Left atrial enlargement (LAE) is a condition where one of the heart's chambers, the left atrium, becomes larger than its normal size. This article explores the causes and implications of left atrial enlargement, particularly focusing on its relationship with obesity and the potential benefits of weight loss.
What is Left Atrial Enlargement?
Left atrial enlargement occurs when the left atrium, a chamber of the heart, becomes bigger than normal. This enlargement typically develops over time as the left atrium attempts to compensate for underlying issues, such as high blood pressure within the heart. Sometimes, problems with the left ventricle, which is responsible for pumping blood to the aorta, can contribute to LAE. Similarly, issues with the mitral valve, which regulates blood flow between the left atrium and left ventricle, can also play a role. These conditions can lead to elevated pressure and/or an increased volume of blood in the left atrium.
As the left atrium tries to adapt to high pressure and/or high volume, it can stretch and enlarge. This stretching can cause scarring and injury to the atrium.
Who is Affected by Left Atrial Enlargement?
Left atrial enlargement affects people with conditions such as:
- High blood pressure
- Left ventricle dysfunction
- Mitral valve disorders
An Italian study of adults revealed that 12% of them developed left atrial enlargement over a 10-year period, suggesting that the condition is not rare in the general population.
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The Connection Between Obesity and Left Atrial Enlargement
Increased cardiovascular risk in obese patients is partly due to hemodynamic and metabolic disturbances caused by obesity-related co-morbidities. Cross-sectional and short-term longitudinal studies suggest that obesity is associated with diastolic dysfunction.
To investigate the association between major weight loss (WL) and improvements in LA volume, a retrospective study was conducted on patients with morbid obesity [body mass index (BMI) ≥35 kg/m2 with obesity-related co-morbidities] and extreme obesity (BMI ≥40 kg/m2), after surgically-induced WL following gastric bypass surgery. The study included patients who underwent Roux-en-Y gastric bypass surgery for morbid or extreme obesity from 1995 to 2005 at Mayo Clinic, Rochester, MN, and had two or more transthoracic echocardiographic examinations, one within 2 years before the operation and one ≥6 months after the procedure. A control group was frequency-matched for sex, age (±2 year), BMI (±2 kg/m2) at the time of the first echocardiogram, and follow-up duration (±6 months).
Patients with past medical history of cardiomyopathy secondary to a specific disease, pericardial disease, and severe valve disease, as well as those with technically limited echocardiograms were excluded. Digital off-line analysis of LA volume was performed in all patients by a single observer blinded to the clinical history, amount of WL, study group, and original echocardiographic report. LA volume was measured using the biplane area-length method. LA volume indexed by height was also determined.
Statistical analyses compared measurements in patients who underwent gastric bypass surgery with measurements in the control group. Multivariate analysis was performed to assess bariatric surgery as a predictor of change in LA volume, adjusting for potential confounders. Pearson’s correlation coefficients were calculated to test univariate relationships between change in body weight and change in LA volume. Multiple linear regressions were performed using change in LA volume as the dependent variable, and change in body weight as an independent variable.
Study Results: Weight Loss and LA Volume
A total of 64 patients who underwent bariatric surgery met the inclusion criteria. Seven patients were excluded because of a history of heart transplantation (n=2), severe cardiac valvular disease (n=4), and cardiac amyloidosis (n=1). Therefore, 57 cases and 57 frequency-matched controls were included.
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At follow-up, patients who underwent bariatric surgery showed a significant reduction in body weight, body surface area, BMI, and heart rate. Only the control group had significant increases in LA volume and height-indexed LA volume at follow-up. Changes in LA volume, height-indexed LA volume, and E/A ratio were different between cases and controls.
Analysis of the pooled data showed a positive and significant correlation between change in LA volume and change in body weight measured by WL, %WL, and ΔBMI.
Key Findings
The study revealed that long-term change in body weight correlated directly with change in LA volume. Although baseline LA volumes were similar in patients who did and did not undergo gastric bypass surgery, patients who lost weight after surgery had a lesser change in LA volume compared with patients who did not undergo the procedure and had only a mild (at best) WL. To the best of our knowledge, this is the first longitudinal study showing a direct correlation between change in body weight and change in LA size independent of changes in blood pressure.
The Significance of Left Atrial Volume Indexing in Obese Patients
Accurate standardization of left atrium volume (LAV) in patients with obesity is challenging. A study aimed to investigate and examine the relation between LAV indexed to height2 and left atrial function in patients with moderate to severe obesity. Echocardiograms of patients with moderate to severe obesity (body mass index (BMI) ≥ 35 kg/m2) without known cardiac disease were analyzed. LAV was indexed to body surface area (BSA) and height2, and patients were divided into those with or without left atrial enlargement (LAE) based on normalization using either BSA (LAEbsa) or height2 (LAEh2). Using speckle tracking echocardiography, LA reservoir strain (LASr), LA conduit strain (LAScd), and LA contractile strain (LASct) were assessed as a measure of LA function. LA dysfunction was defined as LASct < 14%.
Study Design and Methods
Echocardiograms from the CARDIOBESE study and AF OBESE study, multicenter prospective cross-sectional studies in which 192 patients with obesity without known cardiac disease were enrolled, who were referred for bariatric surgery in the Franciscus Gasthuis & Vlietland and Maasstad Ziekenhuis, both in Rotterdam, the Netherlands were used. Patients were enrolled if they were between 35 and 65 years old and had a BMI of ≥ 35 kg/m2. Height (in meters) and weight (in kilograms) were measured at the time of the echocardiogram. BMI was calculated as weight/height2. BSA was calculated by using the Du Bois formula (BSA [m2]) = 0.007184 x height [cm]0.725 x weight [kg]0.425.
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Two-dimensional greyscale harmonic images were obtained using a commercially available ultrasound system (EPIQ 7, Philips, the Netherlands). LAV was measured on the 4-chamber and 2-chamber view and then indexed to height2 (LAVh2) and BSA (LAVBSA). LAEh2 was defined according to the ESC/ESH hypertension guidelines (LAVh2 >18.5 ml/m2 in males and LAVh2 >16.5 ml/m2 in females). LAEBSA was defined as LAVBSA > 34 ml/m2. LA strain was measured with speckle tracking and analyzed offline with dedicated software (TomTec-Arena, integrated in Sectra IDS7). LA function was described according to the three phases of the LA cycle: LA reservoir strain (LASr), LA conduit strain (LAScd), and LA contractile strain (LASct). LA dysfunction was defined as LASct < 14%.
Study Results: LA Volume Indexing
A total of 142 patients were included in the analysis. In the total study population LAVBSA was 25.6 ± 7.5 ml/m2 and LAVh2 was 18.4 ± 5.3 ml/m2, resulting in a total of 26 (18.3%) patients having LAEBSA, and 77 (54.2%) patients having LAEh2. The prevalence of LAEh2 was significantly higher than LAEBSA in both obesity class groups. The LAEh2 group had significantly lower LASct (12.2 ± 3.2% vs. 13.6 ± 4.5%, p = 0.019). Significantly more patients with LA dysfunction would have been correctly classified by LAEh2 as compared to LAEBSA (41.5% vs. 15.0%, p < 0.001). In binary logistic regression LAEh2 was significantly associated with an abnormal LASct (OR 2.64, CI 1.29-5.42, p = 0.008).
Findings
The study demonstrated that, in subjects with moderate and severe obesity without known cardiac disease, LAEh2 was associated with an increased risk for LA dysfunction, in contrast to LAEBSA and other traditional parameters of LV diastolic function. Furthermore, it confirmed findings of previous studies, showing that indexation of LAV to height2 resulted in a higher prevalence of LAE compared to indexation of LAV to BSA in these subjects.
Implications and Future Directions
These findings underscore the importance of considering weight loss as a potential strategy for mitigating left atrial enlargement, particularly in individuals with obesity. Further research is needed to fully elucidate the mechanisms underlying the relationship between weight loss and LA size, as well as to determine the optimal weight loss strategies for improving cardiac health.
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