LVH 12-Lead ECG Findings: Key Criteria and Clinical Clues

Left ventricular hypertrophy (LVH) is a structural heart change detectable on a 12-lead ECG. Identifying LVH is crucial as it may signal underlying conditions such as hypertension or cardiomyopathy and has prognostic implications for cardiovascular outcomes.

Recognizing LVH requires more than assessing voltage criteria; additional ECG patterns provide key diagnostic insights. Understanding these findings helps differentiate primary LVH from secondary causes, improving clinical decision-making.

Voltage-Based Criteria on the 12-Lead

Interpreting LVH on a 12-lead ECG often begins with voltage-based criteria, which assess QRS complex amplitude in specific leads. Increased left ventricular mass generates stronger electrical forces, resulting in taller R waves in left-sided leads and deeper S waves in right-sided leads. Several well-established criteria quantify these voltage changes, with the Sokolow-Lyon and Cornell voltage criteria being the most widely used.

The Sokolow-Lyon criteria define LVH when the sum of the S wave in lead V1 and the R wave in lead V5 or V6 exceeds 35 mm. While straightforward, its sensitivity varies, especially in obese individuals or those with chronic lung disease, where chest wall impedance can reduce QRS voltages. The Cornell voltage criteria, which sum the R wave in aVL and the S wave in V3, use thresholds of >28 mm in men and >20 mm in women. This method has demonstrated better diagnostic accuracy in some populations, particularly when combined with other ECG findings.

The Romhilt-Estes scoring system incorporates voltage thresholds alongside other ECG features to improve specificity. A score of five or more points suggests LVH, with voltage criteria contributing up to three points. Combining multiple criteria enhances sensitivity while maintaining specificity, making it a preferred approach in comprehensive ECG interpretation.

Non-Voltage Clues in 12-Lead ECG Findings

While voltage criteria are central to diagnosing LVH, additional ECG features provide further insight, particularly when voltage abnormalities are borderline or absent. These non-voltage clues reflect how increased left ventricular mass affects electrical conduction, repolarization, and overall cardiac function.

Left axis deviation is a key indicator, occurring when an enlarged left ventricle alters the heart’s electrical vector. This shift, often seen with QRS axis values between -30° and -90°, is more pronounced in patients with conduction abnormalities such as left anterior fascicular block. A widened QRS complex may indicate intraventricular conduction delay due to myocardial hypertrophy, particularly in the absence of bundle branch block.

Repolarization abnormalities also serve as important markers. The strain pattern, characterized by ST-segment depression and asymmetric T-wave inversion in lateral leads (I, aVL, V5, and V6), is strongly associated with LVH and has prognostic significance. This pattern results from subendocardial ischemia and altered repolarization in hypertrophied myocardium. Unlike ischemic ST-T changes, which are more symmetric and diffuse, the LVH strain pattern typically shows a gradual downsloping ST-segment followed by a deep, asymmetric T-wave inversion. These changes are common in patients with longstanding hypertension, where chronic pressure overload exacerbates myocardial remodeling.

Another important clue is increased P-wave duration and amplitude, particularly in lead II and V1, indicating left atrial enlargement due to diastolic dysfunction. As the left ventricle thickens, impaired relaxation raises left atrial pressure, seen on ECG as a broad, notched P-wave in lead II and a biphasic P-wave in V1 with a prominent negative terminal component. These atrial changes reinforce the diagnosis of LVH, especially in patients with hypertension or aortic stenosis.

Distinguishing Primary LVH From Secondary Causes

LVH can result from various conditions, making it essential to distinguish intrinsic myocardial remodeling from secondary systemic or structural abnormalities. Primary LVH typically stems from genetic or idiopathic factors, where hypertrophy develops independently of external stressors. Hypertrophic cardiomyopathy (HCM) exemplifies this, with asymmetric septal thickening and myocyte disarray increasing the risk of arrhythmias and sudden cardiac events. Unlike secondary LVH, HCM often presents with normal or reduced afterload, meaning hypertrophy is not a compensatory response but rather a result of intrinsic myocardial pathology.

Secondary LVH arises from prolonged hemodynamic stress, with hypertension being the most common cause. Chronic pressure overload forces the left ventricle to generate greater contractile force, leading to concentric hypertrophy as an adaptive mechanism. Over time, this structural change can progress to diastolic dysfunction and heart failure with preserved ejection fraction (HFpEF). Aortic stenosis follows a similar pathophysiology, where outflow obstruction increases ventricular workload, driving hypertrophic remodeling. In these cases, the degree of hypertrophy often correlates with disease severity, and regression can occur with effective blood pressure control or valve replacement.

Systemic conditions such as chronic kidney disease (CKD) and obesity also contribute to LVH through mechanisms beyond direct pressure overload. In CKD, elevated circulating uremic toxins and volume overload promote myocardial fibrosis and hypertrophy, even in patients without overt hypertension. Obesity-related LVH results from increased cardiac output, neurohormonal activation, and metabolic changes that drive ventricular thickening. These cases highlight the complex interplay between systemic pathology and myocardial adaptation, underscoring the need for thorough clinical evaluation to determine the underlying cause of hypertrophy.