing or an imaging/electrocardiographic surveillance protocol, can begin at any age and can be influenced by
specifics of the patient/family history and family preference. As screening recommendations for family members
hinge on the pathogenicity of any detected variants, the reported pathogenicity should be reconfirmed every 2 to
3 years

4 Optimal care for patients with HCM requires cardiac imaging to confirm the diagnosis, characterize the
pathophysiology for the individual, and identify risk markers that may inform decisions regarding interventions
for left ventricular outflow tract obstruction and sudden cardiac death (SCD) prevention. Echocardiography continues to be
the foundational imaging modality for patients with HCM. Cardiovascular magnetic resonance imaging will also be helpful
in many patients, especially those in whom there is diagnostic uncertainty, poor echocardiographic imaging windows, or
where uncertainty persists regarding decisions around implantable cardioverter-defibrillator (ICD) placement.

5 Assessment of an individual patient’s risk for SCD continues to evolve as new markers emerge (e.g.,
apical aneurysm, decreased left ventricular systolic function, and extensive gadolinium enhancement).
In addition to a full accounting of an individual’s risk markers, communication with patients regarding not just
the presence of risk markers but also the magnitude of their individualized risk is key. This enables the informed
patient to fully participate in the decision-making regarding ICD placement, which incorporates their own level of
risk tolerance and treatment goals.

“Top Ten Messages” is continued in the next page.

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Top 10 Take-Home Messages (2 of 2)

6 The risk factors for SCD in children with HCM carry different weights than those observed in adult
patients; they vary with age and must account for different body sizes. Coupled with the complexity of
placing ICDs in young patients with anticipated growth and a higher risk of device complications, the threshold
for ICD implantation in children often differs from adults. These differences are best addressed at primary or
comprehensive HCM centers with expertise in children with HCM.

7 Septal reduction therapies (surgical septal myectomy and alcohol septal ablation), when performed by
experienced HCM teams at dedicated centers, continue to improve in safety and efficacy such that earlier
intervention may be possible in select patients with drug-refractory or severe outflow tract obstruction causing signs of
cardiac decompensation. Given the data on the significantly improved outcomes at comprehensive HCM centers, these
decisions represent an optimal referral opportunity.

8 Patients with HCM and persistent or paroxysmal atrial fibrillation have a sufficiently increased
risk of stroke such that oral anticoagulation with direct oral anticoagulants (or alternatively warfarin)
should be considered the default treatment option independent of the CHA2DS2VASc score. As rapid atrial
fibrillation is often poorly tolerated in patients with HCM, maintenance of sinus rhythm and rate control are
key pursuits in successful treatment.

9 Heart failure symptoms in patients with HCM, in the absence of left ventricular outflow tract obstruction,
should be treated similarly to other patients with heart failure symptoms, including consideration of
advanced treatment options (e.g., cardiac resynchronization therapy, left ventricular assist device, transplantation).
In patients with HCM, an ejection fraction <50% connotes significantly impaired systolic function and identifies
individuals with poor prognosis and who are at increased risk for SCD.

10 Increasingly, data affirm that the beneficial effects of exercise on general health can be extended to
patients with HCM. Healthy recreational exercise (moderate intensity) has not been associated with
increased risk of ventricular arrhythmia events in recent studies. Whether an individual patient with HCM wishes to
pursue more rigorous exercise/training is dependent on a comprehensive shared discussion between that patient
and their expert HCM care team regarding the potential risks of that level of training/participation but with the
understanding that exercise-related risk cannot be individualized for a given patient.

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Genetic Testing and Evaluation

Figure 1. Recommended Evaluation and Testing for HCM

HCM Suspected or Family History of HCM

Diagnostic Testing
(ECG, Imaging, Genetics)
(See Figure 2 for details
1 on genetic testing)
Phenotype Negative Phenotype Positive

Complete Baseline Evaluation

• SCD risk assessment
• Stress testing if symptomatic,
if LVOTO is suspected but
unconfirmed, or to determine
baseline functional capacity

2
Family with Every 1-2 years or with change in
known P/LP symptoms* (1)
variant? Serial evaluation for clinical status,
(See Figure 2 for SCD risk (if no ICD present), or
more detail) sooner with change in symptoms:
• Clinical assessment
• Echo
YES NO • Holter

Patient
has family YES, or Unknown Every 3-5 y (2b)
variant?
CMR for SCD risk assessment (if no
NO ICD present), or to evaluate for any
suspected morphologic changes
3
Further clinical or genetic
testing is not recommended
(3: No Benefit)
Asymptomatic Symptomatic

4 5
Reassess variant Screening ECG and Echo Every 2-3 y (2b) Treadmill or Bike Exercise Testing (1)
classification (1) (CMR if echo is inconclusive) Treadmill exercise or Special consideration:
at the intervals in the table Cardiopulmonary exercise testing • Stress echo if gradient <50 mm Hg
below (1) for assessment of functional status
• CPET if considering advanced HF
Variant = P/LP Variant downgraded to VUS
therapies

Screening Asymptomatic First-Degree Relatives of Patients With HCM

Age of First-Degree Relative Initiation of Screening Surveillance Interval
Children and adolescents from At the time of diagnosis in another family member Every 1-2 y
genotype-positive family and/or family
with early onset HCM
All other children and adolescents At any time after the diagnosis in the family, but Every 2-3 y
no later than puberty
Adults At the time of diagnosis in another family member Every 3-5 y

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Table 6. Screening With Electrocardiography and 2D Echocardiography

in Asymptomatic Family Members*

Age of First-Degree Relative Initiation of Screening Repeat ECG, Echo

Pediatric
Children and adolescents from gen- At the time HCM is diagnosed in Every 1-2 y
otype-positive families, and families another family member
with early onset disease
All other pediatric At any time after HCM is diag- Every 2-3 y
nosed in a family member but no
later than puberty
Adults At the time HCM is diagnosed in Every 3-5 y
another family member
*Includes all asymptomatic, phenotype-negative first-degree relatives deemed to be at-risk for developing HCM based on family history or genotype
status and may sometimes include more distant relatives based on clinical judgment. Screening interval may be modified (e.g., at onset of new
symptoms or in families with a malignant clinical course or late-onset HCM).

Strong evidence HCM genes include, at the time of this publication: MYH7, MYBPC3, TNNI3, TNNT2, TPM1,
MYL2, MYL3, and ACTC1.
Determining pathogenicity of variants relies on a weight of collective evidence based on American College of Medical
Genetics and Genomics criteria and may change over time.

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Figure 2. Genetic Testing Process in HCM

HCM Index Case

Targeted Gene Testing

Regular reevaluation
for variant
Disease-causing reclassification VUS, LB/B or
LP/P variant no variant identified
(See Figure 1, Box 4)
(1)

Consider second tier

Reclassified as Reclassified as
LP/P VUS or LB/B
testing in proband if no
variant is identified

Cascade genetic testing Clinical surveillance

in family (1) in family (1)

Variant positive Variant negative No evidence of

HCM diagnosed
HCM

Further clinical or
Regular follow-up genetic testing not Regular clinical
Regular follow-up
recommended surveillance
(See Figure 1, Box 2) (See Figure 1, Box 2)
(1) (See Figure 1, Box 3) (See Figure 1, Box 5)
(1)
(3: No Benefit) (1)

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Diagnosis
Table 5. Clinical Features in Patients With
“HCM Phenocopies (Mimics)”

Typical Presentation Age Systemic Features Possible Etiology Diagnostic Approach

Infants (0-12 mo) and toddlers Dysmorphic features, • RASopathies • Geneticist assessment
failure to thrive, • Glycogen storage • Newborn metabolic
metabolic acidosis diseases, other screening
metabolic or • Specific metabolic
mitochondrial assays
diseases • Genetic testing
• Infant of a mother
with diabetes

Early childhood Delayed or abnormal • RASopathies • Biochemical screening

cognitive development, • Mitochondrial diseas • Genetic testing
visual or hearing
impairment
School age and Skeletal muscle • Friedrich ataxia, • Biochemical screening
adolescence weakness or movement Danon disease • Neuromuscular
disorder • Mitochondrial assessment
disease • Genetic testing

Adulthood Movement disorder, • Anderson-Fabry • Biochemical screening,

peripheral neuropathy, disease, Friedrich • Neuromuscular
renal dysfunction ataxia, infiltrative assessment
disorders (e.g., • Genetic testing
amyloidosis),
glycogen storage
diseases

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HCM 2020 Guideline for the Diagnosis and Treatment of Patients with Hypertrophic Cardiomyopathy

Sudden Cardiac Death Risk Assessment

Table 7. Established Clinical Risk Factors for HCM
Sudden Death Risk Stratification

Family history of sudden Sudden death judged definitively or likely attributable to HCM in ≥1 first-
death from HCM degree or close relatives who are ≤50 years of age. Close relatives would
generally be second-degree relatives; however, multiple SCDs in tertiary
relatives should also be considered relevant.

Massive LVH Wall thickness ≥30 mm in any segment within the chamber by
echocardiography or CMR imaging; consideration for this morphologic
marker is also given to borderline values of ≥28 mm in individual
patients at the discretion of the treating cardiologist. For pediatric
patients with HCM, an absolute or z-score threshold for wall thickness
has not been established; however, a maximal wall that corresponds to
a z-score ≥20 (and >10 in conjunction with other risk factors) appears
reasonable.

Unexplained syncope ≥1 Unexplained episodes involving acute transient loss of consciousness,

judged by history unlikely to be of neurocardiogenic (vasovagal) etiology,
nor attributable to LVOTO, and especially when occurring within 6 months
of evaluation (events beyond 5 years in the past do not appear to have
relevance).

HCM with LV systolic Systolic dysfunction with EF <50% by echocardiography or CMR imaging.
dysfunction

LV apical aneurysm Apical aneurysm defined as a discrete thin-walled dyskinetic or akinetic

segment of the most distal portion of the LV chamber; independent of
size.

Extensive LGE on CMR Diffuse and extensive LGE, representing fibrosis, either quantified or
imaging estimated by visual inspection, comprising ≥15% of LV mass (extent of
LGE conferring risk has not been established in children).

NSVT on ambulatory It would seem most appropriate to place greater weight on NSVT as a
monitor risk marker when runs are frequent (≥3), longer (≥10 beats), and faster
(≥200 bpm) occurring usually over 24 to 48 hours of monitoring. For
pediatric patients, a VT rate that exceeds the baseline sinus rate by >20%
is considered significant.

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Figure 3. ICD Patient Selection

Prior event
YES An ICD is recommended (1)
(SCD, VF, sustained VT)

NO

At least 1 of the
following:
• FH SCD*
• Massive LVH* YES† An ICD is reasonable (2a)
• Unexplained
Syncope*
• Apical aneurysm
• EF ≤50%

NO
Children

NSVT *‡ YES

NO Adults†

Extensive LGE on CMR YES An ICD may be considered (2b)

NO

An ICD is not indicated (3: Harm)

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Management of Symptoms
Figure 4. Management of Symptoms in Patients With HCM

HCM Patients

Treat comorbidities
according to GL
(1)

Obstructive physiology?

See Figure 5 NO YES

Symptoms?

Repeat evaluation as
NO YES
per Figure 1, Box 2

Avoid vasodilators and

high-dose diuretics

Beta-blockade
(1)

Verapamil or diltiazem
(1)

If symptoms persist

Septal reduction
Disopyramide
therapy
(1)
(1)

Surgical
candidate?

NO YES

Septal ablation Other

(1) surgical
indication or
nonstandard
indication?

NO YES

Septal ablation Myectomy

(1) (1)

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Recommendations for Pharmacologic Management of

Patients With Obstructive HCM

COR LOE Recommendations

1 B-NR 1. In patients with obstructive HCM and symptoms* attributable to
LVOTO, nonvasodilating beta-blockers, titrated to effectiveness or
maximally tolerated doses, are recommended.
1 Verapamil 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 (e.g.,
Diltiazem C-LD verapamil, diltiazem) is recommended.

1 B-NR 3. F
 or 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.

1 C-LD 4. F or 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.
2b C-EO 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.
2b C-EO 6. For patients with obstructive HCM, discontinuation of vasodilators
(e.g., angiotensin-converting enzyme 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.
3: Harm C-LD 7. For patients with obstructive HCM and severe dyspnea at rest,
hypotension, very high resting gradients (e.g., >100 mm Hg), as well
as all children <6 weeks of age, verapamil is potentially harmful.
*Symptoms include effort-related dyspnea or chest pain; and occasionally other exertional symptoms (e.g., syncope, near syncope) that are attributed to LVOTO
and interfere with everyday activity or quality of life.

†Comprehensive or primary HCM centers with demonstrated excellence in clinical outcomes for these procedures (Table 3 and 4).

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Table 3. Suggested Competencies of Comprehensive and Primary HCM Centers

Potential HCM Care Delivery Competencies Comprehensive Primary HCM Referring Centers/
HCM Center Center Physicians
Diagnosis X X X
Initial and surveillance TTE X X X
Advanced echocardiographic imaging to detect latent LVOTO X X
Echocardiography to guide SRT X *
CMR imaging for diagnosis and risk stratification X X
Invasive evaluation for LVOTO X * *
Coronary angiography X X X
Stress testing for elicitation of LVOTO or consideration of X X
advanced HF therapies/transplant
Counseling and performing family screening X X X
(imaging and genetic)
Genetic testing/counseling X X *
SCD risk assessment X X X
Class 1 and Class 2a ICD decision-making with adult patients X X X
Class 2B ICD decision-making with adult patients X
ICD implantation (adults) X X *
ICD decision-making and implantation with children/ X *
adolescents and their parents
Initial AF management and stroke prevention X X X
AF catheter ablation X X *
Initial management of HFrEF and HFpEF X X X
Advanced HF management (e.g., transplantation, CRT) X *
Pharmacologic therapy for symptomatic obstructive HCM X X X
Invasive management of symptomatic obstructive HCM X †
Counseling occupational and healthy living choices other X X X
than high-intensity or competitive activities
Counseling options on participation in high-intensity or X
competitive athletics
Managing women with HCM through pregnancy X *
Management of comorbidities X X X

*Optional depending on the core competencies of the institution.

†If these procedures are performed, adequate quality assurance should be in place to demonstrate
outcomes consistent with that achieved by comprehensive centers.

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Table 4. Example Targets for Invasive Septal Reduction Therapies Outcomes

Rate
Myectomy Alcohol Septal Ablation
30-d mortality ≤1% ≤1%
30-d adverse complications ≤10% ≤10%
(tamponade, LAD dissection, infection,
major bleeding)
30-d complete heart block resulting in need for ≤5% ≤10%
permanent pacemaker

Mitral valve replacement within 1 year ≤5%

More than moderate residual mitral regurgitation ≤5% ≤5%
Repeat procedure rate ≤3% ≤10%
Improvement ≥ NYHA class >90% >90%
Rest and provoked LVOT gradient <50 mm Hg >90% >90%

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Sports Participation
Recommendations for Sports and Activity

COR LOE Recommendations

1 B-NR 1. F
 or most patients with HCM, mild- to moderate-intensity recreational*
exercise is beneficial to improve cardiorespiratory fitness, physical
functioning, and quality of life, and for their overall health in keeping with
physical activity guidelines for the general population.
1 C-EO 2. F
 or athletes with HCM, a comprehensive evaluation and shared discussion of
potential risks of sports participation by an expert provider is recommended.
2a C-EO 3. F
 or most patients with HCM, participation in low-intensity competitive sports
is reasonable.

2a C-LD 4. In individuals who are genotype-positive, phenotype-negative for HCM,

participation in competitive athletics of any intensity is reasonable.
2b C-LD 5. F
 or patients with HCM, participation in high-intensity recreational activities or
moderate- to high-intensity competitive sports activities may be considered
after a comprehensive evaluation and shared discussion, repeated annually
with an expert provider who conveys that the risk of sudden death and
ICD shocks may be increased, and with the understanding that eligibility
decisions for competitive sports participation often involve third parties (e.g.,
team physicians, consultants, and other institutional leadership) acting on
behalf of the schools or teams.
3: Harm B-NR 6. In patients with HCM, ICD placement for the sole purpose of participation in
competitive athletics should not be performed.
*Recreational exercise is done for the purpose of leisure with no requirement for systematic training and without the purpose to excel or compete against others.

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Heart Failure Symptoms in Patients with HCM

Figure 5. Heart Failure Algorithm

HCM Patients

Section on
Obstructive
YES obstructive HCM
physiology?
(See Figure 4)

NO

Systolic function

Section on
LVEF <50% LVEF ≥50% symptomatic
nonobstructive HCM

Discontinue
ARNI/ACEI/ARB,
Evaluate for negative inotropic
beta-blocker, and Implantable
other causes of agents (verapamil,
MRA per heart cardiac-defibrillator
reduced EF diltiazem,
failure guideline (2a)
(1) disopyramide)
(1)
(2a)

Reevaluation after
GDMT

Recurrent ventricular
NYHA class I-II NYHA class III-IV
arrhythmias

Continue current LVEF <50% Evaluate for heart

management and LBBB transplant
(1) (1)
YES NO

If patient
Evaluate for heart decompensates
CRT
transplant while listed,
(2a)
(1) evaluate for LVAD
(2a)

Symptoms NYHA class

NO YES
after CRT III-IV
©2020 American College of Cardiology B20177

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