Differentiating ECG Findings in HOCM vs. Cerebral T Waves
The most reliable way to differentiate HOCM from cerebral T waves on ECG is through the presence of LVH voltage criteria with non-voltage abnormalities in HOCM versus diffuse, symmetric, deeply inverted T waves without LVH in cerebral T waves.
Key ECG Characteristics
HOCM ECG Findings
- LVH with non-voltage criteria 1
- Increased QRS voltage (Sokolow-Lyon or Cornell criteria)
- Left atrial enlargement
- Left axis deviation
- Delayed intrinsicoid deflection
- Pathological Q waves (particularly in inferolateral leads)
- ST-segment depression and T-wave inversions (typically in lateral leads)
- Abnormal septal depolarization
Cerebral T Waves (Neurogenic) ECG Findings
- Diffuse, deeply inverted, symmetric T waves
- QT interval prolongation
- No significant LVH voltage criteria
- Normal QRS morphology
- Absence of pathological Q waves
- T waves typically more pronounced in precordial leads
- Often associated with subarachnoid hemorrhage or other acute neurological events
Diagnostic Algorithm
Initial ECG Assessment:
- Evaluate for LVH voltage criteria (Sokolow-Lyon or Cornell)
- Look for non-voltage criteria (pathological Q waves, left atrial enlargement)
- Assess T wave morphology (symmetric vs. asymmetric)
- Examine QT interval
Additional Testing:
For suspected HOCM:
For suspected cerebral T waves:
- Urgent neurological evaluation
- Brain imaging (CT/MRI)
- Assessment for symptoms of increased intracranial pressure
- Serial ECGs to monitor evolution of changes
Management Approach
HOCM Management
Medical therapy for symptomatic patients with LVOT gradients ≥50 mmHg 3:
- Non-vasodilating beta-blockers (first-line)
- Non-dihydropyridine calcium channel blockers (verapamil)
- Disopyramide for refractory symptoms
- Mavacamten (myosin inhibitor) for patients with inadequate response to standard therapy
Septal reduction therapy for drug-refractory symptoms:
- Surgical myectomy
- Alcohol septal ablation (alternative in high surgical risk patients) 4
ICD placement for high-risk patients:
- History of cardiac arrest or sustained VT
- Family history of SCD
- Unexplained syncope
- Multiple risk factors including NSVT on ambulatory monitoring 2
Cerebral T Wave Management
Urgent neurological evaluation and treatment of underlying cause:
- Management of increased intracranial pressure
- Treatment of underlying neurological condition (subarachnoid hemorrhage, stroke, trauma)
Cardiac monitoring to detect arrhythmias
- Continuous telemetry during acute phase
- Serial ECGs to monitor resolution of T wave changes
Important Clinical Pearls
- HOCM ECG findings are typically chronic and stable, while cerebral T waves often evolve rapidly
- The presence of a systolic murmur that increases with Valsalva maneuver strongly suggests HOCM 1
- Cerebral T waves may normalize as the neurological condition improves
- In HOCM, the ECG is abnormal in approximately 94% of patients 1
- The combination of ECG and echocardiography has high sensitivity for HOCM diagnosis 1
- NSVT on ambulatory monitoring is a risk factor for SCD in HOCM patients 2
Common Pitfalls to Avoid
- Misinterpreting athletic heart changes as HOCM (athletes may have LVH voltage criteria but typically lack non-voltage abnormalities) 1
- Failing to recognize that both conditions can coexist (patient with HOCM can develop cerebral T waves from a neurological event)
- Overlooking other causes of T wave inversions (myocardial ischemia, pulmonary embolism, cardiomyopathies)
- Relying solely on ECG for definitive diagnosis (both conditions require additional testing)
- Underestimating the importance of serial ECGs in differentiating the two conditions
By systematically evaluating ECG findings and correlating with clinical presentation and imaging studies, clinicians can effectively differentiate between HOCM and cerebral T waves to guide appropriate management strategies.