ECG in Hypertrophy

Electrocardiography (ECG) is a cornerstone in the diagnosis and assessment of cardiac structural abnormalities, including hypertrophy and atrial enlargement. Hypertrophy refers to an increase in myocardial mass due to pressure or volume overload, while atrial enlargement reflects chamber dilation often secondary to valvular or myocardial disease. Recognizing these changes on ECG is critical, as they provide clues about underlying pathophysiology, disease severity, and guide further management.

This post provides a comprehensive overview of ECG manifestations in left ventricular hypertrophy (LVH), right ventricular hypertrophy (RVH), and atrial enlargement, including diagnostic criteria, associated patterns, clinical implications, and limitations.

1. Introduction to Cardiac Hypertrophy

1.1 Definition and Pathophysiology

Left Ventricular Hypertrophy (LVH): Increased left ventricular mass, usually due to pressure overload (e.g., systemic hypertension, aortic stenosis) or volume overload (e.g., aortic/mitral regurgitation).
Right Ventricular Hypertrophy (RVH): Increased right ventricular mass, commonly caused by pulmonary hypertension, chronic lung disease, or congenital heart defects.
Atrial Enlargement: Enlargement of left atrium (LAE) or right atrium (RAE), typically secondary to valvular disease, myocardial dysfunction, or chronic pressure/volume overload.

1.2 Clinical Importance

ECG signs often precede overt symptoms of hypertrophy.
Help in risk stratification for arrhythmias, heart failure, and sudden cardiac death.
Provide a non-invasive, cost-effective screening tool.

2. Basics of ECG in Hypertrophy

2.1 Electrical Changes in Hypertrophy

Hypertrophy alters the vector and magnitude of depolarization, producing characteristic ECG patterns:

Increased voltage: Due to greater myocardial mass.
Axis deviation: Chamber enlargement can shift the mean QRS axis.
Prolonged conduction times: Changes in PR, QRS, or P wave durations.
Repolarization abnormalities: ST-T changes often secondary to “strain” patterns.

2.2 Key Concepts

ECG is specific but not very sensitive for hypertrophy.
Diagnosis should consider clinical context, imaging (echocardiography), and risk factors.
ECG signs may be attenuated in obesity, COPD, or pericardial effusion.

3. Left Ventricular Hypertrophy (LVH)

3.1 Pathophysiology

LVH results from pressure or volume overload causing myocardial hypertrophy and remodeling:

Pressure overload: Hypertension, aortic stenosis → concentric hypertrophy.
Volume overload: Mitral/aortic regurgitation → eccentric hypertrophy.

Hypertrophied myocardium generates larger QRS amplitudes, alters ventricular depolarization vectors, and produces characteristic ST-T “strain” patterns.

3.2 ECG Features of LVH

3.2.1 Voltage Criteria

Several voltage-based criteria are used:

Sokolow-Lyon Criteria:
- S wave in V1 + R wave in V5 or V6 ≥ 35 mm.
Cornell Criteria:
- R wave in aVL + S wave in V3 > 28 mm (men), 20 mm (women).
R wave in limb leads: Tall R waves in I, aVL.
QRS axis: Usually normal to leftward.

3.2.2 Strain Pattern

ST-segment depression and T wave inversion in lateral leads (I, aVL, V5-V6).
Represents subendocardial ischemia due to hypertrophy.

3.2.3 Other Findings

Prolonged QRS duration (>100 ms) may occur in advanced LVH.
Left atrial enlargement often coexists → broad, notched P waves in lead II.

3.3 Clinical Implications

Common in hypertension, aortic stenosis, hypertrophic cardiomyopathy.
Associated with increased risk of arrhythmias, heart failure, and sudden cardiac death.
ECG diagnosis should ideally be confirmed with echocardiography or cardiac MRI.

3.4 Limitations

ECG has low sensitivity (~30–50%).
Obesity, COPD, and pericardial effusion may mask LVH.
Voltage criteria alone may overestimate hypertrophy in athletes.

4. Right Ventricular Hypertrophy (RVH)

4.1 Pathophysiology

RVH develops in response to chronic pressure overload (pulmonary hypertension, pulmonary stenosis) or volume overload (tricuspid regurgitation, atrial septal defect).

Leads to dominant rightward electrical forces, shifting the QRS axis.
May be associated with right atrial enlargement.

4.2 ECG Features of RVH

4.2.1 Axis Changes

Right axis deviation: QRS axis > +90°.

4.2.2 R Wave in V1

Tall R wave in V1 (>7 mm).
R/S ratio in V1 > 1 suggests RVH.

4.2.3 S Wave in V6

Deep S wave in V6.
R/S ratio < 1 in V6 supports RVH.

4.2.4 P Wave Abnormalities

Right atrial enlargement (RAE) often accompanies RVH:
- P pulmonale: Tall, peaked P waves in lead II (>2.5 mm).

4.2.5 Strain Pattern

ST depression and T wave inversion in right precordial leads (V1-V3).
Reflects ventricular strain due to pressure overload.

4.3 Clinical Implications

Common in pulmonary hypertension, chronic lung disease (cor pulmonale), pulmonary valve disease, congenital heart disease.
Associated with right heart failure and arrhythmias.
Early detection helps guide treatment of underlying pulmonary pathology.

4.4 Limitations

ECG may underestimate RVH in obesity or leftward QRS shift.
R wave in V1 may also appear in posterior myocardial infarction, normal variant, or young athletes.

5. Atrial Enlargement

Atrial enlargement often accompanies ventricular hypertrophy but may occur independently.

5.1 Left Atrial Enlargement (LAE)

5.1.1 ECG Features

P wave in lead II: Notched, broad (“P mitrale”), duration >120 ms.
P wave in V1: Biphasic with prominent terminal negative portion (>1 mm deep, >0.04 sec).
Often coexists with LVH (pressure overload from mitral stenosis, hypertension).

5.1.2 Clinical Significance

Increased risk of atrial fibrillation and thromboembolism.
Common in hypertension, valvular heart disease, diastolic dysfunction.

5.2 Right Atrial Enlargement (RAE)

5.2.1 ECG Features

P wave in lead II: Tall, peaked (>2.5 mm) (“P pulmonale”).
P wave in V1: Dominant initial positive component.
Often coexists with RVH (pulmonary hypertension, chronic lung disease).

5.2.2 Clinical Significance

Can lead to atrial arrhythmias.
May reflect chronic pulmonary disease or tricuspid stenosis/regurgitation.

6. Combined Hypertrophy Patterns

LVH with LAE: Often seen in chronic hypertension or aortic stenosis.
RVH with RAE: Seen in pulmonary hypertension or congenital heart disease.
ECG shows combined P wave, QRS voltage, and axis abnormalities.
Recognition requires systematic evaluation of P waves, QRS, axis, and ST-T changes.

7. ECG Diagnostic Criteria Summary

7.1 LVH

Criteria	Lead(s)	Threshold
Sokolow-Lyon	V1 + V5/V6	≥ 35 mm
Cornell	R aVL + S V3	>28 mm (men), >20 mm (women)
R wave height	aVL	>11 mm
ST-T strain	Lateral leads	ST depression, T inversion

7.2 RVH

Feature	Lead(s)	Threshold
Right axis deviation	Limb leads	> +90°
R wave	V1	>7 mm
R/S ratio	V1	>1
ST-T strain	V1-V3	ST depression, T inversion

7.3 LAE

Lead II: Notched P wave >120 ms.
V1: Terminal negative portion >0.04 sec, >1 mm deep.

7.4 RAE

Lead II: P wave >2.5 mm.
V1: Initial positive component >1.5 mm.

8. Clinical Implications of ECG Hypertrophy

Early detection: ECG can identify hypertrophy before symptomatic heart disease develops.
Arrhythmia risk: LAE and LVH increase susceptibility to atrial fibrillation and ventricular arrhythmias.
Prognostic significance: LVH is associated with increased risk of cardiovascular morbidity and mortality.
Guiding therapy: Identification of hypertrophy can prompt antihypertensive therapy, valve repair, or pulmonary disease management.

9. Limitations and Pitfalls

Sensitivity: ECG may miss mild hypertrophy.
False positives: Tall QRS in athletes, young adults, or thin individuals may mimic LVH.
Obesity and lung disease: May attenuate QRS voltage, masking hypertrophy.
Coexisting conduction abnormalities: Bundle branch blocks can complicate interpretation.
Imaging correlation: Echocardiography remains the gold standard for accurate hypertrophy assessment.

10. Step-by-Step Approach to ECG in Hypertrophy

Assess rhythm and rate (sinus vs. arrhythmia).
Analyze P waves for atrial enlargement.
Evaluate QRS voltage in precordial and limb leads.
Determine axis deviation.
Look for ST-T strain patterns.
Check for conduction delays (QRS duration).
Correlate clinically with history, risk factors, and imaging.

11. Case Examples

Case 1: LVH with LAE

65-year-old male with longstanding hypertension.
ECG: S in V1 + R in V5 = 38 mm, broad P wave in II, terminal negative P in V1.
Diagnosis: LVH with LAE.
Management: Optimize antihypertensive therapy; monitor for arrhythmias.

Case 2: RVH with RAE

55-year-old female with chronic pulmonary hypertension.
ECG: Right axis deviation + tall R in V1, P pulmonale in II.
Diagnosis: RVH with RAE.
Management: Treat underlying pulmonary disease; monitor right heart function.

Case 3: Isolated LAE

70-year-old male with mitral stenosis.
ECG: Notched P wave in II, terminal negative P in V1, normal QRS.
Diagnosis: Isolated LAE.
Management: Consider anticoagulation; monitor for atrial fibrillation.