A global obesity pandemic, coupled with an increasingly ageing population, is exacerbating the burden of cardiovascular disease. Indeed, clinical and experimental evidence underscores a potential connection between obesity and ageing in the pathogenesis of various cardiovascular disorders. This is further supported by the notion that weight reduction not only effectively reduces major cardiovascular events in elderly individuals but is also considered the gold standard for lifespan extension, in obese and non-obese model organisms. This review evaluates the intricate interplay between obesity and ageing from molecular mechanisms to whole organ function within the cardiovascular system. By comparatively analysing their characteristic features, shared molecular and cell biological signatures between obesity and ageing are unveiled, with the intent to shed light on how obesity accelerates cardiovascular ageing. This review also elaborates on how emerging metabolic interventions targeting obesity might protect from cardiovascular diseases largely through antagonizing key molecular mechanisms of the ageing process itself. In sum, this review aims to provide valuable insight into how understanding these interconnected processes could guide the development of novel and effective cardiovascular therapeutics for a growing aged population with a concerning obesity problem.

Cardiovascular effects of obesity may be driven, in part, by the distribution of fat. More recently, epicardial adipose tissue (EAT) has gained recognition as an adverse visceral fat impacting cardiac dysfunction in heart failure with preserved ejection fraction (HFpEF).

EAT can be identified and measured using several non-invasive imaging techniques, including transthoracic echocardiography, computed tomography, and cardiac magnetic resonance. The presence of EAT is associated with increased risk of HFpEF and worse clinical outcomes among patients with established HFpEF, independent of total adiposity. EAT may serve a pivotal role in the pathogenesis of HFpEF by worsening volume distribution, enhancing pericardial restraint and ventricular interaction, worsening right ventricular dysfunction, and diminishing exercise tolerance. No large trials have tested the effects of reducing fat in specific areas of the body on cardiovascular outcomes, but some studies that followed people in communities and trials over time have suggested that drug and non-drug treatments that lower EAT could improve the risk factors for heart problems in patients with HFpEF. Further understanding the role that pathogenic fat depots play in HFpEF incidence and progression may provide future therapeutic targets in treating the obese-HFpEF phenotype.

To investigate the longitudinal changes in left ventricular (LV) structure and function after bariatric surgery in obese individuals and their relationship with preoperative left ventricular ejection fraction (LVEF) by cardiac magnetic resonance (CMR) imaging.

We prospectively enrolled 75 obese subjects scheduled for laparoscopic sleeve gastrectomy and 46 age and sex-matched healthy controls (the control group). All subjects underwent CMR examination to obtain LV structural parameters, LVEF, and strain parameters. According to their preoperative LVEF, the obese subjects were divided into two obesity groups, including the group of patients with LVEF≥60% (n=43) and the group of patients with 50%≤LVEF<60% (n=32). LV structural and functional differences between the control group and the two obesity groups were compared. Eventually, 38 obese subjects completed the CMR follow-up at 1 month and 12 months after bariatric surgery. The longitudinal changes in LV structure and function after surgery in the LVEF≥60% (n=20) group and the 50%≤LVEF<60% group (n=18) were compared.

Before bariatric surgery, the global longitudinal strain was significantly lower in the LVEF≥60% group than that in the control group ([－18.36±1.86]% vs. [－19.50±1.53]%, P<0.05). The global radial ([27.70±3.52]% vs. [34.44±4.11]%, P<0.05), circumferential ([－17.35±1.46]% vs. [－19.85±1.42]%, P<0.05), and longitudinal ([－16.22±1.81]% vs. [－19.50±1.53]%, P<0.05) strain in the 50%≤LVEF<60% group was significantly lower than that in the control group. At 12 months after bariatric surgery, the global radial ([32.52±7.84]% vs. [30.92±4.27]%, P>0.05), circumferential ([－19.02±2.42]% vs. [－18.63±1.49]%, P>0.05), and longitudinal ([－18.18±2.06]% vs. [－17.78±1.66]%, P>0.05) strain in the LVEF≥60% group showed no significant difference compared with the baseline findings. In the 50%≤LVEF<60% group, the global radial ([32.73±5.86]% vs. [26.83±4.85]%, P<0.05) and circumferential ([－19.10±2.00]% vs. [－16.91±2.09]%, P<0.05) strain was significantly higher than that before surgery.

LV remodeling is reversed after bariatric surgery in obese subjects, and the longitudinal changes in LV structure and function vary with the preoperative LVEF.

Epicardial adipose tissue, or epicardial fat, is a type of visceral fat located between the heart and the pericardium. Due to its anatomical proximity to the heart, EAT plays a significant role in both cardiac physiology and pathologies, including cardiac remodeling and cardiovascular diseases (CVD). However, our understanding of how EAT pathology is influenced by risk factors such as obesity and type 2 diabetes mellitus and how altered EAT can drive cardiac remodeling and CVD, remains limited. Herein, we aimed to summarize and discuss the latest findings on EAT and its role in cardiac remodeling, highlighting the outcomes of clinical and observational studies, provide mechanistic insights, and finally introduce emerging therapeutic agents and nutritional guidelines aimed at preventing these conditions.

Surgical weight loss (SWL) improves myocardial mechanics as measured by speckle-tracking imaging. However non-surgical versus SWL and the subsequent impact on myocardial function in overweight Asian subjects has not been evaluated. 66 patients underwent a 16-week lifestyle intervention (LSI) programme consisting of dietary interventions and exercise prescription. Echocardiography with speckle tracking was performed at baseline and post-intervention. This group was compared against a group of 12 subjects who had undergone bariatric surgery and a control group of 10 lean Asian subjects. A generalised structural equation model (gSEM) was constructed to ascertain the effect of modality of weight loss on strain parameters, adjusting for BMI. Participants attained significant weight loss after LSI (28.2 ± 2.66 kg/m2 vs. 25.8 ± 2.84 kg/m2, p = 0.001). This was associated with a non-significant trend towards improvement in strain parameters. SWL participants had significant improvement in the left ventricular global longitudinal strain (- 20.52 ± 3.34 vs. - 16.68 ± 4.15, p < 0.01) and left atrium reservoir strain (44.32 ± 14.23 vs. 34.3 ± 19.31, p = 0.02). Lean subjects had significantly higher strain parameters than overweight subjects. The gSEM model demonstrated surgical modality of weight loss as an independent predictor of improvement in strain parameters. Significant improvement in echocardiographic parameters were documented in patients who underwent bariatric surgery.

Obesity is commonly linked with heart failure (HF) with preserved ejection fraction, with diastolic dysfunction playing an important role in this type of HF. However, diastolic function has not been well clarified in obese patients free of overt comorbidities. We aimed to comprehensively assess diastolic function in adults with uncomplicated obesity by combining left atrial (LA) and left ventricular (LV) strain and ventricular volume-time curve based on cardiac magnetic resonance (CMR), and to evaluate its association with body fat distribution.

A cross-sectional study was conducted with 49 uncomplicated obese participants and 43 healthy controls who were continuously recruited in West China Hospital, Sichuan University from September 2019 to June 2022. LA strain indices [total, passive, and active strains (εs, εe, and εa) and peak positive, early negative, and late negative strain rates (SRs, SRe, and SRa)], LV strain rates [peak diastolic strain rate (PDSR) and peak systolic strain rate (PSSR)], and LV volume-time curve parameters [peak filling rate index (PFRI) and peak ejection rate index (PERI)] were measured. Body fat distribution was assessed by dual-energy X-ray absorptiometry. Correlation between body fat distribution and LA and LV function was evaluated by multiple linear regression.

The obese participants had impaired diastolic function, manifested as lower LV circumferential and longitudinal PDSR (1.3±0.2 vs. 1.5±0.3 s-1, P=0.014; 0.8±0.2 vs. 1.1±0.2 s-1, P<0.001), LV PFRI (3.5±0.6 vs. 3.9±0.7 s-1, P=0.012), and declined LA reservoir function [εs and SRs (46.4%±8.4% vs. 51%±12%, P=0.045; 1.9±0.5 vs. 2.3±0.5 s-1, P<0.001)] and conduit function [εe and SRe (30.8%±8.0% vs. 35.5%±9.8%, P=0.019; -3.1±0.8 vs. -3.5±1.0 s-1, P=0.030)] compared with controls. The LA pumping function (εa and SRa) and LV systolic function [LV ejection fraction (LVEF), PSSR and PERI] were not different between obese and control participants. Multivariable analysis indicated that trunk fat had independent relationships with LA εe (β=-0.520, P<0.001) and LV circumferential PDSR (β=-0.418, P=0.003); visceral fat and peripheral fat were associated with LV longitudinal PDSR (β=-0.342, P=0.038; β=0.376, P=0.024); gynoid fat was associated with LA εs (β=0.384, P=0.014) and PFRI (β=0.286, P=0.047) in obesity.

The obese participants (uncomplicated obese adults with preserved LVEF) had impaired subclinical diastolic function. Central adipose tissue deposits (trunk fat and visceral fat) may exhibit inverse relationships with LV and LA function in obesity. However, peripheral adipose tissue deposits (peripheral fat and gynoid fat) may show positive relationships with LV and LA function.

Epicardial adipose tissue (EAT) is unique type of visceral adipose tissue, sharing the same microcirculation with myocardium. This study aimed to assess the imaging features of EAT in patients with acute myocarditis (AM) and explore the relationships with clinical characteristics.

For this retrospective case-control study, totally 38 AM patients and 52 controls were screened retrospectively from January 2019 to December 2022, and the EAT volume was measured from coronary computed tomography (CT) angiography imaging. Histogram analysis was performed to calculate parameters like the mean, standard deviation, interquartile range and percentiles of EAT attenuation. Whether EAT features change was assessed when clinical characteristics including symptoms, T wave abnormalities, pericardial effusion (PE), impairment of systolic function, and the need for intensive care presented.

The EAT volume (75.2±22.8 mL) and mean EAT attenuation [-75.8±4.4 Hounsfield units (HU)] of the AM group was significantly larger than the control group (64.7±26.0 mL, P=0.049; -77.9±5.0 HU, P=0.044). Among the clinical characteristics, only the presence of PE was associated with changes in EAT features. Patients with PE showed significantly changes in EAT attenuation including mean attenuation [analysis of variance (ANOVA) P=0.001] and quantitative histogram parameters. The mean attenuation of patients with PE (-71.9±4.0 HU) was significantly larger than controls (-77.9±5.0 HU, Bonferroni corrected P<0.001) and patients without PE (-77.4±3.5 HU, Bonferroni corrected P=0.003). Observed in histogram, the overall increase in EAT attenuation could lead to decrease in EAT volume, which resulted in no statistically significant difference in EAT volume between the AM patients with PE and controls (64.7±26.0 vs. 72.2±28.3 mL, Bonferroni corrected P>0.99).

Compared to controls, EAT volume was significantly larger in AM, and EAT attenuation increased notably in the presence of PE. We recommend evaluating EAT volume and attenuation simultaneously when quantifying EAT using CT attenuation thresholds.

Obesity is often associated with multiple comorbidities. However, whether obese subjects with hyperlipidemia in the absence of other complications have worse cardiac indices than metabolically healthy obese subjects is unclear. Therefore, we aimed to determine the effect of hyperlipidemia on subclinical left ventricular (LV) function in obesity and to evaluate the association of cardiac parameters with body fat distribution.

Ninety-two adults were recruited and divided into 3 groups: obesity with hyperlipidemia (n = 24, 14 males), obesity without hyperlipidemia (n = 25, 13 males), and c ntrols (n = 43, 25 males). LV strain parameters (peak strain (PS), peak diastolic strain rate (PDSR), peak systolic strain rate) derived from cardiovascular magnetic resonance tissue tracking were measured and compared. Dual-energy X-ray absorptiometer was used to measure body fat distribution. Correlations of hyperlipidemia and body fat distribution with LV strain were assessed by multivariable linear regression.

Obese individuals with preserved LV ejection fraction showed lower global LV longitudinal, circumferential, and radial PS and longitudinal and circumferential PDSR than controls (all P < 0.05). Among obese patients, those with hyperlipidemia had lower longitudinal PS and PDSR and circumferential PDSR than those without hyperlipidemia (- 12.8 ± 2.9% vs. - 14.2 ± 2.7%, 0.8 ± 0.1 s-1 vs. 0.9 ± 0.3 s-1, 1.2 ± 0.2 s-1 vs. 1.4 ± 0.2 s-1; all P < 0.05). Multivariable linear regression demonstrated that hyperlipidemia was independently associated with circumferential PDSR (β = - 0.477, P < 0.05) in obesity after controlling for growth differences, other cardiovascular risk factors, and central fat distribution. In addition, android fat had an independently negative relationship with longitudinal and radial PS (β = - 0.486 and β = - 0.408, respectively; all P < 0.05); and visceral fat was negatively associated with longitudinal PDSR (β = - 0.563, P < 0.05). Differently, gynoid fat was positively correlated with circumferential PS and PDSR and radial PDSR (β = 0.490, β = 0.481, and β = 0.413, respectively; all P < 0.05).

Hyperlipidemia is independently associated with subclinical LV diastolic dysfunction in obesity. Central fat distribution (android and visceral fat) has a negative association, while peripheral fat distribution (gynoid fat) has a positive association on subclinical LV function. These results suggest that appropriate management of hyperlipidemia may be beneficial for obese patients, and that the differentiation of fat distribution in different regions may facilitate the precise management of obese patients. Clinical trials registration Effect of lifestyle intervention on metabolism of obese patients based on smart phone software (ChiCTR1900026476).

Obesity has become a serious public health issue, significantly elevating the risk of various complications. It is a well-established contributor to Heart failure with preserved ejection fraction (HFpEF). Evaluating HFpEF in obesity is crucial. Epicardial adipose tissue (EAT) has emerged as a valuable tool for validating prognostic biomarkers and guiding treatment targets. Hence, assessing EAT is of paramount importance. Cardiovascular magnetic resonance (CMR) imaging is acknowledged as the gold standard for analyzing cardiac function and morphology. We hope to use CMR to assess EAT as a bioimaging marker to evaluate HFpEF in obese patients.

To assess the diagnostic utility of CMR for evaluating heart failure with preserved ejection fraction [HFpEF; left ventricular (LV) ejection fraction ≥ 50%] by measuring the epicardial adipose tissue (EAT) volumes and EAT mass in obese patients.

Sixty-two obese patients were divided into two groups for a case-control study based on whether or not they had heart failure with HFpEF. The two groups were defined as HFpEF+ and HFpEF-. LV geometry, global systolic function, EAT volumes and EAT mass of all subjects were obtained using cine magnetic resonance sequences.

Forty-five patients of HFpEF- group and seventeen patients of HFpEF+ group were included. LV mass index (g/m2) of HFpEF+ group was higher than HFpEF- group (P < 0.05). In HFpEF+ group, EAT volumes, EAT volume index, EAT mass, EAT mass index and the ratio of EAT/[left atrial (LA) left-right (LR) diameter] were higher compared to HFpEF- group (P < 0.05). In multivariate analysis, Higher EAT/LA LR diameter ratio was associated with higher odds ratio of HFpEF.

EAT/LA LR diameter ratio is highly associated with HFpEF in obese patients. It is plausible that there may be utility in CMR for assessing obese patients for HFpEF using EAT/LA LR diameter ratio as a diagnostic biomarker. Further prospective studies, are needed to validate these proof-of-concept findings.

Glucagon-like peptide-1 receptor agonist(GLP-1RA) is commonly used in patients with cardiovascular disease due to its significant improvement in the prognosis of atherosclerotic cardiovascular disease (ASCVD). However, previous studies have primarily focused on obese patients, leaving uncertainty regarding whether GLP-1RA can yield similar cardiovascular benefits in individuals with normal or low body weight.

In this study, we enrolled patients with ASCVD to establish a retrospective cohort. Patients receiving GLP-1RA treatment were assigned to the GLP-1RA group, while a control group was formed by matching age and body mass index (BMI) among patients not receiving GLP-1RA treatment. Each group was further divided into subgroups based on baseline BMI levels: normal weight, overweight, and obesity. A six-month follow-up was conducted to assess changes in patient weight, metabolic indicators, and cardiac structure and function.

Among the normal weight subgroup, no significant weight change was observed after six months of GLP-1RA treatment (57.4 ± 4.8 vs. 58.7 ± 9.2, p = 0.063). However, significant weight reduction was observed in the other two subgroups (Overweight group: 70.0 ± 9.1 vs. 73.1 ± 8.2, p = 0.003, Obesity group: 90.5 ± 14.3 vs. 95.5 ± 16.6, p<0.001). Regardless of baseline BMI levels, GLP-1RA demonstrated significant glucose-lowering effects in terms of metabolic indicators. However, GLP-1RA have a more significant effect on improving blood lipids in overweight and obese patients. The effects of GLP-1RA on cardiac structure exhibited variations among patients with different baseline BMI levels. Specifically, it was observed that the improvement in atrial structure was more prominent in patients with normal body weight(LAD: 33.0 (30.3, 35.5) vs. 35.0 (32.5, 37.1), p = 0.018, LAA (18.0 (16.0, 21.5) vs. 18.5 (16.5, 20.5), p = 0.008), while the enhancement in ventricular structure was more significant in obese subjects(LEVDD: 49.8 ± 5.8 vs. 50.2 ± 5.0, p < 0.001, LVMI: 65.1 (56.2, 71.4) vs. 65.8 (58.9, 80.4), p < 0.039).

According to the study, it was found that the administration of GLP-1RA can have different effects on cardiac structure in patients with different baseline BMI, In obese patients, improvements in ventricular remodeling may be more associated with weight loss mechanisms, while in patients with normal or low BMI, GLP-1RA may directly improve atrial remodeling through GLP-1 receptors in atrial tissue.

To identify subclinical left ventricle dysfunction (LVD) in obese rats by speckle-tracking echocardiography, and to evaluate the effects of 12-week Moderate-Intensity Continuous Training (MICT) or High-Intensity Interval Training (HIIT) on LV geometry, histology and function in obese rats.

Eighteen male standard or obese Sprague-Dawley rats were randomly divided into the Control group, the MICT group, and the HIIT group. Exercise interventions were conducted for 12 weeks, with equal total load and increased intensity gradient. Using dual-energy X-ray, two-dimensional speckle-tracking echocardiography, pulse Doppler, and HE staining to evalucate body shape, LV morphology, structure, and myocardial mechanics function.

(1) Both MICT and HIIT have good weight loss shaping effect. (2) The LV of obese rats underwent pathological remodeling, with decreased longitudinal contractility and synchrony, and increased circumferential contractility and synchrony. (3) Exercise can inhibit LV pathological remodeling, improve myocardial mechanical function. HIIT is superior to MICT. (4) The global longitudinal strain of obese rats in the HIIT group showed a significant correlation with Fat% and Lean%.

Obesity can induce LV pathological remodeling and subclinical dysfunction. Compared with MICT, 12-week HIIT can effectively inhibit the pathological remodeling of LV and promote the benign development of myocardial mechanical function in obese rats.

Obesity and insulin resistance are prevalent in heart failure with preserved ejection fraction (HFpEF) and are associated with adverse cardiovascular outcomes. Measuring insulin resistance is difficult outside of research settings, and its correlation to parameters of myocardial dysfunction and functional status is unknown.

A total of 92 HFpEF patients with New York Heart Association class II to IV symptoms underwent clinical assessment, 2D echocardiography, and 6-min walk (6 MW) test. Insulin resistance was defined by estimated glucose disposal rate (eGDR) using the formula: eGDR = 19.02 - [0.22 × body mass index (BMI), kg/m2] - (3.26 × hypertension, presence) - (0.61 × glycated hemoglobin, %). Lower eGDR indicates increased insulin resistance (unfavorable). Myocardial structure and function were assessed by left ventricular (LV) mass, average E/e' ratio, right ventricular systolic pressure, left atrial volume, LV ejection fraction, LV longitudinal strain (LVLS), and tricuspid annular plane systolic excursion. Associations between eGDR and adverse myocardial function were evaluated in unadjusted and multivariable-adjusted analyses using analysis of variance testing and multivariable linear regression.

Mean age (SD) was 65 (11) years, 64 % were women, and 95 % had hypertension. Mean (SD) BMI was 39 (9.6) kg/m2, glycated hemoglobin 6.7 (1.6) %, and eGDR 3.3 (2.6) mg × kg-1 min-1. Increased insulin resistance was associated with worse LVLS in a graded fashion [mean (SD) -13.8 % (4.9 %), -14.4 % (5.8 %), -17.5 % (4.4 %) for first, second, and third eGDR tertiles, respectively, p = 0.047]. This association persisted after multivariable adjustment, p = 0.040. There was also a significant association between worse insulin resistance and decreased 6 MW distance on univariate analysis, but not on multivariable adjusted analysis.

Our findings may inform treatment strategies focused on the use of tools to estimate insulin resistance and selection of insulin sensitizing drugs which may improve cardiac function and exercise capacity.

To evaluate the left ventricular (LV) myocardial tissue characteristics in early adult obesity and its association with regional adipose tissue and ectopic fat deposition.

Forty-nine obese adults (mean body mass index: 29.9 ± 2.0 kg/m2) and 44 healthy controls were prospectively studied. LV native and post-contrast T1 values, extracellular volume fraction (ECV), regional adipose tissue (epicardial, visceral, and subcutaneous adipose tissue (EAT, VAT, and SAT)), and ectopic fat deposition (hepatic and pancreatic proton density fat fractions (H-PDFF and P-PDFF)) based on magnetic resonance imaging were compared. The association was assessed by multivariable linear regression.

The obese participants showed reduced global ECV compared to the healthy controls (p < 0.05), but there was no significant difference in global native or post-contrast T1 values between the two groups. Additionally, the obese individuals exhibited higher EAT, VAT, SAT, H-PDFF, and P-PDFF than the controls (p < 0.05). ECV was associated with insulin resistance, dyslipidemia, and systolic blood pressure (SBP) (p < 0.05). Multiple linear regression demonstrated that H-PDFF and SAT were independently associated with ECV in entire population (β =  - 0.123 and - 0.012; p < 0.05).

Reduced myocardial ECV in patients with mild-to-moderate obesity and its relationship to SBP may indicate that cardiomyocyte hypertrophy, rather than extracellular matrix expansion, is primarily responsible for myocardial tissue remodeling in early adult obesity. Our findings further imply that H-PDFF and SAT are linked with LV myocardial tissue remodeling in this cohort beyond the growth difference and cardiovascular risk factors.

Effect of lifestyle intervention on metabolism of obese patients based on smart phone software (ChiCTR1900026476).

Myocardial fibrosis in severe obesity predicts poor prognosis. We showed that cardiomyocyte hypertrophy, not myocardial fibrosis, is the main myocardial tissue characteristic of early obesity. This finding raises the possibility that medical interventions, like weight loss, may prevent cardiac fibrosis.

• Myocardial tissue characteristics in early adult obesity are unclear. • Myocardial extracellular volume fraction (ECV) can be quantitatively evaluated using T1 mapping based on cardiac magnetic resonance imaging (MRI). • Cardiac MRI-derived ECV may noninvasively evaluate myocardial tissue remodeling in early adult obesity.

Epicardial adipose tissue (EAT) contributes to inflammation and fibrosis of the neighboring myocardial tissue via paracrine signaling. In this retrospective study, we investigated the abnormal changes in the amount of EAT in male children with Duchenne muscular dystrophy (DMD) using cardiac magnetic resonance (CMR) imaging. Furthermore, we constructed and validated a nomogram including EAT-related CMR imaging parameter for predicting the occurrence of myocardial fibrosis in patients with DMD.

This study enrolled 283 patients with DMD and 57 healthy participants who underwent CMR acquisitions to measure the quantitative parameters of EAT, pericardial adipose tissue (PAT), paracardial adipose tissue, and subcutaneous adipose tissue. Late gadolinium enhancement (LGE) was performed to confirm myocardial fibrosis in patients with DMD. The DMD group consisted of 200 patients from institution 1 (the ratio of the training set and the internal validation set was 7:3) and 83 patients from four other institutions (the external validation set). Logistic and least absolute shrinkage and selection operator (LASSO) regression was used to select the optimal predictors and to develop and validate the nomogram model predicting LGE risk in the training set, internal validation set, and external validation set.

Compared with those in healthy controls, some regional EAT thicknesses, areas, and global volumes were significantly higher in patients with DMD, and 41.7% of patients with DMD showed positive LGE. These LGE-positive patients with DMD showed significantly higher EAT volume (median 23.9 mL/m3; P<0.001) and PAT volume (median 31.8 mL/m3; P<0.001) compared with the LGE-negative patients with DMD. Age [odds ratio (OR) 2.0; P<0.001], body fat percentage (OR 1.3; P<0.001), and EAT volume (OR 1.4; P<0.001) were independently associated with positive LGE in the training set. The interactive dynamic nomogram showed superior prediction performance, with a high degree of the calibration, discrimination, and clinical net benefit in the training and validation of the DMD datasets. The area under the curve (AUC) values of the nomogram in the training set, internal validation set, and external validation set were 0.95 [95% confidence interval (CI): 0.91-0.98], 0.97 (95% CI: 0.92-0.99), and 0.95 (95% CI: 0.91-0.99), respectively.

The onset of LGE-based myocardial fibrosis was associated with EAT volume in patients with DMD. Additionally, the nomogram with EAT volumes showed superior performance in patients with DMD for predicting the occurrence of myocardial fibrosis.

Cardiac remodeling and dysfunction can be caused by atrial fibrillation (AF). The aim of this research is to investigate the relationship between the systemic inflammatory response index (SIRI) and left ventricular (LV) remodeling and systolic function in individuals with AF.

416 patients with AF who were admitted to the Second Department of Cardiology in the East Ward of the Qingdao Municipal Hospital between January 2020 and May 2022 were included in the present retrospective research. The relationship between SIRI and various cardiac parameters was analyzed. The patients' left atrial (LA) enlargement and left ventricular (LV) hypertrophy and systolic dysfunction were evaluated. SIRI was calculated by the formula: neutrophil × monocyte/lymphocyte.

SIRI significantly correlated with LV end-diastolic diameter (LVDd), LV posterior wall thickness at end-diastole (LVPWTd), interventricular septal thickness at end-diastole (IVSTd), LV mass index (LVMI), LV ejection fraction (LVEF), LA diameter (LAD), C-reactive protein (CRP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in patients with AF. In multivariate linear regression analyses, SIRI was discovered to be significantly related to LVMI (ln-transformed) (p = 0.025), LVEF (ln-transformed) (p = 0.005), and LAD (ln-transformed) (p = 0.007). In multivariate logistic regression, the highest quartile of SIRI (SIRI > 1.62) was significantly associated with LV hypertrophy (p = 0.026), impaired LV systolic function (p = 0.002), and LA enlargement (p = 0.025).

SIRI was significantly associated with LV remodeling and systolic function impairment in patients with AF. SIRI may serve as a reliable and convenient inflammatory biomarker for detecting impaired cardiac structure and systolic function in patients with AF.

We sought to investigate the correlation of pericoronary adipose tissue with coronary artery disease and left ventricular (LV) function.

Participants with clinically suspected coronary artery disease were enrolled. All participants underwent coronary computed tomography angiography (CCTA) and echocardiography followed by invasive coronary angiography (ICA) within 6 months. Pericoronary adipose tissue (PCAT) was extracted to analyze the correlation with the Gensini score and LV function parameters, including IVS, LVPW, LVEDD, LVESD, LVEDV, LVESV, FS, LVEF, LVM, and LVMI. The correlation between PCAT and the Gensini score was assessed using Spearman's correlation analysis, and that between the PCAT volume or FAI and LV function parameters was determined using partial correlation analysis.

One hundred and fifty-nine participants (mean age, 64.55 ± 10.64 years; men, 65.4% [104/159]) were included in the final analysis. Risk factors for coronary artery disease, such as hypertension, diabetes, dyslipidemia, and a history of smoking or drinking, had no significant association with PCAT (P > 0.05), and there was also no correlation between PCAT and the Gensini score. However, the LAD-FAI was positively correlated with the IVS (r = 0.203, P = 0.013), LVPW (r = 0.218, P = 0.008), LVEDD (r = 0.317, P < 0.001), LVESD (r = 0.298, P < 0.001), LVEDV (r = 0.317, P < 0.001), LVESV (r = 0.301, P < 0.001), LVM (r = 0.371, P < 0.001), and LVMI (r = 0.304, P < 0.001). Also, the LCX-FAI was positively correlated with the LVEDD (r = 0.199, P = 0.015), LVESD (r = 0.190, P = 0.021), LVEDV (r = 0.203, P = 0.013), LVESV (r = 0.197, P = 0.016), LVM (r = 0.220, P = 0.007), and LVMI (r = 0.172, P = 0.036), and the RCA-FAI was positively correlated with the LVEDD (r = 0.258, P = 0.002), LVESD (r = 0.238, P = 0.004), LVEDV (r = 0.266, P = 0.001), LVESV (r = 0.249, P = 0.002), LVM (r = 0.237, P = 0.004), and LVMI (r = 0.218, P = 0.008), respectively. Finally, the total volume was positively correlated with FS (r = 0.167, P = 0.042).

The FAI was positively correlated with the LV function but was not associated with the severity of coronary artery disease.