Echocardiography and obstructive hypertrophic cardiomyopathy (oHCM)
Echocardiograms (ECHOs) play a critical role in diagnosing and evaluating cardiomyopathies, including obstructive hypertrophic cardiomyopathy (oHCM), providing valuable insights into disease progression and prognosis.1,2 Additionally, echocardiography aids in risk stratification for HCM patients, assessing the likelihood of sudden cardiac death (SCD), heart failure, atrial fibrillation, and stroke.3
Echocardiograms are important in the initial diagnosis of hypertrophic cardiomyopathies (HCM) and are used alongside personal and family history, physical examination, electrocardiography (ECG), cardiac imaging, and first-line laboratory tests.4
An ECHO can also help differentiate between different forms of HCMs, including obstructive (oHCM), non-obstructive, and apical.5,6 Differentiating between different forms of HCM is important as it helps guide clinicians toward the most appropriate selection of treatment or interventions.5
Echocardiography is considered the first-line imaging modality for identifying left ventricular hypertrophy (LVH) and assessing left ventricular outflow tract (LVOT) obstruction.3
Subsequently, echocardiograms are essential for HCM diagnoses in measuring left ventricular wall thickness. HCM is defined by a left ventricular (LV) wall thickness ≥15 mm in at least one myocardial segment that is not explained solely by loading conditions.4,7
≥15 mm
left ventricular (LV) wall thickness in at least one myocardial segment is defined as hypertrophic
cardiomyopathy (HCM)4,7
Echocardiography can define oHCM by measuring the LVOT gradient, an integral component of the HCM disease phenotype, playing a major role in symptomatology and progression to heart failure.8
The LVOT gradient groups specific to the obstructive forms of HCM are:7
Echocardiograms can also detect systolic anterior motion (SAM) of the mitral valve.2 SAM of the mitral valve is a characteristic finding in oHCM and is defined by a sudden forward displacement of the mitral valve, which occurs prior to the point when the posterior wall reaches its maximum movement.2 The severity of SAM positively correlates with the extent of obstruction in oHCM.2
As well as the assessment of LVH, LVOTO, and SAM, echocardiography can accurately assess systolic and diastolic function.8 A systematic study of cardiac structure and function is fundamental when evaluating patients with suspected oHCM.8
A summary of the key imaging features to assess, and their primary imaging modality, in patients with suspected or confirmed HCM:4,8,9
Complementary use of an ECHO with cardiovascular magnetic resonance (CMR) can be used in oHCM evaluation.10 This is common in cases where echocardiography is inconclusive or where additional information regarding the magnitude and distribution of hypertrophy or anatomy of the mitral valve apparatus is required.10
LVOT gradient can impact available treatments for patients with oHCM. A marked LVOT gradient of ≥50 mm Hg (either at rest or after provocation) is the threshold for considering advanced pharmacological or invasive therapies if symptoms are refractory to standard management.11
≥ 50 mm
Hg LVOT gradient
Beyond its immediate implications for intervention, LVOTO as an ECHO parameter can reveal prognostic implications, such as playing a role in identifying an increased risk of heart failure progression, SCD, and stroke.3 By incorporating LVOT gradient measurement into the clinical decision-making process, clinicians can more accurately identify high-risk patients, optimise timing for intervention, and tailor long-term treatment strategies for improved patient outcomes.3
ECHO permits non-invasive quantification of LVEF. A normal LVEF typically ranges between 52-72% in males, and 54-74% in females, with values below this range indicating systolic dysfunction and reduced cardiac pumping ability.12 The presence of systolic dysfunction (e.g. LVEF <50%) in HCM has been linked to a worse prognosis, with reported mortality as high as 11% per year.9
In HCM, LVEF has emerged as a significant prognostic indicator, with LVEF <50% labelled as a predictor of SCD by AHA/ACC guidelines.13 While HCM is generally characterised by normal or hyperdynamic systolic function, a subset of patients (~4-9%) experience progressive disease leading to reduced LVEF (<50%).9,13 Those with HCM who have a low-normal and reduced LVEF have been shown to have a higher risk of hospitalisation for heart failure and an increased risk of cardiovascular death.13
Patients with oHCM should have their LVEF assessed by echocardiography before initiating treatment.14 Pharmacological therapies aimed at reducing outflow tract obstruction and alleviating symptoms should not be initiated if LVEF is below 55%, including CAMZYOS (mavacamten).14 Accurate LVEF assessment during CAMZYOS treatment surveillance is crucial, since suboptimal endocaridal border definition can lead to errors in LVEF estimation and influence treatment decisions.15 The BSE therefore recommend that contrast echocardiography should be used when two or more segments cannot be visualised.15
ACC, American College of Cardiology; AHA, American Heart Association; BSE, British Society of Echocardiography; CMR, cardiovascular magnetic resonance; ECHO, echocardiogram; HCM, hypertrophic cardiomyopathy; LVEF, left ventricular ejection fraction; LVOT, left ventricular outflow tract; LVOTO, left ventricular outflow tract obstruction; oHCM, obstructive hypertrophic cardiomyopathy; SAM, systolic anterior motion; SCD, sudden cardiac death.
3500-GB-2500258 | December 2025
