How to Do Echo in Left Ventricular Hypertrophy: A Consensus Statement of the Italian Society of Echocardiography and Cardiovascular Imaging

Figures

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  Figure 1. Case of genetically determined obstructive hypertrophic cardiomyopathy due to a pathogenic variant in the myosin heavy chain 7 gene. Marked asymmetric left ventricular hypertrophy, predominantly involving the interventricular septum, with reverse curvature (a, e and h). The mitral valve leaflets appear elongated (a) and show systolic anterior motion, resulting in left ventricular outflow tract obstruction (b-d and f), with evident flow acceleration on color Doppler imaging (g) and significant intraventricular gradient (l). The left ventricle is hyperdynamic, with near-complete cavity obliteration during systole (d, f, and i)

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  Figure 2. Case of mid-ventricular hypertrophic cardiomyopathy with apical aneurysm. Parasternal long-axis view (a) and apical four-chamber view in diastole (b) and systole (c). Mid-ventricular flow acceleration is evident on color Doppler imaging (d). Speckle-tracking analysis demonstrates severely reduced apical longitudinal strain (e)

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  Figure 3. Case of apical hypertrophic cardiomyopathy. Two-dimensional echocardiography in the parasternal long-axis view (a) and apical four-chamber view (b) demonstrates marked hypertrophy of the apical segments. Color-Doppler imaging shows mid-ventricular flow acceleration (c). Speckle-tracking analysis reveals severely reduced longitudinal strain in the apical segments (d). Cardiac magnetic resonance cine steady-state free precession images in the horizontal long-axis (e) and vertical long-axis planes (f) confirm severe apical hypertrophy. (g) Late gadolinium enhancement is present within the hypertrophied apical segments

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  Flowchart 1. Echocardiographic assessment of hypertrophic cardiomyopathy. CW = Continuous wave, EF = Ejection fraction, FAC = Fractional area change, GLS = Global longitudinal strain, IVC = Inferior vena cava, LA = Left atrial, LV = Left ventricle, LVEF = Left ventricular ejection fraction, LVOT = Left ventricular outflow tract, LVOTO = Left ventricular outflow tract obstruction, PLAX = Parasternal long axis, PSAX = Parasternal short axis, PW = Pulsed wave, RV = Right ventricular, SAM = Systolic anterior motion, sPAP = Systolic pulmonary artery pressure, TAPSE = Tricuspid annular plane systolic excursion, TR = Tricuspid regurgitation

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  Flowchart 2. Simplified echocardiographic protocol for patients treated with cardiac myosin inhibitors. CMI = Cardiac myosin inhibitor, ECHO = Echocardiography, HCM = Hypertrophic cardiomyopathy, LVEF = Left ventricular ejection fraction, LVOT = Left ventricular outflow tract, LVOTO = Left ventricular outflow tract obstruction, NYHA = New York Heart Association

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  Figure 4. Cardiac amyloidosis due to a pathogenic variant in the transthyretin gene. Marked concentric left ventricular hypertrophy, right ventricular hypertrophy, thickening of the valvular apparatus, and interatrial septum are evident (a-c). Transmitral Doppler flow pattern (d) and tissue Doppler imaging (e) findings are consistent with diastolic dysfunction. The reduction of s’, e’, and a’ velocities (e), typically < 5 cm/s, is a characteristic finding in cardiac amyloidosis. Speckle-tracking analysis demonstrates reduced longitudinal strain in basal and mid-ventricular segments with relative apical sparing (f). (g) Postcontrast cardiac magnetic resonance imaging shows the characteristic pattern of difficult myocardial nulling, diffuse subendocardial late gadolinium enhancement, and early darkening of the blood pool. (h) T1 mapping reveals diffusely increased myocardial T1 relaxation times. (i) Bone tracer scintigraphy demonstrates significant cardiac uptake

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  Figure 5. Concentric left ventricular hypertrophy in Anderson–Fabry disease (a and b). In the parasternal short-axis view (b), an intramyocardial hyperechogenicity of the posterior wall is evident. Speckle-tracking analysis shows a characteristic reduction in longitudinal strain in the left ventricular posterior wall (c). Cardiac magnetic resonance imaging demonstrates the characteristic intramyocardial late gadolinium enhancement in the posterior wall (d). T1 mapping analysis shows diffusely reduced native T1 relaxation times, with relatively increased values in the posterior segment corresponding to the area of late gadolinium enhancement (e)

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  Figure 6. Left ventricular hypertrophy in Noonan syndrome. (a-d) Severe left ventricular hypertrophy with marked hypertrophy of the papillary muscles. (e and f) Findings consistent with diastolic dysfunction and elevated filling pressure. (g) Presence of a mid-cavitary intraventricular gradient