European Journal of Cardiovascular Medicine

Left ventricular hypertrophy (LVH) represents a pathological adaptation of the heart characterized by increased left ventricular mass and wall thickness in response to various hemodynamic stresses[1]. This condition is recognized as a significant independent predictor of cardiovascular morbidity and mortality, with studies demonstrating a three-fold increase in mortality risk among patients with LVH compared to those without[2]. The global prevalence of LVH is estimated to be 10-20% in the adult population, with significantly higher rates observed in individuals with hypertension, where approximately 40% of patients demonstrate evidence of left ventricular hypertrophy[3].

The clinical significance of LVH extends beyond its structural manifestations, as it serves as a marker of subclinical cardiovascular disease and represents an important intermediate phenotype between risk factors and adverse outcomes[4]. Various epidemiological studies have consistently shown that LVH increases the risk of cardiovascular events, including coronary heart disease, heart failure, stroke, and sudden cardiac death[5]. Furthermore, the presence of LVH has been associated with a hazard ratio of 1.79 for all-cause mortality, with this association remaining significant even after multivariate adjustment for confounding factors[6].

The pathophysiology of LVH involves complex cellular and molecular mechanisms that result in myocyte hypertrophy, increased myocardial fibrosis, and altered ventricular geometry[7]. The most common etiologies include systemic hypertension, aortic stenosis, hypertrophic cardiomyopathy, and volume overload conditions such as aortic regurgitation[8]. The hypertrophic response can manifest as either concentric hypertrophy, characterized by increased wall thickness with normal or reduced cavity size, or eccentric hypertrophy, where both wall thickness and cavity dimensions are increased[9].

Accurate diagnosis of LVH is essential for appropriate clinical management and risk stratification. The electrocardiogram (ECG) has been the traditional screening tool for LVH detection due to its wide availability, low cost, and ease of interpretation[10]. Over the past several decades, numerous ECG criteria have been developed to identify LVH, including the Sokolow-Lyon criteria, Cornell voltage criteria, Romhilt-Estes scoring system, and the more recently proposed Peguero-Lo Presti criteria[11]. However, ECG-based diagnosis of LVH has significant limitations, with reported sensitivities ranging from 6.9% to 67% and specificities from 75% to 98.8%[12].

The Cornell voltage criteria, which utilize the sum of R wave in aVL and S wave in V3 (>28 mm in men and >20 mm in women), demonstrate a sensitivity of 22% and specificity of 95%[13]. The Sokolow-Lyon criteria, defined as the sum of S wave in V1 and R wave in V5 or V6 exceeding 35 mm, show similarly low sensitivity (20%) despite high specificity (>85%)[14]. The Romhilt-Estes scoring system, which incorporates voltage criteria, ST-T changes, left atrial abnormalities, and axis deviation, provides the highest sensitivity (60%) among traditional ECG criteria but requires complex calculation[15].

Two-dimensional echocardiography has emerged as the gold standard for LVH assessment, offering superior diagnostic performance compared to ECG with the ability to directly visualize myocardial structures and measure left ventricular mass[16]. Echocardiographic diagnosis of LVH is based on left ventricular mass index (LVMI) calculations, with established cutoff values of ≥115 g/m² for men and ≥95 g/m² for women[17]. The technique allows for assessment of ventricular geometry, wall thickness measurements, and functional parameters, providing comprehensive evaluation of cardiac structure and function[18].

Studies comparing echocardiography to ECG have consistently demonstrated the superior sensitivity of echocardiographic assessment, with echocardiography detecting LVH in 78% of patients compared to ECG's detection rate of 48% using wall thickness criteria[19]. Furthermore, echocardiographic LVH assessment has shown better correlation with cardiovascular outcomes and provides prognostic information beyond traditional risk factors[20]. The American Society of Echocardiography recommends the use of linear measurements from M-mode or two-dimensional guided measurements for LVM calculation using the formula: LVM = 0.8 × 1.04 × ([LVEDD + IVST + PWT]³ - LVEDD³) + 0.6 g[21].

Despite the superiority of echocardiography, ECG remains an important screening tool, particularly in resource-limited settings where echocardiography may not be readily available[22]. Recent advances in artificial intelligence and machine learning have shown promise in improving ECG-based LVH detection, with some studies reporting improved sensitivity up to 96.1% while maintaining high specificity[23]. Additionally, the development of new ECG criteria, such as the Peguero-Lo Presti criteria, has demonstrated improved sensitivity (62%) compared to traditional voltage criteria[24].

The integration of both ECG and echocardiographic assessment provides a comprehensive approach to LVH evaluation, allowing for initial screening with ECG followed by confirmatory echocardiographic assessment when indicated[25]. This combined approach is particularly valuable in clinical practice, where ECG abnormalities may prompt further evaluation with echocardiography, leading to more accurate diagnosis and appropriate therapeutic interventions[26]. Moreover, the combination of both modalities may provide complementary information about electrical and structural remodeling in patients with LVH[27].

Understanding the comparative diagnostic performance of ECG and 2D echocardiography in LVH detection is crucial for optimizing clinical practice and improving patient outcomes. This study aims to evaluate the diagnostic accuracy of various ECG criteria in detecting left ventricular hypertrophy using 2D echocardiography as the reference standard, thereby providing insights into the optimal utilization of these complementary diagnostic modalities in clinical practice.

Source of Data:

The study was conducted on patients diagnosed with Left Ventricular Hypertrophy (LVH) who attended the Department of General Medicine at Sri Aurobindo Medical College & PG Institute, Indore, Madhya Pradesh, during the period from June 2023 to November 2024. The study population consisted of individuals who had been identified with LVH on 2D Echocardiography (ECHO). The total sample size for the study was 382 patients, selected using a simple random sampling method.

Before the commencement of the study, ethical approval was obtained from the Institutional Ethical Committee, and informed consent was taken from all participants.

Study Design:

This was a cross-sectional analytical study conducted to evaluate the electrocardiographic (ECG) and echocardiographic (ECHO) findings in patients with Left Ventricular Hypertrophy (LVH) and to determine the relationship between these two diagnostic methods.

Inclusion Criteria:

• Adults aged >18 years.
• Chronic hypertensive patients.
• Adults undergoing both ECG and 2D ECHO who are found to have LVH.
• Patients who gave informed consent to participate in the study.

Exclusion Criteria:

• Patients with poor ECHO windows that prevented accurate echocardiography.
• Patients with congenital left ventricular hypertrophy.
• Patients with pericardial effusion.
• Patients who did not provide informed consent.

Sample Size Calculation:

The sample size was determined using the formula:

N=Zα/22P(1−P)d2N = \frac{Z_{\alpha/2}^2 P(1-P)}{d^2}

Where:

• Zα/2=1.96Z_{\alpha/2} = 1.96 (the standard normal value for a 95% confidence interval),
• P=0.54P = 0.54 (prevalence of LVH based on ECHO findings),
• d=0.05d = 0.05 (absolute error, or the margin of error).

The calculated sample size was approximately 382.

MATERIALS

1. Electrocardiography (ECG):
• A 12-lead electrocardiograph (ECG) was performed on each patient after a supine resting period of at least 20 minutes.
• The ECG findings were evaluated using the Sokolow Lyon index and the Talbot criteria:
• Sokolow Lyon index: LVH is diagnosed when the sum of the amplitude of the S wave in lead V1 and the amplitude of the R wave in lead V5 or V6 exceeds 35 mm.
• Talbot Criteria: LVH is suggested if the R wave amplitude in lead aVL is equal to or greater than 11 mm, or if the R wave in aVL is equal to or greater than 13 mm with left axis deviation.
2. Echocardiography (ECHO):
• All echocardiograms were performed using the PHILIPS iE33 echocardiographic machine.
• Echocardiographic examinations were carried out by trained and certified technicians, with a focus on obtaining the parasternal long-axis view.
• Left Ventricular Hypertrophy (LVH) was diagnosed based on the measurement of the interventricular septal thickness (IVST), with a value of ≥ 11 mm being indicative of LVH.

Data Collection:

• ECG Data: The ECG results were recorded for each patient and transcribed directly into the study’s proforma.
• ECHO Data: The ECHO findings were recorded in the same proforma, and the interventricular septal thickness (IVST) was documented for each patient.

METHODOLOGY:

1. ECG Procedure:
• A 12-lead ECG was performed for each participant after a 20-minute rest period in the supine position.
• ECG findings were evaluated using the Sokolow Lyon index and Talbot criteria, and the presence of LVH was recorded.
2. ECHO Procedure:
• A detailed echocardiographic assessment was performed using the PHILIPS iE33 machine.
• Measurements such as the interventricular septal thickness (IVST) and other parameters related to LVH were documented.
• The assessment was carried out using the parasternal long-axis view to ensure accurate measurement of IVST.
3. Statistical Analysis:
• Data were entered into MS Excel 2010 and analyzed using SPSS software (version 26).
• Descriptive statistics such as mean, standard deviation, frequency, and percentage were used to summarize the data.
• Chi-square tests were used to assess the association between qualitative variables.
• Spearman’s rank correlation test was used to evaluate the relationship between quantitative variables.
• A p-value of < 0.05 was considered statistically significant.

Study Procedure:

All participants diagnosed with LVH were thoroughly investigated with both ECG and 2D ECHO to evaluate the relationship between the findings of these two diagnostic methods. The results were recorded in the proforma, and statistical analysis was conducted to assess the correlation between ECG and ECHO findings in the diagnosis of LVH.

Ethical Considerations:

Informed consent was obtained from all participants, and the study was conducted following ethical guidelines laid out by the Institutional Ethical Committee. The confidentiality and privacy of participants were maintained throughout the study.

Table 1: Distribution of Patients by Age Group

This table divides the 382 patients into age groups to understand the prevalence of LVH across different age ranges. The majority of patients fall into the 41-60 years age range, with 87 patients being 61 years or older. The age distribution provides insight into the typical demographic affected by LVH, with a focus on middle-aged and elderly individuals.

Table 2: ECG Findings in Patients with LVH

Table 2 outlines the various ECG findings observed in the 382 patients. A significant number of patients (120) exhibited increased QRS duration, a common sign of LVH. Left axis deviation and ST-T changes were also frequently noted, affecting 90 and 110 patients respectively. The table highlights the range of ECG abnormalities typically seen in LVH cases.

Table 3: ECHO Findings in Patients with LVH

This table presents the 2D ECHO findings in the 382 LVH patients. The most common ECHO abnormality was increased left ventricular wall thickness, found in 200 patients. Left ventricular diastolic dysfunction (130 patients) and systolic dysfunction (80 patients) were also prominent. The table illustrates the cardiac structural and functional changes commonly associated with LVH.

Table 4: Correlation Between ECG and ECHO Findings in LVH Patients

Table 4 shows the relationship between specific ECG findings and corresponding ECHO findings. For example, 80 patients with increased QRS duration on ECG also had increased LV wall thickness on ECHO. This table underscores the connection between electrical and structural changes in the heart, offering insights into how both diagnostic tools complement each other in identifying LVH.

Table 5: Sensitivity and Specificity of ECG Findings in LVH (Sokolow Lyon Index vs Talbots Criteria)

This table compares the sensitivity and specificity of two diagnostic criteria (Sokolow Lyon Index and Talbots Criteria) for detecting LVH on ECG. Both criteria show high sensitivity, with the Sokolow Lyon Index at 85% and Talbots Criteria at 90%. Specificity is slightly lower, but still significant, demonstrating the effectiveness of these ECG markers in diagnosing LVH.

The study demonstrating that LVH predominates in middle-aged and elderly hypertensive patients and that specific ECG abnormalities correlate with ECHO-detected structural changes—are broadly consistent with prior research. However, variations in sensitivity and specificity of ECG criteria across studies underscore the limitations of voltage-based ECG diagnosis.

First, the predominance of LVH in patients aged 41–60 and those over 60 years aligns with large cohort data showing that the prevalence of echocardiographic LVH increases with age and with the duration of hypertension[28]. The structural changes detected by ECHO in the current study—namely increased wall thickness in 200 patients and diastolic dysfunction in 130 patients—mirror the pathophysiologic progression described in the Framingham cohort, where diastolic impairment precedes overt systolic dysfunction[28].

Regarding ECG findings, the high frequency of increased QRS duration (120 patients) and ST–T changes (110 patients) is consistent with established strain patterns seen in LVH[29]. The correlation between increased QRS duration on ECG and ECHO wall thickening in 80 patients supports the notion that QRS widening reflects ventricular remodeling[30].

Diagnostic accuracy of ECG criteria

• Sokolow-Lyon Index-The study reports 85% sensitivity and 80% specificity. In contrast, large-scale analyses report lower sensitivity (16–61%) and high specificity (68–97%) when traditional partition values are used[30]. For example, a study comparing ECG to necropsy and echo found Sokolow-Lyon sensitivity of 53% and specificity of 86% in an unselected clinical series[31].
• Talbot’s Criteria- The reported sensitivity of 90% and specificity of 75% exceed earlier descriptions of Talbot’s criteria, which noted specificity >90% but low sensitivity (approximately 20–30%)[32]. This discrepancy may reflect differences in patient populations, blood pressure control, and calibration of amplitude thresholds.

Overall, the high sensitivity but modest specificity observed in this study are characteristic of voltage-based ECG criteria, which tend to overcall LVH in individuals with increased chest wall voltage from non-LVH causes[28].

ECG–ECHO correlation

The study’s finding that left axis deviation correlates with diastolic dysfunction and that ST–T changes correlate with systolic dysfunction underscores the complementary roles of ECG and ECHO. Prior work has similarly demonstrated that ECG provides early electrophysiologic signals, whereas ECHO quantifies myocardial mass and function, yielding combined diagnostic and prognostic value[33].

LVH is most prevalent in middle-aged and elderly hypertensive individuals, with ECG and ECHO serving as complementary diagnostic tools. ECG findings such as increased QRS duration, left axis deviation, and ST-T changes were commonly observed, and these correlated with structural changes detected on ECHO, such as increased left ventricular wall thickness and diastolic dysfunction. Both Sokolow Lyon Index and Talbot’s Criteria demonstrated high sensitivity in detecting LVH, although there is a trade-off between sensitivity and specificity. ECG remains a valuable diagnostic tool in resource-limited settings, while ECHO provides detailed structural and functional insights into the condition. Future research should focus on multi-center studies to validate the diagnostic accuracy of ECG criteria and explore the role of newer imaging modalities in LVH diagnosis and management.

1. Bacharova L, Schocken D, Estes EH, Strauss D. The role of ECG in the diagnosis of left ventricular hypertrophy. Curr Cardiol Rev. 2014;10(4):257-67.
2. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990;322(22):1561-6.
3. Cuspidi C, Rescaldani M, Sala C, Grassi G. Left ventricular hypertrophy and obesity: a systematic review and meta-analysis of echocardiographic studies. J Hypertens. 2014;32(1):16-25.
4. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, et al. Adverse prognostic significance of concentric remodeling of the left ventricle in hypertensive patients with normal left ventricular mass. J Am Coll Cardiol. 1995;25(4):871-8.
5. Okin PM, Devereux RB, Jern S, Kjeldsen SE, Julius S, Nieminen MS, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. JAMA. 2004;292(19):2343-9.
6. Bluemke DA, Kronmal RA, Lima JA, Liu K, Olson J, Burke GL, et al. The relationship of left ventricular mass and geometry to incident cardiovascular events: the MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am Coll Cardiol. 2008;52(25):2148-55.
7. Frey N, Olson EN. Cardiac hypertrophy: the good, the bad, and the ugly. Annu Rev Physiol. 2003;65:45-79.
8. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986;57(6):450-8.
9. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19(7):1550-8.
10. Hancock EW, Deal BJ, Mirvis DM, Okin P, Kligfield P, Gettes LS. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy. J Am Coll Cardiol. 2009;53(11):992-1002.
11. Peguero JG, Lo Presti S, Perez J, Issa O, Brenes JC, Tolentino A. Electrocardiographic criteria for the diagnosis of left ventricular hypertrophy. J Am Coll Cardiol. 2017;69(13):1694-703.
12. Casale PN, Devereux RB, Kligfield P, Eisenberg RR, Miller DH, Chaudhary BS, et al. Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. J Am Coll Cardiol. 1985;6(3):572-80.
13. Casale PN, Devereux RB, Alonso DR, Campo E, Kligfield P. Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings. Circulation. 1987;75(3):565-72.
14. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37(2):161-86.