HOCM is one of the most common inheritable diseases and is the most common cause of sudden-cardiac death in young athletes. It is a heterogenous disease affecting the myocardium, with autosomal dominant inheritance and variable penetrance. The degree and location of ventricular hypertrophy is variable, though most commonly causes asymmetric septal hypertrophy, which can produce dynamic left ventricular outflow tract (LVOT) obstruction. However, LVOT obstruction only occurs in ~25% of cases. In addition to possible outflow tract obstruction, it can also cause diastolic dysfunction and chaotic cellular array, predisposing to both microvascular ischemia and arrhythmias.
EKG findings are consistent with increased precordial voltages and nonspecific repolarization abnormalities (ST/T changes). Essentially, it produces findings consistent with LVH. This can eventually also lead to left atrial enlargement. Patients with asymmetric septal hypertrophy have deep, dagger-like Q waves in the lateral and inferior leads. These Q waves are not those of ischemia, which are wide (>40ms). Additionally, patients may have a tall, needle-like R wave in V1 (usually LVH alone will not produce larger R waves in the right precordial leads) or a deep S wave in V6.
There is a subset called apical hypertrophic cardiomyopathy, with localized hypertrophy of the apex. This is most commonly seen in those of Japanese descent. The classic EKG finding is giant T wave inversion in the precordial leads.
There is also some overlap between HCM and WPW as some patients have findings of both. EKG findings may be consistent with WPW as well. Additionally, these patients are prone to arrhythmias (SVT, PAC, PVC, atrial fibrillation, VT).
One thing that this is important to differentiate from is benign T wave inversion from early repolarization that is commonly seen in young, African American athletes. These patients have short QT intervals due to early repolarization, though commonly have large voltage R waves and T wave inversions or nonspecific ST/T changes. Additionally, these patients commonly have J-waves.
Early repolarization with large voltage QRS complexes and T wave changes in V4-V6. This EKG also clearly shows J-waves and discordant ST elevation in V2-V3. Furthermore, the QTc is short.
Examples: