Cardiovascular · PANCE / PANRE

Hypertrophic Cardiomyopathy (HCM)

Genetic LVH (often asymmetric septal) with dynamic LVOT obstruction — leading cause of SCD in young athletes.

Also known as: HCM, hypertrophic cardiomyopathy, HOCM, IHSS, asymmetric septal hypertrophy

Overview

Primary myocardial disease defined by unexplained left ventricular hypertrophy (wall thickness ≥15 mm, or ≥13 mm with family history) in the absence of another cardiac or systemic cause. Often features dynamic left ventricular outflow tract obstruction from systolic anterior motion (SAM) of the mitral valve.

Epidemiology

Prevalence ~1 in 500. Autosomal dominant inheritance in most familial cases. Most common cause of sudden cardiac death in young athletes in the US.

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Risk factors

  • Autosomal dominant mutations in sarcomere genes (most commonly MYH7 β-myosin heavy chain, MYBPC3 myosin-binding protein C)
  • Family history of HCM or sudden cardiac death
  • Syndromic associations: Noonan syndrome, Fabry disease, Friedreich ataxia, mitochondrial disorders, amyloidosis (phenocopies)
  • Male sex (slightly higher prevalence)

Pathophysiology

Sarcomere mutations produce myocyte hypertrophy, disarray, and interstitial fibrosis. Asymmetric septal hypertrophy narrows the LVOT, and during systole the anterior mitral leaflet is pulled into the septum (SAM), creating dynamic obstruction and posteriorly-directed mitral regurgitation. Diastolic dysfunction is universal. The disorganized myocardium serves as a substrate for ventricular arrhythmia.

Clinical presentation

Symptoms

  • Often asymptomatic; HCM detected on screening or after sudden death of a family member
  • Exertional dyspnea, fatigue (most common symptom)
  • Anginal chest pain
  • Palpitations, presyncope, syncope (especially exertional — ominous)
  • Sudden cardiac death may be the first manifestation

Signs / physical exam

  • Brisk, bisferiens carotid pulse (spike-and-dome)
  • Sustained, displaced apical impulse with palpable presystolic component (S4)
  • Harsh systolic ejection murmur at LLSB — INCREASES with Valsalva strain and standing (decreased preload), DECREASES with squatting or handgrip (increased afterload/preload)
  • Holosystolic apical murmur of MR from SAM
  • S4 gallop from forceful atrial contraction into stiff LV

Differential diagnosis

  • Aortic stenosis — Fixed obstruction — murmur DECREASES with Valsalva; calcified valve on echo
  • Athlete's heart — Symmetric hypertrophy ≤13 mm, regresses with detraining, normal diastolic function, larger LV cavity
  • Hypertensive LVH — Symmetric concentric LVH in patient with chronic HTN; usually wall thickness <15 mm
  • Cardiac amyloidosis — Thickened walls but LOW voltage on ECG, granular sparkling myocardium, pseudo-Q waves; confirm with PYP scan or biopsy
  • Anderson-Fabry disease — X-linked, low α-galactosidase, angiokeratomas, renal failure, neuropathy; LVH on echo
  • Mitral valve prolapse — Mid-systolic click; murmur shifts with Valsalva but no LVH

Diagnostic workup

Diagnostic criteria

Adult: maximum LV wall thickness ≥15 mm unexplained by loading conditions, or ≥13 mm with affected family member or positive genetic testing. LVOT gradient ≥30 mmHg at rest or ≥50 mmHg with provocation defines obstructive HCM.

Labs

  • Basic labs; consider genetic testing in proband and cascade screen of first-degree relatives
  • BNP/NT-proBNP for severity assessment
  • Cardiac enzymes if chest pain

Imaging

  • Transthoracic echo — diagnostic; document septal thickness, LVOT gradient at rest and with provocation (Valsalva, exercise), SAM, MR
  • Cardiac MRI with late gadolinium enhancement — extent of fibrosis and SCD risk stratification, mass quantification, apical HCM identification
  • ECG — LVH with strain, deep narrow Q waves (septal hypertrophy), giant precordial T-wave inversions in apical HCM (Yamaguchi)
  • Holter monitor — screen for non-sustained VT (SCD risk factor)
  • Exercise stress echo to provoke LVOT gradient

Diagnostic algorithm

ManeuverPreload / AfterloadHCM murmurAortic stenosis murmurMVP click-murmur
Valsalva (strain)↓ PreloadLOUDERSofterClick earlier, murmur longer
Standing from squat↓ PreloadLOUDERSofterClick earlier, murmur longer
Squatting↑ Preload, ↑ AfterloadSofterLouderClick later, murmur shorter
Sustained handgrip↑ AfterloadSofterSofterClick later, murmur louder if MR
Passive leg raise↑ PreloadSofterLouderClick later, murmur shorter
Bedside maneuvers help distinguish HCM from AS and MVP.

Treatment

First-line

  • Avoid dehydration, alcohol, sudden standing, and intense competitive athletics (per 2020 ACC/AHA — shared decision-making for participation)
  • Symptomatic obstructive HCM: non-vasodilating beta-blocker (metoprolol, atenolol, propranolol) titrated to symptoms and HR
  • Non-dihydropyridine CCB (verapamil, diltiazem) if beta-blocker not tolerated
  • AVOID: dihydropyridine CCBs, ACEi/ARBs, digoxin, nitrates, diuretics in obstructive HCM (worsen gradient)
  • Disopyramide added for refractory symptoms (negative inotrope)
  • Mavacamten (cardiac myosin inhibitor) — newer option for symptomatic obstructive HCM (EXPLORER-HCM, VALOR-HCM)

Second-line / adjunct

  • Septal reduction therapy — surgical septal myectomy (preferred in young patients, experienced center) or alcohol septal ablation — for refractory symptoms with LVOT gradient ≥50 mmHg despite optimal medical therapy
  • ICD placement — Class I for survivors of cardiac arrest or sustained VT; Class IIa for ≥1 major risk factor (family history of SCD, unexplained syncope, LV thickness ≥30 mm, non-sustained VT on Holter, abnormal BP response to exercise, extensive LGE on MRI)
  • Family screening — first-degree relatives by ECG and echo every 1-3 years from childhood; genetic testing if a pathogenic variant is identified in proband
  • Heart transplant for end-stage HCM with refractory heart failure

Complications

  • Sudden cardiac death (annual risk ~1% overall, higher in those with risk factors)
  • Atrial fibrillation with embolic stroke
  • Heart failure (obstructive and end-stage burnout/dilated phase)
  • Infective endocarditis (rare)
  • Conduction disease after septal ablation/myectomy

PANCE pearls

  • HCM murmur INCREASES with Valsalva or standing (decreased preload) — opposite of most systolic murmurs.
  • Mavacamten (EXPLORER-HCM) reduces LVOT gradient and improves symptoms in obstructive HCM.
  • First-degree relatives need cascade screening — even asymptomatic carriers may carry SCD risk.
  • Avoid dihydropyridine CCBs (nifedipine, amlodipine), ACE inhibitors, nitrates, and digoxin in obstructive HCM — they worsen LVOT gradient.
  • Apical (Yamaguchi) HCM: giant precordial T-wave inversions and spade-shaped LV cavity on echo/MRI — Japanese predominance, generally favorable prognosis.

References

  • AHA/ACC 2020 HCM — 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy (Ommen et al., Circulation 2020)
  • ESC 2023 HCM — 2023 ESC Guidelines for the Management of Cardiomyopathies (Arbelo et al., Eur Heart J 2023)
  • EXPLORER-HCM — Mavacamten for Treatment of Symptomatic Obstructive HCM (Olivotto et al., Lancet 2020)
  • VALOR-HCM — Mavacamten in Patients with Obstructive HCM Referred for Septal Reduction (Desai et al., JACC 2022)

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