Abstract
Introduction
Currently, the interaction between heart failure with preserved ejection fraction (HFpEF) and obesity is discussed. As part of a complex echocardiographic examination, the two-dimensional speckle tracking (2D-STE) method is a significant tool for assessing dysfunction of the left atrium. Our study aimed to compare left atrial function using the 2D-STE in patients with class III obesity and a control group.
Methods
This was an observational, prospective, pilot /preliminary/ study that enrolled 20 patients with class III obesity (Body mass index (BMI) > 40 kg/m²) and a group of nineteen healthy individuals with a BMI of 20–25 kg/m² as controls. The following parameters were observed: Reservoir Left Atrial Strain (R-LAS), Conduit Time (CT-LAS), and Contractile Displacement (CD-LAS).
Results
The study patient group included sixteen women and four men (average age 42.4 years, ranging 19–63). The mean BMI was 47.69 ± 8.86 kg/m². The control group was created from fifteen women and four men (average age 27.2 ± 3.7 years, average BMI 22.48 kg/m²). The study found significant differences in R-LAS (29.9 ± 7.0 vs. 45.0 ± 11.7;p < 0.001) and CT-LAS (-16.8 ± 5.89 vs. -29.7 ± 8.71;p < 0.001) between patients with class III obesity and controls. No significant difference was seen in the remaining studied parameter /CD-LAS/ (-13.2 ± 4.77 vs. -15.1 ± 6.28;p = 0.305).
Conclusion
The R-LAS and CT-LAS were significantly changed (reduced) in patients with class III obesity compared to the controls.
Keywords: Obesity, Left atrium dysfunction, Echocardiology, Speckle tracking, Strain
Introduction
Obesity is a chronic metabolic disorder that significantly affects the cardiovascular system and is characterized by excessive weight gain and fat accumulation. Abdominal obesity, or the build-up of fat around the visceral organs within the abdomen, is directly associated with an increased risk of heart disease. Numerous cardiovascular conditions, including coronary heart disease [1], atrial fibrillation [2], arterial hypertension [3], and heart failure [4], have been linked to obesity as closely associated complications.
Up to 80% of heart failure patients with preserved ejection fraction (HFpEF) are obese (BMI > 30 kg/m²) or overweight (BMI 25–30 kg/m²) [5]. Increased preload, increased afterload, pulmonary hypertension, and chronic inflammation are some of the factors that contribute to the complex link between obesity and HFpEF. Unlike heart failure with reduced ejection fraction, HFpEF is more challenging to diagnose in clinical settings. It is frequently underdiagnosed, which can delay the correct diagnosis and initiation of appropriate treatment and, ultimately, worsen the overall prognosis. There is a correlation between the degree of left atrial dysfunction and left ventricular diastolic dysfunction according to the strain methodology that focuses on the left atrium [6].
A non-invasive echocardiographic imaging technique called two-dimensional speckle-tracking echocardiographic analysis (2D STE) uses 2D echocardiograms frame by frame to quantitatively evaluate regional myocardial function [7].
The intra-observer and inter-observer variability of 2D STE left atrial strain (LAS) assessment appears to be good. For intra-observer reliability, the previously reported Interclass Correlation Coefficient (ICC) values for LA STE analysis were 0.88–0.97 and for inter-observer reliability, the ICC values were 0.81–0.90, respectively [8–10]. Good intraobserver variability was reported also with a novice examiner performing the assessment [9]. Nevertheless, there might be a significant inter-vendor variability in LAS assessment [11]; and therefore, the use of different vendors for LAS assessment is currently not recommended. When compared to standard echocardiographic imaging, the 2D ST technique with the reservoir left atrial strain (R-LAS) and conduit strain (CT) parameters can reach higher diagnostic accuracy, allowing us to distinguish between individuals with HFpEF, who have dyspnea and those with non-cardiac dyspnea [12]. This method also provides a more sensitive echocardiographic marker of left ventricular diastolic dysfunction than conventional parameters (left atrial volume index, tissue doppler imaging and assessment of transmitral flow) [13]. Additionally, it was reported that LAS can be use for prediction of early left atrial/left ventricular diastolic dysfunction in several other clinical scenarios such as in patients with end stage chronic kidney disease on hemodialysis/after kidney transplant [14], in patients with non-alcoholic metabolic dysfunction associated liver steatosis [15], or to predict treatment outcomes in atrial fibrillation patients undergoing percutaneous or surgical ablation procedures [16, 17]. As there are no data regarding the impact of severe obesity on left atrial deformation, our study aimed to compare left atrial deformation using the 2D STE method in patients with class III obesity and a control group.
Methods
Study design and patients
A prospective, observational pilot study was performed. The study was carried out between September 1, 2024, and January 31, 2025. The study comprised patients, who were scheduled for hospitalisation at the University of Martin’s Department of Internal Medicine I during the relevant time period. The differential diagnosis of obesity, the exclusion of secondary aetiology, and the start of anti-obesity treatment were carried out if they met the study inclusion and did not meet the study exclusion criteria listed below.
The inclusion criteria were selected as follows: patients with class III obesity (BMI above 40 kg/m²) without any previous obesity interventions (pharmacological or surgical), availability to achieve good imaging quality via echocardiography to perform 2D STE analysis. The exclusion criteria included patients under 18 years of age and hospitalized patients, who did not want to participate in the study (all patients included in the study had to sign a written informed consent with participation). Likewise, patients were not eligible for enrolment if they had severe liver disease such as Child-Pugh class C or severe kidney damage such as end-stage chronic kidney disease (stage 5 KDIGO).
The control group consisted of healthy individuals without obesity with a BMI in the range of 20 to 25 kg/m², no history of cardiovascular disease and normal echocardiogram.
Each study participant underwent an echocardiographic examination using the 2D ST methodology. The monitored parameters were Reservoir Left Atrial Strain (R-LAS), Conduit Time (CT), and Contractile Displacement (CD). These parameters were subsequently compared with the parameters in healthy individuals without obesity. For the examination, we used a transthoracic echocardiography device (Vivid® E95, GE Medical Systems, Milwaukee, WI, USA). The echocardiographic study to record at least three ECG-matched cardiac cycles in apical 4-chamber and apical 2-chamber projections for external 2D STE assessment was performed by two board-certified echocardiographers. Subsequently, the echocardiographic images were sent to an external certified in echocardiographer, who was unaware to the patient status (obesity/control individual) and who performed the 2D STE analysis off-line using a specified echocardiographic workstation (EchoPAC™, GE Medical Systems, Milwaukee, WI, USA). For 2D STE analysis, end-systole was set at a moment of aortic valve closure. Left atrial wall was tracked automatically using specified software (AFI LA®, GE Medical Systems, Milwaukee, WI, USA) and adjusted manually by the echocardiographer if automatic software misidentified the atrial wall in apical 2- and 4-chamber projections. Subsequently, automatic analysis of LA strain was performed (Fig. 1), and the mean of the values from the two echocardiographic views were reported as strain results in % of change.
Fig. 1.
Example of 2-dimensional speckle tracking echocardiographic (2D STE) assessment of left atrial strain (LAS)
Statistical analysis
The results of the study were processed using the statistical software Jamovi v2.6.26.0 (Sydney, Australia). Continuous variables are presented by mean and median; variability was summarized by standard deviation and interquartile range. Discrete variables were summarized in numbers and percentages. A boxplot was used to check the distribution of continuous variables. Data distribution was tested using the Shapiro-Wilk normality test. In the case of normal data distribution, the statistical significance was assessed by Student’s paired t-test, for abnormal distribution, the Mann-Whitney U test was used. Nominal variables were tested using the chi-square test. We considered a p-value < 0.05 as statistically significant.
Results
Patients and Controls
A total of 20 patients (4 men and 16 women, average age 42.4 years, ranging 19–63) with class III obesity (the mean BMI 47.69 ± 8.86 kg/m²) meeting the inclusion criteria were included in the patient cohort during the study and a total of 19 healthy individuals (4 men and 15 women, average age 27.2 ± 3.7 years, average BMI 22.48 kg/m²) were included in the control group. As for the patient group, the majority were women (80%). Most patients had arterial hypertension (65%) and hyperlipidaemia (70%). Exactly half of the patients had fatty liver associated with metabolic dysfunction. Similarly, half of the patients had problems with glucose metabolism, where 30% of patients had type 2 diabetes mellitus and 20% had impaired glucose tolerance. Complete basic demographic data of the patients can be found in Table 1.
Table 1.
Basic review of demographic information of patients, selected laboratory parameters and comorbidities of patients with patients with class III obesity
| Studied group of obese patients with class III obesity | |
|---|---|
| Number of patients (women/men) | 20 (16/4) |
| Age | 42.4 (19–63) |
| Height (cm) | 168.4 ± 7.91 |
|
Weight (kg) (before treatment) |
135.31 ± 26.65 |
|
BMI (kg/m2) (before treatment) |
47.69 ± 8.86 |
|
Waist circumference (cm) (before treatment) |
133.9 ± 16.26 |
|
Hip circumference (cm) (before treatment) |
143.7 ± 14.62 |
|
Waist to height ratio (before treatment) |
0.8 ± 0.1 |
| Serum creatinine (µmol/L) | 65.7 ± 12.57 |
| Calculated GFR – Cockcroft Gault (ml/min/1.73 m²) | 100.65 ± 15.22 |
| ALT (µkat/L) | 0.52 ± 0.23 |
| AST (µkat/L) | 0.44 ± 0.10 |
| Haemoglobin (g/L) | 132.8 ± 14.19 |
| Total Serum Protein (g/L) | 70.65 ± 3.96 |
| Total cholesterol (mmol/l) | 4.5 ± 0.644 |
| LDL cholesterol (mmol/l) | 3.17 ± 0.58 |
| HDL cholesterol (mmol/l) | 1.1 ± 0.25 |
| Triacylglycerols (mmol/l) | 1.83 ± 0.73 |
| Type 2 Diabetes / Impaired Fasting Glucose (%) | 30 / 20 |
| Hyperlipidemia (%) | 70 |
| Metabolic dysfunction-associated steatotic liver disease (%) | 50 |
| Active oncological disease (%) | 0 |
| Chronic kidney disease (%) | 5 |
| Coronary artery disease (%) | 5 |
| Atrial fibrillation (%) | 0 |
| Arterial hypertension (%) | 65 |
| Bariatric surgery – gastric sleeve resection (%) | 0 |
| Gastroesophageal reflux disease (%) | 15 |
| Hypothyroidism (%) | 20 |
| Asthma bronchiale (%) | 15 |
| Hyperandrogenic syndrome (%) | 5 |
| Valve disease – moderate to severe (%) | 0 |
BMI body mass index, GFR glomerular filtration rate, ALT alanine aminotransferase, AST aspartate aminotransferase, LDL low-density lipoprotein, HDL high-density lipoprotein
Left atrial function STE analysis
Looking at the LAS analysis, there was a significant difference in R-LAS (+ 29.9 ± 7.0 versus + 45.0 ± 11.7; p < 0.001) and CT-LAS (-16.8 ± 5.89 versus − 29.7 ± 8.71; p < 0.001) between the obese patients and the control group. No significant difference was observed in CD-LAS values (-13.2 ± 4.77 versus − 15.1 ± 6.28; p = 0.305) as can be seen in Figs. 2, 3 and 4 (Figs. 2, 3 and 4).
Fig. 2.
Comparison of R-LAS (%) between patients with class III obesity and control group
Fig. 3.
Comparison of conduit (CD) left atrial strain (%) between patients with class III obesity and control group
Fig. 4.
Comparison of contraction (CT) left atrial strain (%) between patients with class III obesity and control group
Discussion
As mentioned, 2D ST could be used for an early detection of left atrial dysfunction and that this dysfunction correlates with impaired left ventricular filling. This impairment in atrial/ventricular filling could be used for early diagnosis of HFpEF, which is the most frequent form of HF in patients with obesity. In our study, we have shown significant differences in R-LAS and CT-LAS in patients with class III obesity, which could be used to identify myocardial injury before the onset of clinically obvious signs of heart failure. Taking into account the fact that the number of patients with obesity continues to increase dramatically, and obesity as well as cardiac comorbidities pose a significant public health problem, early identification of incipient cardiac abnormalities through non-invasive techniques such as 2D STE could provide crucial information for early detection of the disease, early treatment intervention and subsequent improvement of patient outcomes. To support this suggestion, we would like to point out the results of the cardiac magnetic resonance study performed by Bayer et al. [18], which showed that in patients with obesity (with or without T2D) impaired LA structure and function (LA dysfunction) emerged as the only independent discriminator of HFpEF. Unfortunately, to the best of our knowledge, there are no other published studies investigating the relationship of class III adult obesity with left atrial damage using 2D ST echocardiography at this time. Therefore, there is no study for direct confirmation of our results, and our results are preliminary and would need to be confirmed in future larger trials.
However, there are several studies examining the use of 2D ST in patients with T2D. Based on one of these studies, left atrial function strain can be used to detect early changes in diastolic dysfunction. In this study [19], consisting of 331 patients divided into three groups (101 with normal weight, 114 with obesity, and 116 with T2D), echocardiographic parameters of left ventricular diastolic function were examined. It was found that obese patients, as well as patients with T2D, had significant reductions in atrial reservoir, conduit, and booster strain compared to a third healthy group. These patients also had worse reservoir and conduit strain rates. However, the group studied included patients with obesity but without T2D, who had a weight equal to or above the 95th percentile of BMI. Similarly, the patients in the T2D group were patients with a normal weight equal to or below the 85th percentile of BMI.
A recent study [20] conducted in 2024 on a Vietnamese population of 111 participants examined the relationship between T2D and heart injury. The study was focused on examining the parameters of the stiffness of the left atrium and left ventricle, as well as the left atrioventricular coupling index (LACI). The results showed that in patients with T2D, increased stiffness of the left atrium as well as the left ventricle was significantly more frequent and their LACI (%) values were significantly higher compared to the control group.
Our results add novel data on the obesity-related left atrial functional alterations. In previous observation, Gulel et al. examined left atrial function using doppler-based echocardiography in individuals with BMI ≥ 30 kg/m2 (compared to those with BMI < 30 kg/m2) and found that all left atrial systolic and diastolic function parameters were similar between the compared groups [21]. In fact, this observation does not correspond with our results. There are two possible explanations of these differences. First, the study performed by Gulel et al. included mostly patients with class II obesity (mean BMI of 38 ± 6 kg/m2), and the differences in BMI between patients and controls (24 ± 2 kg/m2) were lower compared with our study, which enrolled patients with class III obesity (47.69 ± 8.86 kg/m²) and compared the studied LA parameters with a group of individuals with normal body weight (and an average BMI of 22.48 kg/m²). Second, it is possible, that doppler-based echocardiographic parameters are less sensitive in identifying left atrial dysfunction than left atrial 2D STE analysis [22, 23]. In more recent analysis [24], the authors found that LAS and the longitudinal strain rate during the contraction phase and the longitudinal strain rate during the reservoir phase were decreased in patients with obesity and diabetes (compared to non-obese patients with diabetes). This corresponds with our observation in non-diabetic patients with obesity, suggesting the obesity is the key player in left atrial dysfunction development. Furthermore, another recent study [25] showed in a population of older adults with metabolic syndrome and overweight or obesity that left atrial structure and function were abnormal (including abnormal LAS values), but did not significantly differ across different glycemic status (diabetes, prediabetes, normal), again suggesting obesity as the main pathophysiological factor in left atrial structural/functional dysfunction development.
Now, the exact mechanism of how obesity affects left atrial function remains unclear. As mentioned in the Introduction, obesity leads to an increased preload and afterload, pulmonary hypertension, chronic inflammation and metabolic dysregulation; nevertheless, one should think also on the possible contribution of extrinsic mechanical factors to the observed impairment in LAS parameters. Recent evidence in metabolically healthy individuals with obesity suggests that reduced myocardial strain may not solely reflect intrinsic myocardial dysfunction but may be strongly influenced by abdominal adiposity and changed thoracic geometry, leading to external cardiac compression [26]. In particular, altered anteroposterior chest diameter and increased waist circumference have been shown to independently predict reduced left ventricular global longitudinal strain, supporting a “mechanical” rather than purely metabolic mechanism. Integrating this perspective could help contextualize the reduced left atrial strain observed in the present study and may explain why functional abnormalities occur even in the absence of overt structural heart disease. Summarizing, this is a still unexplained issue, which is open for future research evaluation.
Limitations
Firstly, the sample size of the study is small, and the conclusions of the study certainly need to be confirmed by further studies on a larger sample of patients. A larger number of patients would help to refine the results and make them more generalizable for further application.
Secondly, the study included many more women than men, which inevitably creates some bias in the results. This can be explained by the greater tendency to admit the problem with obesity and its complications in women compared to men, as well as the perceived ignorance in men to admit weight issues due to the stigmatization of the disease of obesity.
Thirdly, the measurements were performed by two cardiologists, which may introduce some extent of interindividual variability.
Fourthly, there was a slight age imbalance between groups. As we wanted to compare the LAS values between patients with class III obesity and truly healthy controls (with no cardiovascular diseases) we needed to accept this limitation (it would be very hard to enrol totally age-matched healthy controls for the study, as the prevalence of LAS-affecting diseases such as arterial hypertension, type 2 diabetes increases with increased age).
Lastly, obese patients generally have poorer echocardiographic imaging quality, making it difficult to obtain adequate images and ensure unambiguous accuracy of measurements. Therefore only those individuals in whom echocardiographic examination allowed to obtain images with good quality to perform STE were included. Therefore, our results might not be interpolated to all obese patients, and there is a low possibility of a selection bias.
All these limitations should be definitely taken into account when the results of our observations are interpreted.
Conclusion
The R-LAS and CT-LAS parameters were significantly reduced in patients with class III obesity compared to the control group. These results certainly advocate further research into the role of 2D-STE for early detection of left atrial impairment in patients with class III obesity and, perhaps, could provide a novel diagnostic marker for early detection of HFpEF in patients with obesity. However, studies with larger sample sizes will be definitely required to validate these results.
Acknowledgements
Peter Tudík and Jakub Jurica share first authorship and contributed equally to this work.
Informed consent statement
Patients signed an written informed consent prior the enrollment to the study.
Authors’ contributions
T.B., and M.S. designed the study; P.T. and J.J. drafted the manuscript; T.B. and M.S. performed the echocardiographic studies; M.B.V. performed the independent 2D speckle tracking analysis; P.T., J.J., M.J.P., B.F., Z.M., A.M., L.K., N.N., and P.L. collected, analyzed and interpreted the clinical data, and performed the search of the literature; I.S., T.B., M.M and M.S. supervised the study and acquired the funding; T.B., I.S., M.M., and M.S. revised the manuscript critically. P.T and J.J. share first authorship, they contributed to this work equally. All the authors have read and approved the final version of the manuscript.
Funding
This study is a part of the research project the Research Agency of Slovak Ministry of Education, Science, and Sports (VEGA) 1/0168/25 and was supported by the project Operational Programme Integrated Infrastructure ITMS 2014+:313011V344.
Data availability
All data are available from the corresponding author upon a reasonable request.
Declarations
Ethics approval and consent to participate
The research was performed according the all ethical standards, and the study adhered to the Declaration of Helsinki. The study was approved by the local ethics committee (Ethics Committee of Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Slovakia, approval code EK 37/2024, approval date 4th June 2024).
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Peter Tudík and Jakub Jurica share the first authorship and contributed equally to this work.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All data are available from the corresponding author upon a reasonable request.