Visceral Adiposity：A Potential Marker for Mortality Risk in Heart Failure with Preserved Ejection Fraction?

doi:10.21203/rs.3.rs-2324354/v1

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Research Article

Visceral Adiposity：A Potential Marker for Mortality Risk in Heart Failure with Preserved Ejection Fraction?

https://doi.org/10.21203/rs.3.rs-2324354/v1

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Background

Recent research reports that regional adiposity, notably epicardial and visceral fat, may serve a pivotal pathophysiologic role in heart failure with preserved ejection fraction (HFpEF). We aimed to describe the role of regional adiposity in predicting all-cause death in patients with HFpEF.

Methods

This was a prospective cohort study in patients with HFpEF, and the primary outcome of this study was all-cause mortality. Visceral fat area (VFA) was measured through the multifrequency bioelectrical impedance analyzer (BIA). The thickness of epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) was measured by echocardiography. Cox regression analysis was used to evaluate the predicted effect of the potential risk factors. Test for interaction was used to estimate whether the prognostic value of VFA was affected by subgroups of potential risk confounders.

Results

A total of 172 patients with an average age of 72 years were analyzed, of which 59.9% (n = 103) were females. 66% were hypertensive and 40% had atrial fibrillation (AF). The best cutoff value of VFA for all-cause death was 148.3cm². The all-cause mortality rate in the VFA ≥ 148.3 cm² group was significantly higher than in the VFA < 148.3 cm² group. Patients with higher VFA were older, with higher body mass index (BMI), and more frequently with pre-existing hypertension and atrial fibrillation. Age, smoking, BMI, H2PEFF score, and VFA were significantly associated with higher mortality in HFpEF by univariable Cox analysis. However, PAT thickness, EAT thickness, waist/hip ratio, body fat mass, and abdominal obesity were not effective predictors of HFpEF outcomes. After adjusting for cofounders of other underlining risk factors, VFA could independently predict all-cause mortality in HFpEF. In addition, results were broadly consistent in participants with different baseline characteristics.

Conclusions

VFA may be a useful prognostic risk factor for all-cause mortality in patients with HFpEF.

Trial registration

NCT05496439 (08/10/2022), retrospectively registered.

Prospective cohort study

HFpEF

VFA

regional adiposity

Obesity is one of the main factors in the development of heart failure (HF), especially HF with preserved ejection fraction (HFpEF) (1). Recent studies reported that regional adiposity, notably epicardial and visceral fat, might serve a pivotal pathophysiologic role in HFpEF, contributing to the loss of cardiopulmonary fitness, left ventricular compliance, and neurohormonal balance, and to the increase of local and systemic inflammation, intra-abdominal pressure and vascular congestion(2).

The accumulations in epicardial and visceral adiposity, rather than body mass index (BMI), subcutaneous fat or body components are associated with the incidence of HFpEF (2, 3). Our previous studies have demonstrated that both epicardial and visceral fat were closely related to arterial stiffness in patients with HFpEF (4, 5). And the latest study reported excess visceral fat was associated with cardiometabolic risk factors by compositional data analysis (6). The TOPCAT trial reported the prognostic value of abdominal obesity on adverse outcomes of HFpEF (7). However, a cohort of 572 adults, in which 64% without HF (n = 367), 20% with heart failure with reduced ejection fraction (HFrEF) (n = 113) and 16% with HFpEF (n = 92), revealed visceral abdominal fat failed to predict poor outcomes (8). Notably, research also reported that HFpEF patients in Asia possess a high burden of co-morbidities but a low scale of overweight (5, 9). Whether regional adiposities could predict outcomes of patients with HFpEF is not clear, and the issue is even more little known across Asia.

The aim of the present study is to describe the role of regional adiposity and anthropometric indicators such as waist/hip ratio and body fat mass in predicting all-cause death in patients with HFpEF in Asia. We also compared the effect of visceral fat area (VFA) on predicting mortality in subgroups considering sex, age, BMI, smoking and co-morbidities. We hope this study will provide some insights for Asia HFpEF and useful guidance for future clinical work on HFpEF.

Study Population

This is a prospective study that collected data from inpatients with HFpEF who were recruited at the First Affiliated Hospital of Chongqing Medical University from September 2020 to January 2022. A total of 297 inpatients diagnosed with HFpEF were initially considered for inclusion. Patients with severe liver insufficiency (elevated liver enzymes: 3 times over upper reference limit, or liver cirrhosis), severe kidney insufficiency (eGFR < 30ml/min/1.73m², based on CKD-EPI formula), history of autoimmune disease, cancer diagnosis at the beginning of the study, and left ventricular ejection fraction (LVEF) less than 50% at any time were not included. Finally, 172 participants recruited for this study and completed follow-up and the flow chart of participants were shown in supplemental Fig. 1. The study protocol was approved by the Ethics Committee of the First Affiliated Hospital of Chongqing Medical University and conformed to the Helsinki Declaration and registered with clinicaltrials.gov with the identifier NCT05496439. All participants provided written informed consent.

Definition Of Hfpef

All patients in the trial were required preserved ejection fraction (LVEF ≥ 50%) and decreased activity tolerance with New York Heart Association (NYHA) class II to IV. And, participants were also accorded with at least one criteria to evidence the relevant cardiac structural or functional change including left atrial volume index (LAVI) > 29 mL/m² for sinus rhythm or > 34 mL/m² for fibrillation and/or flutter rhythm, left ventricular mass index (LVMI) ≥ 115 g/m² for males or ≥ 95 for females, diastolic dysfunction (E/e’ ≥ 13; Septal e’ < 9cm/s, E/A > 2 or < 1), fibrillation and/or futter rhythm, or NT-proBNP ≥ 125 pg/mL for sinus rhythm or ≥ 375 pg/mL for fibrillation and/or flutter rhythm.

Data Collection

Subject demographics and clinical characteristics, including gender, age, vital signs, BMI, waist circumference, hip circumference, concomitant disease, smoking history, drinking history, laboratory tests, echocardiographic data, and body composition measurement data were recorded. The follow-up of the participants was completed via telephone contact under standard process.

Anthropometric Measurements

Body fat mass, muscle mass, skeletal muscle mass as well as the VFA of the subjects were measured through the multifrequency bioelectrical impedance analyzer (DBA-210, DONGHWA, China, certificate number 20202070083). Briefly, the subjects were asked to measure on an empty stomach, wearing light clothes, and stand barefoot vertically on the body composition analyzer in a quiet state. Data was gathered during the subjects held the hand electrode and kept their arms straight, and not in contact with the sides of the body. The body height and weight were measured using a rangefinder accurate to 0.1cm, and a digital scale accurate to 0.1 kg, respectively. Waist circumference and hip circumference were measured by a soft ruler while subjects were asked to stand with their feet 25 to 30 cm apart. All measurements were performed twice within 3 days after the admission, and the average of the 2 values was adopted.

Echocardiography

All the echocardiography data was examined using the same cardiac ultrasound machine (models: Vivid E95, AU11403, GE Vingmed Ultrasound AS). Epicardial adipose tissue (EAT) thickness and pericardial adipose tissue (PAT) thickness were measured on the free wall of the right ventricle (RV) in the parasternal long-axis view as previously reported (4).

Statistical Analysis

The study population was divided into VFA < 148.3 cm² group and VFA ≥ 148.3 cm² group based on the optimal prognostic cutoff from the receiver operating characteristic (ROC) curve. Continuous variables were expressed as mean ± SD or median (IQR), and conformity to normal distribution was tested using the Kolmogorov-Smirnov test (K-S test) or Shapiro-Wilk test (S-W test); categorical variables were expressed as percentages using independent samples T-test. Mann-Whitney U test or the Chi-square test to assess the difference between the two groups. Survival curves were constructed using the Kaplan-Meier method using the log-rank test. Cox regression analysis was used to evaluate the role of potential risk factors in prognosis. Variance inflation factor (VIF) values were calculated to measure the degree of multicollinearity among the variables, and a VIF of > 5 was considered indicative high correlation of the variables. To explore whether VFA interacts with different baseline characteristics including gender, age, BMI, smoking, hypertension, atrial fibrillation, coronary artery disease, and diabetes mellitus history, test for interaction was used in subgroup analysis. Differences with P value of < 0.05 were considered statistically significant, and all data analyses were performed using SPSS (Version 25.0. Armonk, NY: IBM Corp.).

Baseline Characteristics

The baseline characteristics of the study population were described in Table 1. According to the established selection process, the trial included 172 patients with an average age of 72 years, of which 40.1% (n = 69) were males, 59.9% (n = 103) were females, 66% with hypertension, and 40% with atrial fibrillation (AF). Patients were divided into the low VFA group (VFA < 148.3 cm²) and the high VFA group (VFA ≥ 148.3 cm²) based on the optimal prognostic cutoff. The median follow-up duration was 395.5 days (interquartile range: 207.5 to 535.5 days), during which 7 patients died.

Table 1

Characteristics of the Study Population According to Visceral Fat Area.
Variables	Entire cohort (n = 172)		VFA < 148.3cm² (n = 135)	VFA ≥ 148.3 cm² (n = 37)	P value
Gender (Women, %)	103 (59.88%)		80 (59.26%)	23 (62.16%)	0.750
Age (years)	72.0 (65.0, 80.0)		71.0 (61.0, 78.0)	79.0 (72.5, 83.5)	< 0.001
Smoking (n, %)	38 (22.09%)		30 (22.22%)	8 (21.62%)	0.938
H2PEFF risk score	3.0 (2.0, 5.0)		3.0 (2.0, 5.0)	5.0 (4.0, 6.5)	< 0.001
HFA-PEFF risk score	5 (4, 6)		4 (4, 6)	5 (4, 6)	0.244
Death (%)	7 (4.07%)		1 (0.74%)	6 (16.22%)	< 0.001
Anthropometrics
BMI (kg/m²)	23.82 ± 3.55		22.95 ± 3.06	27.01 ± 3.42	< 0.001
Waist/Hip ratio	0.92 (0.88, 0.96)		0.92 (0.88, 0.96)	0.94 (0.90, 0.99)	0.043
Body fat mass (kg)	16.43 ± 7.23		14.25 ± 5.59	24.37 ± 7.02	< 0.001
Muscle mass (kg)	40.08 ± 7.96		39.90 ± 8.16	40.73 ± 7.28	0.583
Skeletal muscle mass (kg)	22.70 (19.78, 26.45)		22.70 (19.50, 26.45)	22.90 (20.30, 26.73)	0.813
VFA (cm²)	131.35 (109.60, 145.95)		124.30 (105.00, 136.00)	157.80 (152.90, 173.10)	< 0.001
Abdominal obesity* by WC (n, %)	41 (27.33%^#)		21 (18.42%)	20 (55.56%)	< 0.001
Abdominal obesity** by VFA (n, %)	144 (83.72%)		107 (79.26%)	37 (100%)	0.002
Concomitant disease
Hypertension (n, %)	114(66.28%)		82 (60.74%)	32 (86.49%)	0.003
AF (n, %)	70 (40.70%)		46 (34.07%)	24 (64.86%)	0.001
CAD (n, %)	70 (40.70%)		55 (40.74%)	15 (40.54%)	0.982
DM (n, %)	60 (34.88%)		45 (33.33%)	15 (40.54%)	0.581
Laboratory data
CRP (mg/L)	4.15 (2.25, 9.95)		4.19 (2.17, 10.40)	3.61 (2.46, 8.78)	0.871
FBG (mmol/L)	5.35 (4.83, 6.28)		5.10 (4.75, 6.35)	5.60 (5.40, 6.10)	0.016
Ur (mmol/L)	7.00 (5.60, 9.28)		7.00 (5.60, 9.30)	6.50 (5.55, 8.60)	0.465
Cr (umol/L)	79.00 (63.25, 95.75)		78.00 (62.00, 94.00)	82.00 (72.50, 107.50)	0.148
TC (mmol/L)	3.62 (2.99, 4.61)		3.65 (3.08, 4.62)	3.61 (2.98, 4.37)	0.945
LDL (mmol/L)	2.04 (1.50, 2.63)		2.11 (1.51, 2.82)	1.92 (1.47, 2.53)	0.624
NT-proBNP (pg/mL)	1200 (500, 2671)		1071 (470, 2680)	1498 (870, 2550)	0.257
Echocardiographic data
LA (mm)		36 (31, 40)	36 (31, 39)	39 (35, 44)	0.004
LV (mm)		46 (43, 50)	45 (42, 50)	48 (45, 51)	0.008
RA (mm)		38.5 (35.0, 44.0)	37.0 (34.0, 45.0)	40.0 (36.5, 43.0)	0.357
RV (mm)		21 (20, 22)	21 (20, 24)	21 (20, 22)	0.466
LVPW (mm)		10.00 (9.75, 11.00)	10.00 (9.00, 11.00)	11.00 (10.00, 12.00)	0.013
IVST (mm)		11 (10, 12)	11 (9, 12)	11 (10, 12)	0.243
EF (%)		61 (58, 65)	62 (58, 66)	61 (57, 64)	0.100
e', septal (cm/s)		4.80 (3.90, 6.40)	4.80 (3.85, 6.40)	4.80 (3.90, 6.00)	0.889
E wave (cm/s)		70.55 (56.20, 93.25)	69.00 (56.90, 87.20)	84.40 (53.80, 108.00)	0.153
Mean E/e'		11.74 (8.97, 15.57)	11.48 (8.87, 15.16)	13.06 (9.41, 17.93)	0.195
TRV (cm/s)		263.00 (242.00, 311.80)	262.05 (242.00, 330.75)	263.00 (238.00, 308.00)	0.709
PASP (mmHg)		36.0 (30.0, 54.0)	36.0 (29.0, 56.0)	38.5 (30.0, 49.5)	0.827
LAVI (ml/m²)		39.00 (28.40, 50.60)	36.30 (27.60, 48.10)	45.07 (33.01, 60.20)	0.028
LVMI (g/m²)		109.00 (86.25, 137.00)	107.5 (85.30, 131.53)	116.95 (98.40, 140.53)	0.193
PAT (mm)		4.60 (3.70, 5.90)	4.35 (3.60, 5.58)	5.40 (4.10, 6.50)	0.041
EAT (mm)		4.10 (3.10, 5.80)	4.00 (3.00, 5.70)	4.50 (3.30, 6.20)	0.079
Values are mean ± standard deviation, number (%), or median (interquartile range).
*Defined as a waist circumference (WC) of ≥ 102 cm in men and ≥ 88 cm in women (21).
#Regarding abdominal obesity by WC, analyses were performed using 150 cases.
**Defined as visceral fat area ≥ 100 cm².

Patients in high VFA group were older and exhibited higher H2PEFF risk scores, more frequently pre-existing hypertension, and AF (P < 0.005). Patients with greater VFA were more likely to combine with obesity reflected by pericardial fat thickness, BMI, waist/hip ratio, abdominal obesity, and body fat mass (P < 0.05). The levels of fasting blood glucose (FBG), left atrial (LA), left ventricular (LV), left ventricular posterior wall (LVPW), and LAVI were higher in high VFA group than those in low VFA group (P < 0.05).

(We prefer to show Table 1 here)

Roc Curve For Prediction Of All-cause Mortality By Vfa In Patients With Hfpef

The primary outcome of this study was the death of HFpEF patients regardless of cause. Figure 1 showed the ROC curve of VFA for predicting mortality in patients with HFpEF. The area under the curve (AUC) was 0.842 (95% CI 0.666-1.000, P = 0.002), and the most sensitive and specific cutoff value of VFA was 148.3 cm² with 85.7% sensitivity and 81.2% specificity.

Prognostic Value Of Regional Adiposity

All patients underwent the survival outcome measurements. At the cutoff date for this study, 1 patient in the low VFA group and 6 patients in the high VFA group had died. One patient died from new onset cancer in the low VFA group. In the high VFA group, 4 patients happened cardiovascular death, 1 patient died from infection, and 1 patient passed away due to unclear reasons.

Figure 2 showed the relationship between visceral adiposity and long-term survival using the Kaplan–Meier curve. The survival was significantly better in patients with low VFA (P < 0.001).

In the univariable Cox analysis, the results showed that age, smoking, H2PEFF score, BMI, and VFA were significantly associated with higher mortality (Table 2), patients in high VFA group tended to display a higher risk of overall mortality (HR, 1.042; 95% CI 1.015–1.069; P = 0.002). However, other regional adiposity parameters including body fat mass, waist/hip ratio and abdominal obesity failed to predict outcomes. EAT thickness, PAT thickness, and the risk score of HFA-PEFF also had no statistical significance to predict all-cause death of HFpEF patients in the present study.

Table 2

Univariate analysis for all-cause mortality.
Variables	Univariable analysis
Variables	HR (95% CI)	P value
Age	1.117 (1.009, 1.236)	0.033
Gender	3.692 (0.716, 19.035)	0.119
Smoking	4.658 (1.042, 20.820)	0.044
BMI	1.188 (1.006, 1.402)	0.042
Waist/Hip ratio	0.363 (0.000, 386.109)	0.776
Abdominal obesity	1.982 (0.443, 8.866)	0.371
Body fat mass	1.071 (0.988, 1.161)	0.095
VFA	1.042 (1.015, 1.069)	0.002
FBG	0.993 (0.686, 1.438)	0.971
NT-proBNP	1.000 (1.000, 1.000)	0.333
PAT	0.985 (0.829, 1.170)	0.861
EAT	1.236 (0.849, 1.800)	0.268
H2PEFF	1.855 (1.150, 2.990)	0.011
HFA-PEFF	1.373 (0.714, 2.642)	0.342

(We prefer to show Table 2 here)

Multivariable And Subgroup Analyses

Figure 3 showed the results of multivariate analysis including VFA and other meaningful risk factors. In designed models, the VIFs were less than 5 for variables, and results of collinearity diagnosis were shown in supplemental table 1. After adjusting for age in Model 1, VFA (HR, 1.039; 95% CI 1.010–1.070; P = 0.009) was associated with overall mortality. In Model 2, the gender-adjusted HR for VFA was 1.043 (95% CI 1.016–1.071; P = 0.002). In Model 3, after adjusted for BMI, the association between VFA and mortality remained significant (HR, 1.056; 95% CI 1.006–1.109; P = 0.027). In Model 4, after adjusting for H2PEFF risk score and NT-proBNP, which were both confirmed as powerful prognostic factors in HFpEF (10, 11), VFA maintained significant relation with the adverse outcome (HR, 1.048; 95% CI 1.005–1.092; P = 0.026).

In the pre-specified subgroup analyses (total, 14 sub-cohorts, Fig. 4), there’s no interaction among VFA and gender, age, BMI, smoking, hypertension, AF, coronary artery disease, or diabetes mellitus history.

In the setting of a prospective study, patients with excess visceral adiposity possessed a phenotype of older, higher BMI, and more frequently with pre-existing hypertension and atrial fibrillation, and it was a novel finding to identify visceral adiposity as a risk factor of all-cause mortality during a median follow-up of 395.5 days in patients with HFpEF. The role of VFA on prediction outcomes was consistent in participants with different baseline characteristics.

Obesity and related metabolic syndrome are now regarded as one of the major drivers of HFpEF pathophysiology (3). Excess adipose promotes inflammation, hypertension, insulin resistance, dyslipidemia and impairs function of heart, arterial and skeletal muscle (12). BMI, on which the current definition of obesity was based, had been identified as a common risk factor for HFpEF, and higher BMI (BMI ≥ 35 kg/m²) was believed to be a distinct obese phenotype of HFpEF (13, 14). However, in contrast to western populations, the majority of eastern Asian patients with HFpEF are normal weight or even underweight (15), which highlights the limitations of BMI as the distinct phenotype for Asian HFpEF. In the present study, the average BMI of the patients was 23.82 kg/m² (far below the standard of obesity with BMI above 28 kg/m²) (16), while the rate of abdominal obesity was 27.33% calculated by waist circumference and 79.26% by VFA, indicating the different role of regional obesity in pathogenesis of HFpEF in Asia. It was further verified in cox regressions that VFA but not BMI were corelated with poor outcome in HFpEF (Fig. 3), indicating VFA might be better to depict the adverse outcomes of HFpEF.

Regional adiposities were reported to be highly heterogeneous according to the location, density, and composition (12). Visceral adipose tissue was believed to associate with deleterious metabolic consequences (17). And the deep subcutaneous adipose tissue (SAT) might have more adverse metabolic traits than the superficial (18, 19). Viscera-surrounding adipose tissues like EAT and perivascular adipose tissue, establish an important link between the dysfunctional metabolic profile and the adjacent cardiovascular remodeling (20), which was further verified by our previous studies in Asian population with HFpEF (4, 5). It was also reported that visceral adiposity might serve a role on the development of cardiometabolic disease by promoting diabetes, dyslipidaemia, and hypertension (2). These heterogeneous traits of adipose tissue endow regional adiposities with different roles on the pathological progress and perhaps the prognosis of HFpEF. In the current cohort, the effect of VFA on predicting all-cause death in HFpEF seemly surpassed the other regional adipose including PAT, EAT, body fat mass and abdominal obesity (Table 2).

To date, little is known about how visceral adiposities affect prognosis in HFpEF. The TOPCAT trial demonstrated that the all-cause mortality risk was significantly higher in patients with abdominal obesity (7). However, a post hoc analysis from the TOPCAT showed abdominal obesity is associated with an increased risk of death only in males but not in females with HFpEF (21). Evidence also supported that visceral adipose tissue was higher in men than women, while it was only associated with the elevation in pulmonary capillary wedge pressure in women, but not in men (22). Though gender differences might exist in the pathophysiologic role of VFA in HFpEF, there was no difference in predicting outcomes in the gender sub-group or adjusted for gender (Fig. 3, 4). In addition, in subgroup analysis, no interactions were unearthed among visceral obesity and age, BMI, smoking, hypertension, AF, coronary artery disease or diabetes mellitus history (Fig. 4). The study of whether excess visceral adiposity may confer adverse outcome in HFpEF through adding risks on cardiometabolic profiles is in progress. Further research of other potential mechanism was needed to fully understand the role of regional adiposities on HFpEF.

Successful risk stratification is a key to enhancing clinical care in HFpEF (23). A prospective study from China, which included 41708 hospitalized HFpEF patients, reported that the 1-year rate of cardiovascular death was 3.1% with the most common comorbidities of hypertension, coronary heart disease and AF(24), which is similar to our study findings. An analysis of the ESC Heart Failure Long-Term Registry associated the increased hazard with baseline characteristics such as age, NYHA class, pulmonary congestion, aortic stenosis, AF, peripheral artery disease and chronic kidney disease (25). The previous research also showed that higher HFA-PEFF or H2FPEF score was associated with all-cause death of HFpEF patients (11). The prognostic role of H2FPEF score was further verified by our study in Asian HFpEF populations (Table 2). However, when considering VFA, H2FPEF score and NT-proBNP in a model, only VFA was associated with the risks of death in patients with HFpEF.

Future study with a larger sample size and muti-centers is required to verify the initial study findings. Owing to the small number of events, a more rigorous regression analysis was unattainable, and the results of the analysis may have bias that we have not yet identified and resolved. Also, diagnosis of HFpEF is not straightforward. In the present study, only patients had signs or symptoms of heart failure is included, which may leave some asymptomatic people not being enrolled, and falsely diagnosed as HFpEF due to dyspnea that is not owing to cardiac origin.

In this prospective study, all-cause mortality rate in the high VFA group was significantly higher than in the low VFA group. Assessing VFA at baseline is meaningful to risk stratification and prognostic assessment in patients with HFpEF.

AF, Atrial Fibrillation; AUC, area under the curve; BIA, bioelectrical impedance analyzer; BMI, body mass index; CI, confidence interval; EAT, epicardial adipose tissue; FBG, fasting blood glucose; HF, heart failure; HR, hazard ratio; HFpEF, heart failure with preserved ejection fraction; LA, left atrial; LAVI, left atrial volume index; LV, left ventricular; LVEF, left ventricular ejection fraction; LVMI, left ventricular mass index; LVPW, left ventricular posterior wall; NT-proBNP, N-terminal pro-brain type natriuretic peptide; PAT, pericardial adipose tissue; RV, right ventricle; ROC, receiver operating characteristic; SAT, subcutaneous adipose tissue; VFA, Visceral fat area; VIF, Variance inflation factor.

Ethics approval and consent to participate

The study was approved by the Ethics Committee of the First Affiliated Hospital of Chongqing Medical University (approval number: 2021-473) and conformed to the Helsinki Declaration. Patients gave their written informed consent.

Consent for publication

Not applicable

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Competing interests

All authors declare that they have no conflict of interest.

Funding

This work was supported by National Natural Science Foundation of China [82270406, 81570212]; Chongqing Science and Technology Joint Project 2021; Basic Science and Foreword Technology Research Project [cstc2018jcyjAX0058]; Chongqing Returnees Stay and Create Fund 2020, Chongqing High-end Talent Fund; China Cardiovascular Health Alliance-Access Research Fund [2021-CCA-ACCESS-130] and Chongqing Science and Health Union Medical Research Project [2019ZLXM003].

Authors’ contributions

Study concept and design: LG, DZ. Data acquisition: JZ, XZ, JX, HY, XD, MS, HB, XT and ZL. Data analysis and interpretation: JZ, LG, DZ, XW. Statistical analysis: JZ, LG. Drafting of the manuscript: JZ, LG. Critical revision of the manuscript: XW, PG, LG, DZ.

Acknowledgements

We thank Dr. Dong Qian (department of cardiac ultrasound in the First Affiliated Hospital of Chongqing Medical University) for her help in performing echocardiograph.

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No competing interests reported.

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Visceral Adiposity：A Potential Marker for Mortality Risk in Heart Failure with Preserved Ejection Fraction?

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Abstract

Background

Methods

Results

Conclusions

Trial registration

Figures

Background

Materials And Methods

Study Population

Definition Of Hfpef

Data Collection

Anthropometric Measurements

Echocardiography

Statistical Analysis

Results

Baseline Characteristics

Roc Curve For Prediction Of All-cause Mortality By Vfa In Patients With Hfpef

Prognostic Value Of Regional Adiposity

Multivariable And Subgroup Analyses

Discussion

Conclusion

Abbreviations

Declarations

References

Additional Declarations

Supplementary Files

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