ECG Case 124

Patients with HCM can have a normal ECG

Echocardiography is more sensitive than the ECG in diagnosing HCM, and around 5% of patients with echocardiographic evidence of HCM will have a normal ECG. These patients generally have a less severe phenotypic expression of disease, but early diagnosis is important to ensure close monitoring and prevention of complications. Patients with a normal ECG but clinical and echocardiography features concerning for HCM should undergo further investigation with cardiac MRI.

HCM presents with a wide spectrum of disease

Formerly known as hypertrophic obstructive cardiomyopathy, the majority (75%) of HCM cases are mild and are not associated with LVOT obstruction. Patients with HCM present with a broad spectrum of disease and symptomatology — they may remain asymptomatic until diagnosis or sudden cardiac death, or present with progressive symptoms of exertional chest pain or shortness of breath. Exertional syncope is the most concerning symptom and suggests dynamic left ventricular outflow tract (LVOT) obstruction +/- ventricular dysrhythmia.

The clinical diagnosis of HCM is based on the presence of left ventricular hypertrophy (LVH), typically defined by an end-diastolic ventricular septal thickness ≥ 13mm in adults, occurring in the absence of any inciting stimulus such as hypertension or aortic stenosis. The most commonly observed pattern is asymmetrical thickening of the interventricular septum. However, the degree and distribution of hypertrophy is variable, ranging from mild hypertrophy (13-15mm) to extreme myocardial thickening (30-60mm).

Adolescents and adults that are competitive athletes may demonstrate significant physiological left ventricular hypertrophy (≥ 13mm) which can mimic HCM. In these patients, an enlarged LV cavity, and symmetrical LV hypertrophy, favours a physiological cause of changes seen. Cardiac MRI is required to definitively differentiate between the two causes.

Q waves: differentiating HCM versus MI

Deep Q waves seen in HCM are the result of depolarisation through a hypertrophied septum. Although thickened, conduction through this tissue is normal. This produces deep, narrow Q waves with a different morphology to those of myocardial infarction:

• Infarction Q waves are typically > 40 ms duration
• Septal Q waves in HCM are < 40 ms

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