European Journal of Cardiovascular Medicine

Aortic Stenosis (AS) is one of the most common valvular heart diseases, particularly in the aging population, and represents a significant cause of morbidity and mortality in both developed & developing countries. The disease is characterized by the progressive narrowing of the aortic valve orifice, which leads to an increase in left ventricular (LV) afterload and subsequently results in left ventricular hypertrophy (LVH) and myocardial dysfunction. The clinical spectrum of AS ranges from a long asymptomatic period to the development of disabling symptoms and life-threatening complications such as heart failure. The early detection and accurate assessment of LV dysfunction in AS patients are critical for timely intervention and optimal management.^[1]

Traditionally, the assessment of LV function in AS patients has relied on measuring the left ventricular ejection fraction (LVEF) using echocardiography. However, LVEF has limitations, particularly in its ability to detect subclinical LV dysfunction, which can occur even when LVEF values are preserved (≥50%). This is because LVEF can remain normal until later stages of the disease due to compensatory mechanisms that maintain cardiac output despite increasing afterload. Current guidelines identify LV ejection fraction (LVEF) as an objective marker of elevated cardiac risk.^[2]  However, when compared with patients undergoing AVR with a normal LVEF, patients with an impaired LVEF have increased operative mortality, inferior long-term prognosis and in up to 50% of cases do not recover a normal LV function following AVR, suggesting that an impaired LVEF is an advanced stage of dysfunction associated with permanent myocardial damage ^[3-5]

Hence, Objective markers are required to assist risk stratification of patients with AS and to identify high-risk patients before LVEF declines Speckle tracking echocardiography (STE) is a new, validated technique which enables highly reproducible, angle-independent assessment of regional and global LV systolic function in longitudinal, circumferential and radial planes.[6-7] In recent years, global longitudinal strain (GLS) measured by speckle tracking echocardiography has emerged as a more sensitive and specific method for assessing myocardial function offering an insight into the subclinical stages of cardiac muscle impairment which precede overt systolic dysfunction.

GLS has been shown to detect subtle changes in myocardial function that are not apparent on traditional echocardiographic measures like LVEF.^[2]

Longitudinal strain, which is predominantly governed by the subendocardial layer, is most sensitive in the presence of myocardial disease.^[8] There is a subendocardial ischemia in AS patients, which is known to affect longitudinal myocardial fibers first. This sensitivity to early myocardial dysfunction makes GLS particularly valuable in the context of AS, where early detection of cardiac involvement has significant prognostic implications. The potential of GLS to serve as an early biomarker for cardiac dysfunction in AS could lead to earlier interventions, potentially delaying the progression of disease and improving patient outcomes.^[9] Hence highlighting the role of GLS in improving risk assessment in AS patients. GLS has been shown to correlate with histopathological changes in myocardial fibrosis, which are common in AS and contribute to progressive LV dysfunction. Moreover, GLS has been associated with outcomes; a reduced GLS in AS patients has been linked to increased mortality and morbidity, independent of LVEF and other traditional risk factors.^[5]

Due to its non-invasiveness, reproducibility, and sensitivity, GLS has gained attention as a potential tool for assessing cardiac function in various cardiovascular conditions. Given the intimate relationship between AS and myocardial function, it is plausible that GLS may be correlated with the severity of AS. Understanding this potential correlation could provide clinicians with an additional tool for evaluating AS severity and monitoring disease progression. Moreover, it may offer insights into the underlying pathophysiological mechanisms and aid in risk stratification and treatment planning.^[10] There is paucity of studies correlating Global Longitudinal Strain with severity of Aortic Stenosis in Indian sub-continent. Hence this research paper aims to investigate the correlation between GLS and AS severity in India. By reviewing existing literature and analyzing clinical data, we seek to determine whether GLS can serve as a reliable and informative marker for assessing AS severity & detecting subclinical dysfunction in patients of AS with preserved LVEF.^[10]

AIMS & OBJECTIVES

• To assess the capacity of global longitudinal strain (GLS) in patients with aortic stenosis (AS) to detect the subclinical left ventricular (LV) dysfunction [LV ejection fraction (LVEF) ≥50% patients
• To evaluate correlation of Global longitudinal strain with severity of Aortic stenosis.

This investigation was designed as a hospital based observational cross-sectional study was conducted at the Cardiology department of SMS Hospital, Jaipur, a tertiary care hospital known for its comprehensive cardiovascular care services.

The duration of the study spanned 18 months, during which all eligible patients were enrolled and followed up to complete the necessary evaluations.

Consecutive patients diagnosed with aortic stenosis to the Cardiology departmentof SMS Hospital, Jaipur during the study period.

Sample Size

The reference study by Manzo R et al.[10] depicts a negative correlation from baseline to increasing severity of aortic stenosis with GLS score. However the value of r is not available.Hence initially, a sample size calculation was performed based on the assumptions of a correlation coefficient (r) of 0.4 at a 95% confidence level and 80% power.

The calculation utilized the formula: N = ([Zα+Zβ]/ C)2 + 3

Where, C = 0.5 * ln[(1+r)/(1-r)]

Zα​=1.96 (for a 5% error), and Zβ=0.84(for 80% power).

The derived sample size was approximately 47, rounded to 50 for feasibility. However, to enhance the robustness of the study findings and allow for a comprehensive analysis across varying degrees of aortic stenosis severity, the sample size was increased to 100 patients.

Inclusion criteria:

Age > 18 Years

Patients of Aortic stenosis.

EF > 50%

Giving Informed Consent

Exclusion criteria:

• Patients having significant multi valvular heart disease
• Patients with AS & hemodynamically significant AR
• Patients with known coronary artery disease, congenital heart disease
• Patients with hypertrophic cardiomyopathy

METHODOLOGY

• Institutional Ethics Approval was taken
• Patient Selection and Consent

Patients diagnosed with aortic stenosis attending the Cardiology Outpatient Department (OPD), ECHO room or Inpatient Department (IPD) at our facility, who met the inclusion and exclusion criteria, were considered for the study. Informed consent was obtained from all participants, ensuring they understand the nature of the study and their involvement in it.

• Clinical Assessment and Data Collection

Upon enrollment, participants were evaluated for symptoms related to aortic stenosis. A comprehensive clinical examination was conducted for each patient. Routine laboratory investigations were performed, including Complete Blood Count (CBC), Kidney Function Tests (KFT), Liver Function Tests (LFT), Fasting Blood Sugar (FBS) & Post Prandial Blood Sugar (PPBS),

Lipid Profile & NTproBNP.

• A 12-lead Electrocardiogram (ECG) and 2D transthoracic echocardiography was acquired from all patients.

2D Transthoracic Echocardiography (TTE)

• TTE was performed using the Philips EPIQ 7C medical system equipped with S5 broadband phased-array transducers. Echocardiographic measurements and recordings adhered to the American Society of Echocardiography (ASE) guidelines. Standard measurements captured in the parasternal long-axis and short-axis views, and apical four-chamber view. Left ventricular dimensions were assessed using M-mode echocardiography, with the left ventricular mass index (LVMI) calculated using the ASE formula. Left ventricular ejection fraction (LVEF) was calculated by Simpson’s biplane method. Mitral Annular plane systolic excursion was calculated from m-mode in 4c view
• Pulsed-wave and continuous-wave Doppler ultrasound was utilized to record velocities through the LV outflow tract (LVOT) and aortic valve (AV), respectively. The AV was examined from multiple view to accurately measure the peak AV velocity and the mean AV gradient. The aortic valve area (AVA) was calculated using the continuity equation.

Global Longitudinal Strain (GLS) Measurement

• Strain was evaluated off-line from digitally stored images using Qlab 9 (cardiac motion quantification (aCMQ); Phillips Medical Systems) software package.
• Longitudinal strain for individual myocardial segments measured from all 3 apical views.
• In end-systolic frame, automated border tracking was enabled, before manual adjustment using a point and click approach to ensure that the endocardial and epicardial borders were included in the region of interest.
• The software then divided the LV myocardium into six segments in each view and generated segmental and global longitudinal strain.
• The strain values for all the segments were recorded and averaged to obtain the global longitudinal strain (GLS), and also Bull’s eye display of the regional and global longitudinal strain were generated

Definitions

Aortic stenosis severity was classified according to the 2020 ACC/AHA guidelines as follows:

• Mild: AVA > 1.5 cm² or mean AV gradient < 20 mmHg
• Moderate: AVA 1.0 – 1.5 cm² or mean AV gradient 20 – 39 mmHg
• Severe: AVA < 1.0 cm² or mean AV gradient ≥ 40 mmHg

According to Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging

GLS divided into following categories

• Normal GLS: Approximately -18% to -22%
• Mildly abnormal GLS -16% to -18%
• Moderately abnormal GLS value: -14% to -16%
• Severely abnormal GLS value: >-14% (less negative)

FLOW CHART OF STUDY DESIGN

Data Management and Statistical Analysis

All collected parameters were systematically entered in a tabulated form using Microsoft Excel™. Data were analyzed using SPSS software version 22 (SPSS Inc., Chicago, IL, USA). Descriptive statistics were used to summarize the baseline characteristics and clinical data of the study population, with continuous variables presented as means ± standard deviations (SD) and categorical variables as percentages. Differences between groups based on the severity of aortic stenosis were analyzed using ANOVA for parametric variables, with Bonferroni correction applied for multiple comparisons. Pearson’s correlation coefficient (r) was calculated to assess the relationship between GLS and the severity of aortic stenosis.

To further explore the independent determinants of GLS, univariate linear regression was initially performed to identify significant factors, followed by multivariate linear regression to adjust for potential confounders. Statistical significance was defined as a P-value of less than 0.05. In addition, odds ratios (ORs) were calculated to assess the likelihood of subclinical LV dysfunction in different GLS categories, and 95% CIs were used to quantify the precision of these estimates. All statistical analyses were conducted with a significance level set at P < 0.05.

Table 1: BASELINE CHARACTERISTICS

The baseline characteristics of the study population, categorized by aortic stenosis (AS) severity (mild, moderate, and severe), show no statistically significant differences across the groups. The mean age of the overall cohort was 71.2 ± 8.8 years, with a similar age distribution among the severity groups (p = 0.788). Males comprised 58% of the total population, with proportions slightly higher in the moderate (64%) and severe (73%) AS groups compared to the mild group (46%, p = 0.362). Hypertension was prevalent in 69% of patients, while 54% had hyperlipidemia and 30% had diabetes mellitus, with no significant variation among groups (p > 0.1 for all). Smoking was observed in 11% of the cohort, and the mean serum creatinine was 0.88 ± 0.40 mg/dL, both showing no significant differences across the AS severity groups (p = 0.383 and 0.369, respectively). Overall, the groups were comparable in terms of age, gender, comorbidities, and serum creatinine levels.

Table 2: ECHOCARDIOGRAPHIC PARAMETRS

The table summarizes the echocardiographic and laboratory measurements across different severities of aortic stenosis (AS). Significant differences were observed in septal thickness, posterior wall thickness, and LV mass index, which increased with AS severity (p = 0.003, 0.006, and 0.015, respectively). Peak velocity, mean pressure gradient, and aortic valve area showed strong correlations with AS severity, with peak velocity and mean gradient increasing significantly (p < 0.0001), while aortic valve area decreased (p < 0.0001). Markers such as e’, and E/e’ did not differ significantly across the groups (p > 0.05). Measures of systolic function, like GLS, MAPSE, decreased significantly with worsening AS (p = 0.003). NT-proBNP levels were notably higher in severe AS (550 ± 300 pg/mL) compared to mild and moderate AS, reflecting increased hemodynamic stress (p = 0.001). Overall, parameters like wall thickness, LV mass, and hemodynamic indices demonstrated clear differentiation between AS severity groups.

Table 3: Capacity of GLS to Detect Subclinical LV Dysfunction in Patients with AS and LVEF ≥50%

The findings demonstrate the capacity of Global Longitudinal Strain (GLS) to detect subclinical left ventricular (LV) dysfunction in patients with aortic stenosis (AS). Patients with progressively abnormal GLS categories were more likely to have subclinical LV dysfunction. Among those with normal GLS (> -18%), only 16% exhibited LV dysfunction. This proportion increased significantly in mildly abnormal GLS (-18% to -16%), moderately abnormal GLS (-16% to -14%), and severely abnormal GLS (< -14%) groups, with LV dysfunction present in 40%, 48%, and 68% of patients, respectively.

The odds of subclinical LV dysfunction increased markedly with worsening GLS. Patients with moderately abnormal GLS had an odds ratio (OR) of 3.24 (p = 0.03), and those with severely abnormal GLS had an OR of 6.2 (p = 0.001) compared to the reference group with normal GLS. The findings indicate that GLS provides a strong, independent marker for detecting subclinical LV dysfunction, with its predictive power significantly improving as GLS values worsen.

Figure 1

Table 4: Correlation of GLS with severity of AS

The table highlights the correlation between Global Longitudinal Strain (GLS) categories and the severity of Aortic Stenosis (AS). In patients with mild AS, most had normal GLS (> -18%, 51%), with no patients in the severely abnormal GLS category (< -14%). In moderate AS, the distribution shifted, with only 14% having normal GLS, while 42% had mildly abnormal GLS, 32% had moderately abnormal GLS. Among patients with severe AS, the majority (57%) had severely abnormal GLS followed by moderately abnormal (33%). The correlation coefficient between GLS and AS severity strengthens as AS severity increases. For mild AS, the correlation coefficient is 0.3 (95% CI: 0.10–0.50, p = 0.1), indicating a weak and statistically non-significant relationship. In moderate AS, the correlation coefficient rises to 0.5 (95% CI: 0.28–0.72, p = 0.03), showing a moderate and statistically significant association. For severe AS, the correlation coefficient is 0.8 (95% CI: 0.50–0.90, p = 0.001), reflecting a strong and highly significant relationship between worsening GLS and increasing AS severity. These findings demonstrate a clear trend where GLS deteriorates progressively with increasing AS severity, indicating its utility as a sensitive marker for disease progression.

Figure 2

Figure 3

The graphs illustrate a strong relationship between Global Longitudinal Strain (GLS) and two key hemodynamic parameters of aortic stenosis (AS): aortic valve area and mean gradient. GLS shows a strong inverse correlation with aortic valve area (correlation coefficient: -0.7), where worsening AS severity, marked by decreasing valve area (from ~1.6 cm² in mild AS to ~0.8 cm² in severe AS), is associated with GLS values becoming less negative. GLS also more strongly inversely correlates with mean gradient across the aortic valve (correlation coefficient: -0.8), with increasing mean gradient (from ~15 mmHg in mild AS to ~50 mmHg in severe AS) aligning with a worsening GLS. These findings emphasize GLS as a reliable marker for both the structural (valve area) and functional (mean gradient) severity of AS, reflecting progressive subclinical myocardial dysfunction.

Table 5: The Relation between Global Longitudinal Strain and the Echocardiographic and Clinical Parameters

Global Longitudinal Strain (GLS) demonstrates significant correlations with several echocardiographic and clinical parameters, reflecting its utility in assessing myocardial function in aortic stenosis (AS). Univariate analysis revealed that relative wall thickness, ejection fraction, LV mass index, mean pressure gradient (PG), aortic valve area, NT-proBNP, and MAPSE were significantly associated with GLS. However, in multivariate analysis, only mean PG (beta = -0.33),(p < 0.0001), ejection fraction (beta = 0.318), (p < 0.0001), MAPSE (beta = 0.211), (p = 0.047), and NT-proBNP (beta = -0.245), (p = 0.025) remained independent predictors of GLS. Variables like relative wall thickness, LV mass index, and aortic valve area, which were significant in the univariate analysis, lost their significance in multivariate analysis, likely due to overlapping contributions to GLS variability. These findings underscore the multifactorial nature of GLS and its ability to integrate structural, functional, and hemodynamic changes, establishing it as a robust marker for subclinical myocardial dysfunction and AS severity.

Figure 4

Global Longitudinal Strain (GLS) has emerged as a superior marker for detecting subclinical left ventricular (LV) dysfunction in aortic stenosis (AS) compared to ejection fraction (EF), which has significant limitations. EF is load-dependent and influenced by LV geometry and remodeling, often masking reduced myocardial contractility or overestimating function in AS.

There exists an independent relationship between LVEF and relative wall thickness; thus, for a similar extent of intrinsic myocardial shortening, the LVEF will tend to increase in relation to the extent of LV concentric remodeling. LVEF may thus be maintained despite reduced myocardial contractility by the use of preload reserve or changes in LV geometry. In contrast, a decreased LVEF may occur in the setting of preserved contractility due to afterload mismatch but could also represent a failing LV.Furthermore, EF poorly correlates with AS severity and has a low predictive value for LV structural impairments and outcomes.

Cardiac magnetic resonance (CMR) studies using late gadolinium enhancement (LGE) and T1 mapping have revealed myocardial abnormalities in AS patients with preserved EF, suggesting that preserved EF does not equate to normal LV function. However, the high cost and limited feasibility of CMR underscore the need for alternatives like GLS. Derived from speckle-tracking echocardiography, GLS offers a cost-effective, feasible and sensitive measure of myocardial deformation, providing a reliable tool for early detection of subclinical LV dysfunction and timely intervention in AS.

Our study confirms that GLS can detect subtle myocardial impairments even in patients with preserved EF (≥50%), aligning with findings by Abdel Mawla TS et al.(2023)[11], who reported that GLS decreases progressively with AS severity despite unchanged EF. Patients with severely abnormal(< -14%) & moderately GLS (-16 to -14%) demonstrated a significantly higher likelihood of subclinical LV dysfunction (OR = 6.2 & 3.24) This finding is consistent with studies by Abdel Mawla TS et al.(2023)[11] and Tan ES et al.(2023)[12], which demonstrated that GLS is impaired early in AS, often before EF declines. This supports the notion that GLS is a sensitive marker for early myocardial changes, as also highlighted by Bonow RO et al.(2006)[13], who emphasized its prognostic value in asymptomatic AS.

GLS identifies myocardial dysfunction earlier than EF by measuring longitudinal fiber strain, which is most affected in the subendocardium by the increased afterload in AS. Amato MC et al.(2001)[14] demonstrated that impaired GLS predicts the onset of heart failure symptoms before EF reduction occurs. Similarly, Lund O et al.(1997)[15] showed that even in AS patients with preserved EF, reduced GLS was associated with adverse cardiovascular events and symptomatic progression, underlining its clinical utility in early risk stratification.

Our study demonstrates a strong correlation between worsening GLS and the severity of AS, with a significant increase in GLS abnormalities as AS progresses. These findings are in line with Vaquette B et al.(2005)[16], who found GLS significantly decreased across mild, moderate, and severe AS (p = 0.003), correlating with increased mean pressure gradient (PG) and reduced aortic valve area (AVA). These changes reflect the hemodynamic burden of AS, consistent with the findings of Cheitlin MD.et al.(2005)[17], who showed that GLS deterioration parallels the biomechanical effects of increasing afterload.

Furthermore, our multivariate analysis revealed mean PG as an independent predictor of GLS (beta = -0.33), (p < 0.0001), indicating that GLS integrates structural and functional effects of AS. Similar results by Amundsen BH et al.(2006)[18] demonstrated that deteriorating GLS corresponds to higher transvalvular gradients and more advanced AS. Such findings reinforce the utility of GLS as a reliable marker of AS progression and severity.

Clinical Implications: Risk Stratification and Early TAVR

The integration of GLS into routine AS evaluations holds significant clinical implications. By detecting subclinical LV dysfunction, GLS enables early risk stratification and guides timely interventions such as transcatheter aortic valve replacement (TAVR). Abdel Mawla TS et al.(2023)[11] highlighted that patients with impaired GLS but preserved EF benefit from early TAVR, showing improved symptomatic relief and survival. In asymptomatic severe AS, Amato MC et al.(2001)[14] proposed that GLS can help identify high-risk patients who may benefit from earlier valve intervention, particularly when GLS is worse than -14.7%.

GLS also provides critical information in asymptomatic severe AS, where traditional markers such as EF and valve area may be inadequate for decision-making. In such patients, GLS can identify those at higher risk for adverse outcomes and justify early TAVR. Vaquette B et al.(2005)[16] found that GLS was superior to EF in predicting symptom development and mortality in asymptomatic severe AS​. Early intervention in these patients has been associated with improved long-term survival and reduced progression to heart failure, further supporting the integration of GLS into routine clinical practice.

Furthermore, TAVR has been shown to improve GLS in patients with impaired baseline values, supporting its role in myocardial recovery. Studies by Notomi Y et al.(2005)[19] & Mor-Avi V et al.(2011)[20] demonstrated that GLS can predict post-TAVR outcomes, including recovery of LV function and reduced mortality. This highlights GLS’s prognostic importance, particularly in asymptomatic patients, where intervention decisions are often challenging.

The most recent American College of Cardiology/American Heart Association and European Society of Cardiology valvular heart disease guidelines do not include a role for GLS assessment. However, in light of  the cumulative evidence demonstrating its powerful prognostic value, Notomi Y et al.(2005)[19] in a review article in JACC proposed algorithm in asymptomatic severe AS patients with preserved LVEF .In the absence of other current guideline indications for aortic valve intervention or exercise stress echocardiography abnormalities, the measurement of impaired LVGLS worse than <14.7% may be one of many features to guide a decision to intervene. If the optimal management is still unclear, patients with impaired GLS could be further studied using CMR; midwall LGE, abnormal native T1, or increased extracellular volume all provide evidence of LV impairment that could prompt surgery. In the absence of such CMR findings, close follow-up could be recommended (i.e., 3 to 6 months) to detect any changes in symptoms or LV function.

GLS is a cost effective, feasible and sensitive marker for detecting subclinical LV dysfunction and correlates strongly with AS severity.

Incorporating GLS into clinical practice enables earlier detection of high-risk patients, personalized treatment strategies, and improved long-term outcomes.

Its ability to predict outcomes in patients with preserved EF and guide early interventions like TAVR underscores its value in modern AS management.

LIMITATIONS

1. Cross-sectional Design: The cross-sectional nature of the study limits our ability to establish causality between GLS impairment and progressive AS or predict long-term outcomes. Longitudinal studies are needed to better understand the temporal relationship and to ascertain whether early GLS changes can predict future cardiac events or mortality in this population.
2. Single-Center Data: Data were collected from a single tertiary care center, which may not be representative of broader patient populations. This limits the generalizability of the findings to other settings or regions where patient demographics and baseline health statuses may vary.
3. Sample Size: Although the sample size was calculated to provide statistical power for primary outcomes, the relatively small sample size, especially when stratified into various categories of GLS and AS severity, might limit the statistical power to detect smaller yet clinically significant differences. This might also increase the risk of Type II errors.
4. Technique Dependency: The accuracy of GLS measurements depends heavily on the image quality and the expertise of the operator. Variability in imaging quality and interpretation could have influenced the GLS values, potentially introducing measurement bias.
5. Exclusion Criteria: The exclusion of patients with significant co-morbid conditions such as coronary artery disease, congenital heart diseases, and hypertrophic cardiomyopathy could limit the applicability of the findings to all patients with AS. Patients with these conditions frequently present in clinical settings and may show different GLS dynamics.
6. Lack of Multiple Imaging Modalities: This study relied solely on echocardiographic GLS measurements. Incorporating other imaging modalities, like cardiac MRI, which can provide additional insights into myocardial fibrosis and function, might have enriched the understanding of the myocardial changes in AS.
7. Interpretation of GLS: The interpretation of what constitutes normal and abnormal GLS values can vary, and the thresholds used in this study may not align with those employed in other studies or clinical practices, potentially affecting the comparison of results across different studies.

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