Obesity remains one of the most important diseases of the twenty-first century, increasing the risk of heart failure, diabetes mellitus, dyslipidemia, sleep apnea, and cancers [16]. At first, it was thought that bariatric surgeries only restrict the intake volume; later research depicted the metabolic and systematic effects [17, 18]. It has been shown that morbid obesity can increase preload and afterload over time, leading to increased LV wall stress. LV dilatation and hypertrophy can ensue, increasing myocardial stiffness and resulting in LV diastolic and systolic dysfunction. Obesity is associated with activating the renin–angiotensin–aldosterone axis, which changes the cardiac structure and size [19, 20]. Expectedly, weight loss can reverse obesity-related cardiac changes if remodeling and fibrosis have not happened [21]. This supports the importance of early intervention, especially bariatric surgeries, at younger ages. Improved cardiac outcomes following bariatric surgery seem much further than decreased preload, afterload, and mechanical pressure on the myocardium [22].

Most studies generally assessed the favorable echocardiographic changes of bariatric surgery on the myocardium after six months. The presenting study tried to detect early echocardiographic changes in morbidly obese patients undergoing bariatric surgery. The main findings of this research were improved GLS, GCS, and dyssynchrony of circumferential movement of the left ventricle in six months after bariatric surgery. Despite significant weight loss three months after the surgery, only the LV's basal and apical circumferential strains showed improvement.

In a study by Grymyr in 2021, the one-year impact of bariatric surgery on LV mechanics was assessed, and the absolute value of GLS improvement was 4.6% at six months, and LVEF remained unchanged [23]. In multivariate regression analyses, 1-year improvement in GLS was predicted by lower preoperative GLS, more considerable mean blood pressure, and BMI reduction (all P < 0.05). In our study, the absolute increase in GLS was 2%, with no change in LVEF, and the improvement in GLS and GCS after six months did not necessarily correlate with the baseline weight or weight loss. As in Grymyr's study, the lower baseline GLS predicted more improvement in GLS six months after the surgery. Circumferential strains were not calculated in the Grymyr study.

In 2019, Santos et al. measured the GLS, GCS, GRS (global radial strain), and LV twist in 25 patients about three months after sleeve gastrectomy [24]. Only GLS improved by about 2%, and GCS, GRS, and LV twist remained unchanged. Contrarily, we found a significant increase in the absolute value of GCS (increment of 3% from baseline to three months after the surgery and 4% from baseline to six months after the surgery). Regarding the type of surgery, the absolute values of the GCS were significantly lower in the mini-bypass group than in classic surgery (at baseline and after three and six months) in our research. Unfortunately, our study sample size was not large enough to conclude the superiority of any procedure over the others.

A meta-analysis by Gherbesi, published in 2022, included 11 studies with follow-ups ≥ 6 months that confirmed GLS but not LVEF improved after bariatric surgery [25]. GCS was not an endpoint in this meta-analysis.

In another study in 2017 in South Korea, 37 patients undergoing bariatric surgery were studied by Shin et al. Echocardiography was performed before and after at least one year of bariatric surgery [26]. Bariatric surgery led to significant decreases in left ventricular (LV) size and mass and LV longitudinal strain (14.1 ± 1.9–16.2 ± 1.4%, p < 0.001 for longitudinal strain). Changes in LV longitudinal strain were related to LV mass reduction (p = 0.04). However, LV ejection fraction and LV circumferential and radial strains were comparable at follow-ups. Our study showed improved GLS, GCS, and dyssynchrony of circumferential movement of the left ventricle six months after bariatric surgery. Only the LV's basal and apical circumferential strains showed improvement three months after the surgery. GCS was not measured in Shin’s study.

In this study, the change in GLS and GCS after six months did not correlate with the baseline weight or weight loss, but it did correlate with the baseline GLS and GCS values. Further studies should reassess the mechanism behind different observed responses of longitudinal and circumferential strains to weight loss. The main practical finding was that patients with lower absolute GLS values had a greater increase in GLS after weight loss.

In this study, we did not assess blood pressure changes or metabolic alterations such as blood sugar level, as there was much evidence supporting their beneficial effects of improved metabolic state in morbidly obese patients after bariatric surgery. Enhanced glucose metabolism or the release of adipocytokines is responsible for these favorable outcomes [27, 28].

In practice, encountering an obese patient with RV enlargement usually requires multiple additional workups to exclude cardiac disorders, notably left-to-right shunts, and evidence of pulmonary hypertension. In contrast, the definite effect of obesity on RV size cannot be estimated. Unfortunately, the upper limit of normal RV size in obese patients has not been provided. Multiple studies focused on the effects of bariatric surgery on the right ventricular size and function; all showed a favorable impact on RV size and function [11]. In a retrospective cohort study, the changes in different RV sizes were assessed, and RV mid-cavity and longitudinal dimensions significantly decreased after surgery. They did not report the RV size as “normal” or” abnormal” based on the latest guidelines. The chamber quantification guideline [13] 2015 emphasized measuring RV size in an “RV-focused view” with suggestions to minimize the significant variability in acquiring RV views. The retrospective nature of their study (2008–2017) and the presence of different echocardiographers that may image RV before the widespread acceptance of the “RV-focused view” limits reliance on the change in RV size in the long follow after bariatric surgery [29].

We tried to elucidate the early effect of bariatric surgery on multiple echocardiographic right ventricular sizes and find which RV size shows the most remarkable change relative to the baseline measurement. In the presenting study, RVOT in PLAX view was abnormal in 91.2% of the study population at baseline and remained abnormal in 76.5% even after significant weight loss. On the other hand, basal RV diameter was normal in all of the participants. Despite the small study population, the following conclusions can be drawn from this study: First, the basal RV enlargement should not be explained by obesity, and other etiologies for RV enlargements, such as left to right shunt and pulmonary hypertension, should be in mind during echocardiography. Second, RVOT size in the PLAX view should not be relied on as a sole measurement for diagnosing RV enlargement in obese patients. Lastly, despite significant weight loss in six months after bariatric surgery, abnormal RV size did not return to the normal range in all participants. In a study by Eslami and colleagues [30], multiple echocardiographic planes were measured and indexed to body mass index (BMI) and body surface area (BSA) in 80 normal participants. They proposed a formula to predict maximum RV diameter based on BMI. The main problem with their proposed formula for estimating RV diameter in obese patients was the small number of people with a BMI of more than 25 kg/m2 in this study. Long-term studies of the effect of bariatric surgery on the right ventricular size are needed to find the threshold of abnormal RV diameter in obese patients.

Detailed clinical and laboratory data of the patients were documented in the registry of metabolic surgery at Firoozgar Hospital, and patients were referred to us only if they met the criteria. As we aimed to assess the early cardiac effect of weight loss, patients with clinical conditions that may have concurrent cardiac effects, such as uncontrolled hypertension, a history of cardiomyopathy, myocardial infarction, myocarditis, pericardial disease, and moderate or severe valvular disease, were excluded. Tachycardia and atrial fibrillation were among the other risk factors that were excluded. Laboratory data, including kidney function, lipids, and pro-BNP, were documented in the Firoozgar database but were not included in our research as we solely focused on echocardiographic changes.

Bariatric surgery and 2D speckle echocardiography were performed in two different hospitals, which resulted in the loss of follow-up. After significant weight loss, some patients did not return for echocardiographic follow-up. Endocardial detection and performing strain studies are challenging in morbidly obese patients. We tried to overcome this limitation by including patients with satisfactory views, and obese patients were excluded if the endocardial border was not traceable in more than two segments in a view. As we excluded patients with underlying cardiac disease (cardiomyopathies, history of previous myocardial infarction or myocarditis), generalization of the study results to these groups of patients is impossible. The reason behind this strict exclusion criteria was to attribute the observed influence to the direct effect of weight loss following bariatric surgery. Clarifying why GCS improvement precedes GLS and its explanation requires further investigation with a larger sample size to elucidate the early impact of bariatric surgery on enhancing layer-specific strain. This study assessed only proximal RVOT in the parasternal long-axis view, as acquiring the true short-axis view of the RVOT needs stable and constant landmarks, which is challenging in obese patients.

Besides, as we did not evaluate patients’ clinical outcomes, taking this improvement in GLS and GCS and mechanical dispersion into clinical practice is not applicable. Considering RV size in echocardiography is challenging, and adhering to chamber quantification guidelines was pursued to minimize the variability in RV measurement. Due to the small sample size, defining a new threshold for abnormal RV size was impossible. The lack of significant changes in RV size post-surgery despite significant weight loss may be due to the early time of follow-ups and the relatively healthy groups of morbidly obese patients. Again, the small study population prevents extrapolating the improvement of 2D speckle indices and RV size to all post-bariatric surgery patients.

Speckle-tracking echocardiography has proven that bariatric surgery may enhance left ventricular function. Changes in right ventricular size should be considered and assessed during echocardiography in obese patients after weight loss.