Left Ventricular Hypertrophy on ECG: ECG Diagnosis Explained

Secondary repolarization abnormalities consist of downsloping ST segment depression followed by T-wave inversion, most commonly seen in leads over the hypertrophied ventricle. These were formerly called 'strain patterns' but this term is no longer recommended as the underlying mechanism is more complex than simply an overworked ventricle. Other causes include bundle branch blocks and preexcitation syndromes.

Strain patterns on EKG are ST-T wave abnormalities caused by abnormal ventricular repolarization; RVH with strain is diagnosed using the acronym STRAIN (ST concave downward, R:S ratio >1 in V1, check for biphasic T waves or S1Q3T3 pattern, and inverted T waves), while LVH with strain is diagnosed using the same acronym but looking for ST depression in lateral leads (V4-V6) with ST elevation in right leads (V1-V3), all left precordials depressed, and inverted T waves in laterals; however, ST elevation alone cannot definitively diagnose strain versus STEMI without clinical correlation.

Left ventricular overload produces secondary repolarization changes including ST segment depression and T wave inversion in lateral precordial leads (V5, V6). This occurs because hypertrophied muscle has relatively less coronary blood supply, creating an ischemia-like pattern. These changes are secondary to overload and should not be interpreted as primary ischemia. The pattern of ST depression and T inversion in V5-V6 is called the 'strain pattern' or 'estrem pattern' when in left precordial leads. This pattern indicates left ventricular overload.

Secondary repolarization abnormalities, termed strain patterns, occur when ventricular hypertrophy impairs normal repolarization, causing ST segment depression and T wave inversions. In LVH, strain pattern appears in lateral leads (V5-V6, aVL) as T wave inversion and ST depression. In RVH, strain pattern appears in right precordial leads (V1-V3) and inferior leads (II, III, aVF). These changes result from delayed and abnormal repolarization in the hypertrophied myocardium. While ECG provides initial screening, echocardiography is essential for confirmation—measuring wall thickness and calculating mass index to differentiate pathological hypertrophy from physiological adaptations like athlete's heart. The key distinction: LVH exaggerates normal R wave progression; RVH reverses it.

Left ventricular hypertrophy (LVH) with strain pattern is characterized by high voltage QRS complexes in left-sided leads (V5, V6, I, aVL) with specific repolarization abnormalities. The Sokolow-Lyon criteria (S in V1 + R in V5 or V6 > 35 mm) or Cornell criteria (R in aVL + S in V3 > 28 mm in men, > 20 mm in women) can be used for diagnosis. The strain pattern shows ST-segment depression and T-wave inversion in lateral leads (I, aVL, V5, V6), representing subendocardial ischemia from increased wall stress. This pattern is distinct from acute ischemia and indicates chronic pressure overload of the left ventricle.

Wide QRS patterns resembling bundle branch blocks may not always indicate true BBB. Pacemaker rhythms can mimic BBB: right ventricular pacing mimics LBBB by activating ventricles from the RV apex, while left ventricular pacing resembles RBBB by activating from back to front toward V1. Left ventricular hypertrophy (LVH) can mimic LBBB with prolonged QRS, increased voltage, and T-wave discordance, but is distinguished by prolonged intrinsicoid deflection (>60ms) in V5-V6. Ventricular pre-excitation (Wolff-Parkinson-White syndrome) creates BBB-like patterns: left ventricular pre-excitation produces positive R wave in V1, while right ventricular pre-excitation creates deep S waves in V1, with short PR interval and Delta wave as clues. Ventricular arrhythmias at slower rates can also resemble BBB. The left bundle system subdivides into anterior and posterior fascicles, while the right bundle is a single pathway. Fascicular blocks shift QRS axis without widening: Left Anterior Fascicular Block (LAFB) causes left axis deviation (-45° or more), while Left Posterior Fascicular Block (LPFB) causes right axis deviation (+120° or more). Bifascicular block indicates blockage of any two fascicles.

Left Ventricular Hypertrophy (LVH) is diagnosed using the Sokolow-Lyon criteria: sum of S wave in V1 plus R wave in V5/V6 exceeding 35 mm, or R wave in aVL exceeding 11 mm. Left Bundle Branch Block (LBBB) is identified by a broad QRS complex (>120ms) with a W pattern in V1 and M pattern in V6, along with broad QRS complexes in leads I and aVL. These conditions can coexist and should be evaluated together for comprehensive cardiac assessment.

Left ventricular hypertrophy (LVH) in young athletes may be a physiological response to intense training (athlete's heart). If there are no other risk factors (hypertension, rhythm disturbances), this may not require intervention. However, ongoing cardiology monitoring is recommended.

Complete left bundle branch block (LBBB) is always abnormal in athletes, defined by QRS >120ms, dominant S in V1, and broad R waves in lateral leads. LBBB is rare in athletes (<1/1000) but common in cardiomyopathies (31% of dilated cardiomyopathy patients). LBBB predicts mortality and requires full diagnostic workup. Ventricular pre-excitation (WPW) shows short PR <120ms and delta wave, the second most common ECG finding in athletes. Despite being common (2 found in 100 screened), it carries sudden cardiac death risk and requires EP study regardless of symptoms.

This section covers conduction abnormalities and special syndromes. Left bundle branch block (LBBB) shows wide QRS complexes (>0.12 seconds) with characteristic morphology. The Sgarbossa criteria identify acute MI in LBBB: concordant ST elevation >1 mm, concordant ST depression >1 mm, or discordant ST elevation >5 mm. Wolff-Parkinson-White (WPW) syndrome shows delta wave (slurred QRS upstroke) and short PR interval (<0.12 seconds), representing early ventricular activation through an accessory pathway. WPW can lead to reentrant tachycardias and ventricular fibrillation. Treatment involves ablation of the accessory pathway. Left ventricular hypertrophy (LVH) is diagnosed using Cornell criteria: R in aVL + S in V3 >28 mm in men, >20 mm in women.

When LVH criteria are positive: (1) Consider clinical context (hypertension, aortic stenosis, etc.); (2) Use echocardiography for confirmation; (3) Consider serial EKGs to track changes; (4) Differentiate LVH from ischemia (LVH strain shows asymmetric ST depression, ischemia shows symmetric patterns). The key is to use EKG criteria as screening tools, not definitive diagnoses, and always correlate with clinical findings.

Beyond hypertension, multiple conditions cause LVH: aortic stenosis (narrowed valve increases cardiac workload), amyloidosis/Fabry disease (abnormal protein deposition in heart muscle), kidney dysfunction (fluid retention and pressure elevation), and hypertrophic cardiomyopathy (genetic inheritance causing abnormal wall thickening). When LVH is diagnosed, clinicians must systematically investigate underlying causes through 24-hour blood pressure monitoring, echocardiography for valvular assessment, kidney function tests, and family history evaluation. Identifying the root cause is critical because treating the underlying condition can reverse LVH and prevent progression to serious complications.

Left Ventricular Hypertrophy (LVH) is defined as an increase in left ventricular mass due to increased wall thickness, cavity size, or both, primarily caused by chronic pressure or volume overload from conditions like hypertension, aortic stenosis, or valvular diseases; it presents with characteristic ECG findings including increased QRS voltage, prolonged QRS duration, left axis deviation, and ST-T wave changes, though echocardiography remains the gold standard for diagnosis and quantification; management focuses on treating the underlying cause rather than LVH itself, as untreated LVH can progress to heart failure, ischemia, and arrhythmias.

Echocardiography evaluates LVH by measuring interventricular septum and posterior wall thickness with end-diastolic diameter to calculate left ventricular mass. Eccentric hypertrophy shows increased wall thickness with normal chamber dimensions, while concentric hypertrophy shows increased wall thickness with normal wall-to-radius ratio. ECG can identify LVH changes over time, which is important given the high prevalence of hypertension makes annual echocardiography unsustainable. Patients whose LV mass regresses have significantly better prognosis than those with persistent LVH. The LIFE study showed losartan 100 mg reduced primary composite endpoint, particularly stroke, with benefit anticipated within the first year by LVH regression. Meta-analyses show ACE inhibitors, ARBs, and calcium channel blockers determine greater blood pressure reduction and LVH regression. ECG findings include left axis deviation, left anterior fascicular block, intraventricular conduction abnormalities, and arrhythmias like ventricular extrasystoles causing ECG artifacts.

Two instrumental methods diagnose LVH: ECG and echocardiography. ECG has low sensitivity (5-50%) but high specificity (85-95%), while echocardiography achieves 85-100% sensitivity and is the gold standard. Three ECG criteria exist: (1) Sokolow-Lyon index (S in V1 + R in V5/V6 > 35 mm); (2) R wave in aVL > 11 mm; (3) Cornell product (S in V3 + R in aVL × QRS duration > 28 mm for men, > 20 mm for women, or > 2400 mm·ms). Echocardiography directly measures wall thickness and calculates left ventricular mass index (LVMI), with thresholds of 95 g/m² for women and 115 g/m² for men when indexed to body surface area.