HOCM

HOCM TTE Algorithm

4. What is the resting peak LVOT gradient? Peak gradient = 4 × Vmax²
≥50 mmHg

Clinically significant obstruction

Resting obstruction is sufficient to explain exertional symptoms when the clinical picture fits.

Obstructive HCM
This is the threshold generally used when considering advanced obstruction-directed therapy in symptomatic patients.
<50 mmHg

Provoke the gradient

Perform Valsalva and/or standing maneuvers rather than labeling the patient nonobstructive from the resting study alone.

Valsalva / standing Measure the highest provoked LVOT gradient
≥50 mmHg Provocable obstructive HCM
<50 mmHg No clinically significant gradient yet
If symptomatic and still <50 mmHg:
perform exercise TTE. A gradient ≥50 mmHg with exercise identifies latent / exercise-induced obstruction.
Report: maximal LV wall thickness and pattern, SAM, site of obstruction, resting LVOT gradient, provoked/exercise gradient and method, MR mechanism/severity, LA size, LV systolic function, and relevant diastolic findings.

What you are measuring

  • In A5C, A3C and subcostal views
    • Peak instantaneous LVOT gradient using CW Doppler
    • Convert velocity to gradient: Peak ΔP (mmHg) = 4 × (Vmax in m/s)²
    • Report rest and provoked values, and specify the provocation method

How to acquire it correctly

  • Use color Doppler first to locate aliasing/turbulence in LVOT
  • Place CW Doppler cursor through LVOT, aligned as parallel to flow as possible
  • Sweep multiple windows and pick the highest Vmax (best aligned, cleanest envelope)
  • Optimize settings: higher sweep speed, appropriate gain to avoid blooming, avoid under-gaining (you will clip the peak)

How to confirm it is LVOT and not MR

  • LVOT obstruction: “dagger-shaped” late-peaking systolic CW envelope
  • MR: denser, often earlier-peaking signal that extends into/through systole (may appear more holosystolic), usually higher velocity than LVOT
  • If unsure, compare timing and shape, and correlate with color jet direction and MR severity
  • Use PW Doppler mapping: step from LVOT toward apex to localize the site of acceleration (helps distinguish mid-cavity vs LVOT)

What to report

  • Resting LVOT Vmax and peak gradient (mmHg)
  • Provoked LVOT Vmax and peak gradient, plus provocation method
  • Presence/absence of SAM of MV and severity of MR (qualitative is fine)
  • If mid-cavity obstruction: state location and report peak gradient there (and clarify it is mid-cavity, not LVOT)
LVOT Gradient Interpretation
Interpretation Peak gradient Meaning Next step
No obstruction by gradient <30 mmHg Does not meet the hemodynamic definition of LVOT obstruction If resting gradient is <50 mmHg, perform provocative maneuvers when evaluating HCM
LVOT obstruction present 30-49 mmHg Dynamic LVOT obstruction is present If symptoms are suspected to be obstruction-related, look for a provoked or exercise gradient ≥50 mmHg
Clinically significant obstruction ≥50 mmHg Resting or provoked gradient capable of causing symptoms Key threshold for obstruction-directed treatment decisions when symptoms persist

Provocative Testing

  • Valsalva or exercise can unmask gradients ≥50 mmHg in symptomatic patients
  • These thresholds guide decisions for septal reduction therapies

SAM

Left ventricular outflow tract obstruction occurs when fast-flowing blood through the LV outflow tract pulls the mitral valve anteriorly due to a Venturi effect. This phenomenon is called systolic anterior motion (SAM) of the mitral valve.

SAM leads to 2 key consequences

  • Outflow obstruction
    • The anteriorly displaced mitral valve obstructs the LV outflow tract
    • This impairs systolic ejection into the aorta, reducing cardiac output
    • Can lead to hypotension or cardiogenic shock
  • Mitral regurgitation

TTE

  • Septal hypertrophy (often asymmetric, IVS ≥15 mm)
  • Systolic anterior motion (SAM) of mitral valve
  • Dynamic obstruction: Late-peaking “dagger-shaped” continuous-wave Doppler curve
  • Mitral regurgitation: Posteriorly directed jet due to SAM
  • Hyperkinetic LV: Often with near obliteration of the left ventricular cavity during systole

Does this patient with HCM need an ICD?

HCM ICD Decision

Prior cardiac arrest, VF, or sustained VT?

Secondary prevention

ICD recommended Class I
IF NO

Any major SCD risk factor?

  • HCM-related SCD in a close relative ≤50 years
  • Massive LVH ≥30 mm
  • Recent suspected arrhythmic syncope
  • LV apical aneurysm with scar / LGE
  • LVEF <50%
ICD reasonable Class IIa
IF NONE

NSVT or extensive LGE?

Give NSVT more weight when runs are frequent, longer, or faster. Extensive LGE is generally ≥15% of LV mass in adults.

ICD may be considered Class IIb
IF ABSENT

No recognized SCD risk factors

Continue routine reassessment as the phenotype evolves.

Do not implant ICD for primary prevention Class III: Harm

HCM ICD Risk Assessment

1

Patient age group

2

Prior cardiac arrest or sustained VT?

3

Sudden cardiac death risk markers

Recommendation

Why
Interpretation

References

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  5. O’Mahony, C., Jichi, F., Pavlou, M., Monserrat, L., Anastasakis, A., Rapezzi, C., Biagini, E., Gimeno, J. R., Limongelli, G., McKenna, W. J., Omar, R. Z., Elliott, P. M., & Hypertrophic Cardiomyopathy Outcomes Investigators. (2014). A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy: HCM Risk-SCD. European Heart Journal, 35(30), 2010–2020. https://doi.org/10.1093/eurheartj/eht439
  6. Maron, B. J., Rowin, E. J., Casey, S. A., Link, M. S., Lesser, J. R., Chan, R. H. M., Garberich, R. F., Udelson, J. E., & Maron, M. S. (2019). Hypertrophic cardiomyopathy in adulthood associated with low cardiovascular mortality with contemporary management strategies. Journal of the American College of Cardiology, 73(16), 2061–2072. https://doi.org/10.1016/j.jacc.2019.02.009