Hypertrophic cardiomyopathy echocardiography and ultrasound

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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]

Overview

Echocardiography is the imaging modality of choice in the diagnosis of hypertrophic cardiomyopathy. Classically there is a small left ventricular cavity with hypertrophy out of proportion to any underlying condition that would cause LVH. The hypertrophy is often asymmetric.

Echocardiography

Echo with doppler is the primary procedure used to diagnose hypertrophic cardiomyopathy. There is a prolonged isovolumic relaxation time, reduced peak E velocity, prolonged deceleration time, increased peak A velocity and decreased E/A ratio as compared to normal controls.

Proper examination should evaluate: [1]

  • Dynamic outflow tract obstruction
    • SAM (systolic anterior motion) of the mitral leaflet
    • Mid-systolic closure of the aortic valve
    • Late peaking, high-velocity flow in the outflow tract
    • Variability of obstruction with maneuvers (exercise, amyl nitrate inhalation, and post-PVC beats)
  • Doppler Techniques
    • Use continuous wave doppler to measure the systolic flow velocity in the LV outflow tract and mid-cavity (both at rest and during maneuvers such as the Valsalva maneuver or during dobutamine administration.

Because of the turbulent, high-velocity jet in the left ventricular outflow tract (LVOT), the anterior mitral leaflet moves anteriorly in systole, exacerbating the outflow tract obstruction, and promoting mitral regurgitation. The following images show classic systolic anterior motion (SAM) of the mitral valve leaflets:

Frequency of Hypertrophy

While LVH is usually present, not all carriers with HCM demonstrate left ventricular hypertrophy. Left ventricular hypertrophy may be absent in childhood. It may then appear following the rapid growth of adolescence and may first appear at age 17 to 18.[2][3][4] LVH may be time-dependent and may appear late, particularly in patients with a mutation in the myosin-binding protein C gene. Patients generally present later in life and in general, have a better prognosis than beta myosin heavy chain or cardiac troponin T mutations. Up to 60% of patients at age 50 years have no evidence of LVH. LVH may appear later in life in these patients. Because of this, a normal EKG and a normal ECHO at maturity does not exclude the presence of an HCM mutation. [5]

Diagnostic Features of Hypertrophy

  • Left ventricular hypertrophy (LVH) most often in an asymmetric distribution,
  • Thickening of the left ventricular wall in the absence of cavitary dilation and the presence of hyperdynamic activity (in fact there may be systolic cavity obliteration or near obliteration)
  • Absence of any other cause of left ventricular hypertrophy such as aortic stenosis or hypertension

Left Ventricular Wall Thickness

  • The traditional definition requires a wall thickness > 15 mm.
  • Borderline wall thicknesses of 13-14 mm must be distinguished from extreme variants of athletes heart
  • There are some genetic variants that yield a normal wall thickness. [6][7][8][9][10]
  • Among children < 13 years of age, LVH is often absent.

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[11]

Echocardiography (DO NOT EDIT)[11]

Class I
"1. A TTE is recommended in the initial evaluation of all patients with suspected HCM.[12][13][14][15][16][17][18][19] (Level of Evidence: B) "
"2. A TTE is recommended as a component of the screening algorithm for family members of patients with HCM unless the family member is genotype negative in a family with known definitive mutations.[20][21][22][23] (Level of Evidence: B) "
"3. Periodic (12 to 18 months) TTE screening is recommended for children of patients with HCM, starting by age 12 years or earlier if a growth spurt or signs of puberty are evident and/or when there are plans for engaging in intense competitive sports or there is a family history of SCD.[21][24] (Level of Evidence: C) "
"4. Repeat TTE is recommended for the evaluation of patients with HCM with a change in clinical status or new cardiovascular event.[25][26][27][28][29][30][31] (Level of Evidence: B) "
"5. A transesophageal echocardiogram (TEE) is recommended for the intraoperative guidance of surgical myectomy.[32][33][34] (Level of Evidence: B) "
"6. TTE or TEE with intracoronary contrast injection of the candidate’s septal perforator(s) is recommended for the intraprocedural guidance of alcohol septal ablation.[35][36][37][38] (Level of Evidence: B) "
"7. TTE should be used to evaluate the effects of surgical myectomy or alcohol septal ablation for obstructive HCM.[35][39][40][41][42][43][44] (Level of Evidence: C) "
Class IIa
"1. TTE studies performed every 1 to 2 years can be useful in the serial evaluation of symptomatically stable patients with HCM to assess the degree of myocardial hypertrophy, dynamic obstruction, and myocardial function.[13][15][17] (Level of Evidence: C) "
"2. Exercise TTE can be useful in the detection and quantification of dynamic LVOT obstruction in the absence of resting outflow tract obstruction in patients with HCM.[26][29][31][45][46] (Level of Evidence: B) "
"3. TEE can be useful if TTE is inconclusive for clinical decision making about medical therapy and in situations such as planning for myectomy, exclusion of sub-aortic membrane or mitral regurgitation secondary to structural abnormalities of the mitral valve apparatus, or in assessment for the feasibility of alcohol septal ablation.[32][33][34] (Level of Evidence: C) "
"4. TTE combined with the injection of an intravenous contrast agent is reasonable if the diagnosis of apical HCM or apical infarction or severity of hypertrophy is in doubt, particularly when other imaging modalities such as cardiovascular magnetic resonance (CMR) are not readily available, not diagnostic, or are contraindicated. (Level of Evidence: C)"
"5. Serial TTE studies are reasonable for clinically unaffected patients who have a first-degree relative with HCM when genetic status is unknown. Such follow-up may be considered every 12 to 18 months for children or adolescents from high-risk families and every 5 years for adult family members.[20][21][23][24] (Level of Evidence: C)"
Class III (No Benefit)
"1. TTE studies should not be performed more frequently than every 12 months in patients with HCM when it is unlikely that any changes have occurred that would have an impact on clinical decision making. (Level of Evidence: C) "
"2. Routine TEE and/or contrast echocardiography is not recommended when TTE images are diagnostic of HCM and/or there is no suspicion of fixed obstruction or intrinsic mitral valve pathology.(Level of Evidence: C) "

Detection of Concomitant Coronary Disease [11]

Class III (No Benefit)
"1. Routine SPECT MPI or stress echocardiography is not indicated for detection of silent CAD-related ischemia in patients with HOCM who are asymptomatic. (Level of Evidence: C) "

References

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