(2024) 22:367
Wei et al. BMC Medicine
https://doi.org/10.1186/s12916-024-03576-9

BMC Medicine

RESEARCH ARTICLE

Open Access

Association of lifestyle with valvular heartdisease progression and life expectancy
among elderly people from different
socioeconomic backgrounds
Yanxia Wei1,2,3, Dawei Sun4, Sanjay Jaiswal1,2,3, Yuxin He1,2,3, Xianbao Liu1,2,3* and Jian’an Wang1,2,3*

Abstract
Background Current cardiovascular prevention strategies are based on studies that seldom include valvular heartdisease (VHD). The role of modifiable lifestyle factors on VHD progression and life expectancy among the elderlywith different socioeconomic statuses (SES) remains unknown.
Methods This cohort study included 164,775 UK Biobank participants aged 60 years and older. Lifestyle was determinedusing a five-factor scoring system covering smoking status, obesity, physical activity, diet, and sleep patterns. Basedon this score, participants were then classified into “poor,”“moderate,” or “ideal” lifestyle groups. SES was classified as highor low based on the Townsend Deprivation Index. The association of lifestyle with major VHD progression was evaluatedusing a multistate mode. The life table method was employed to determine life expectancy with VHD and without VHD.
Results The UK Biobank documented 5132 incident VHD cases with a mean follow-up of 12.3 years and 1418 deaths
following VHD with a mean follow-up of 6.0 years. Compared to those with a poor lifestyle, women and men followed
an ideal lifestyle had lower hazard ratios for incident VHD (0.66 with 95% CI, 0.59–0.73 for women and 0.77 with 95%
CI, 0.71–0.83 for men) and for post-VHD mortality (0.58 for women, 95% CI 0.46–0.74 and 0.62 for men, 95% CI 0.54–0.73). When lifestyle and SES were combined, the lower risk of incident VHD and mortality were observed among participants with an ideal lifestyle and high SES compared to participants with an unhealthy lifestyle and low SES. There
was no significant interaction between lifestyle and SES in their correlation with the incidence and subsequent mortality of VHD. Among low SES populations, 60-year-old women and men with VHD who followed ideal lifestyles lived
4.2 years (95% CI, 3.8–4.7) and 5.1 years (95% CI, 4.5–5.6) longer, respectively, compared to those with poor lifestyles. In
contrast, the life expectancy gain for those without VHD was 4.4 years (95% CI, 4.0–4.8) for women and 5.3 years (95%CI, 4.8–5.7) for men when adhering to an ideal lifestyle versus a poor one.
Conclusions Adopting a healthier lifestyle can significantly slow down the progression from free of VHD to incident
VHD and further to death and increase life expectancy for both individuals with and without VHD within diverse
socioeconomic elderly populations.
Keywords Valvular heart disease, Socioeconomic status, Lifestyle, Life expectancy, Multistate model*Correspondence:
Xianbao Liu
liuxb@zju.edu.cn
Jian’an Wangwangjianan111@zju.edu.cn
Full list of author information is available at the end of the article© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0
International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as longas you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if
you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article orparts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicatedotherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not
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Wei et al. BMC Medicine(2024) 22:367

Background
Valvular heart disease (VHD) ranks as the third mostfrequent cardiovascular disease, after hypertension andcoronary artery disease [1], with aortic valve stenosis andmitral regurgitation being the most common diagnoses[2]. The prevalence of VHD rises sharply with age—it
affects 5–10% of people aged 65–74 years and 10–20%
of those over 75 [3]. However, these figures might not
fully capture the actual situation. In a UK study involving 2500 individuals over 65, 51% were found to have previously undiagnosed VHD, which was primarily mild innature [4]. As the global population ages, VHD is likely
to become the next cardiovascular pandemic. Nonetheless, most cardiovascular disease prevention studies haveoverlooked VHD [5–7], and there is currently no established preventive strategy that can decelerate the risk of
VHD, particularly among the elderly.
A healthy lifestyle is one of the potential modifications
for VHD. Some studies have demonstrated that no current smoking [8], no obesity [9], healthy sleep patterns[10, 11], healthy dietary habits [12], and physical activity[13] are linked to a reduced risk of VHD. These lifestyle factors have been shown to be interrelated, andtheir combined effects lead to stronger associations withhealth outcomes [14]. And a recent study revealed that acomprehensive score of these healthy lifestyle factors is
significantly linked to the occurrence of VHD [15]. However, those previous studies focused on only one diseasestage and did not consider morbidity and mortality as
a continuum in their analysis. Thus, it is imperative tobridge this gap by explore the role of a healthy lifestyleon the progression from health to the onset of VHD andsubsequently to mortality.
An established association exists between socioeconomic status (SES) and an increased risk of cardiovascular disease [16]. Studies have also shown that lower SES islinked to a higher risk of developing aortic valve stenosis
as well as its associated mortality [17, 18]. It is unclear
whether a high lifestyle level can attenuate the risk of
VHD associated with low socioeconomic level. Addressing only lifestyle factors while neglecting social determinants may lead to wider health disparities [19]. To ensurea fair distribution of healthcare resources, it is essential
to better understand the role of lifestyle in populations
with varying SES levels, especially those at higher risk.
Here, we took advantage of the UK Biobank cohort
study to investigate the potential role of overall lifestyles
on major VHD risk among older adults. In addition topresenting results through the widely used hazard ratios(HRs), we also adopted an easily understood metric oflife expectancy, to provide comprehensive evidence support for health professionals and the general public toplan their future healthcare. Our objective was to assess

Page 2 of 12

the role of healthy lifestyle on the progression from being
free of VHD, transitioning to disease onset, and eventually advancing to mortality. Specifically, we analyzed towhat extent a healthy lifestyle correlates with longevity inpeople with and without VHD. Furthermore, we explored
how these changes vary across different SES.

Methods
Study population

The UK Biobank is a large-scale prospective cohort
study with an open-access protocol [20]. Approximately
500,000 individuals aged 40–69 years were recruitedfrom 22 assessment centers across England, Scotland,
and Wales between 2006 and 2010. Baseline information on participants’ lifestyle, socioeconomic, and healthrelated factors were obtained through questionnaires,interviews, and physical measurements, while blood
samples were also collected and processed. All participants provided written informed consent. This study
was approved by the National Information Governance
Board for Health and Social Care and the North West
Multi-Center Research Ethics Committee. Our analysis
was restricted to participants who were 60 years old andabove. We excluded individuals with missing data on lifestyle factors, SES, or other covariates.
Lifestyle factors

A lifestyle score was created based on 5 risk factors(tobacco smoking, obesity, physical inactivity, unhealthy
diet, and unhealthy sleep patterns) measured by the UK
Biobank questionnaire at baseline. We adopted threehealthy lifestyle criteria based on the cardiovascular
health promotion goals of the American Heart Association [21]: not smoking for over a year, maintaining abody mass index (BMI) below 30, and engaging in regular physical activity (at least 150 min per week of moderate intensity, 75 min per week of vigorous intensity,or a combination of moderate and vigorous activities
totaling at least 150 min per week). A healthy diet wasdetermined according to the 2021 dietary guidance for
cardiovascular health from the AHA [22]. Since 6 of the
13 recommended dietary priorities were unavailable in
the UK Biobank, a healthy diet pattern was identified
based on increased consumption of fruits, vegetables,
whole grains, and fish and decreased or no consumptionof refined grains, processed meats, and unprocessed redmeats. Additionally, a healthy sleep pattern was definedby the presence of at least four of the following characteristics: being an early riser, sleeping 7–8 h per day, seldomor never having insomnia symptoms, not snoring, andnot experiencing excessive daytime sleepiness [23]. We
assigned one point to each favorable lifestyle factor andcategorized overall lifestyle into three levels: poor (zeroWei et al. BMC Medicine(2024) 22:367

to two points), moderate (three points), and ideal (fourto five points). Table S1 in Additional file 1 describes thelifestyle factors in greater detail.
SES and covariates

The Townsend Deprivation Index (TDI) was sourced
from national census data within the UK Biobank, signifying an area-level socioeconomic status (SES) measure
based on variables including car ownership, household
overcrowding, owner occupation, and employment [24].
The Townsend scores are a continuous variable, where
higher values indicate a lower SES. Participants weredivided into two groups, with those scoring above the60th percentile defined as having low SES.
We also selected two individual-level measures of SES
available within the UK Biobank: household income andeducational qualifications. Average household income
information was self-reported, with low income defined
as less than £31,000. Participants also disclosed theirhighest educational qualifications, choosing from a listthat included “College or university degree,” “A levels/
AS levels or equivalent,” “O levels/GCSEs or equivalent,”“CSEs or equivalent,” “NVQ or HND or HNC or equivalent,” “Other professional qualifications,” “None of theabove,” or “Prefer not to answer.” According to the International Standard Classification of Education [25], we
categorized educational attainment into two levels: low,which included “O levels/GCSEs/CSEs or equivalent”
and “None of the above,” and high, which encompassed“College or university degree,” “A levels/AS levels or
equivalent,” “NVQ or HND or HNC or equivalent,” and“Other professional qualifications.
Covariates including age, ethnicity, the medication
use for cholesterol and blood pressure, and a history of
hypertension, dyslipidemia, diabetes, coronary arterydisease, atrial fibrillation, cardiomyopathy, heart failure,chronic kidney disease, and cancer were collected via aself-administered touchscreen questionnaire. Operative
procedures for VHD were coded according to the Officeof Population Censuses and Surveys Classification ofInterventions and Procedures, version 4 (OPCS-4), using
hospital inpatient records (K25, K26, K311, K312, K341,
K351, K352).
Outcomes

The outcome was major VHD, defined as a composite of
the two most common types in the UK Biobank: aortic
stenosis and mitral regurgitation. We excluded congenital and rheumatic valve diseases. Incident cases of VHD
were identified through linkage with Hospital Episode
Statistics (HES) and national death registries. For ouranalysis, we considered only the first VHD event in compound cases, disregarding any subsequent events. The

Page 3 of 12

International Classification of Diseases 10th Revision(ICD 10) was used to code VHD cases. Vital status was
obtained from Death Registries. The date of each VHD
event was pinpointed as the earliest recorded occurrence within the UK Biobank data. A detailed outcome
definition can be found in Table S2 in Additional file 1.
Participants were followed-up in the database from theirassessment date until July 31, 2021, for Scotland, October
31, 2022, for England, or February 28, 2018, for Wales.
Statistical analysis

Participants of the UK Biobank were followed up frombaseline until the date of diagnosis, death, withdrawal, orcompletion of follow-up, whichever came first. To investigate the role of lifestyle on the progression of VHD, weemployed a multistate model with a Gompertz distribution [26]. This model included three states: “NO-VHD,”“VHD,” and “death.” Three transitions were observed inparticipants: (1) from no VHD to incidence of VHD, (2)from no VHD directly to death, and (3) from VHD diagnosis to death. We only considered the first occurrenceof transitioning into a new state and did not allow forreversal.
When analyzing transitions 1 and 2, participants who
had prevalent VHD at the baseline were excluded. For
transition 3, we included those with prevalent VHD at
the baseline as well as those who developed VHD duringfollow-up. The multistate survival analysis was controlled
for covariates including age, ethnicity, histories of hypertension, dyslipidemia, and diabetes, as well as medication
use for cholesterol and blood pressure. Age at diagnosis
of VHD was further adjusted in the analysis of transition
3. We estimated hazard ratios (HRs) to measure the association of lifestyle alone, the combination of lifestyle and
SES, and lifestyle within SES-stratified subpopulations
with VHD incidence and mortality. In addition, we calculated the dose–response relationship between lifestylecategory and health outcomes, in which lifestyle category
was treated as a continuous variable. To explore multiplicative interactions, a product term combining the socioeconomic and lifestyle scores was additionally included
in our model.
We assessed the life expectancy of individuals with orwithout VHD categorized by lifestyle categories across
SES levels. First, the Gompertz multistate model was
employed, utilizing age from 60 years as the time scale,to determine the age-specific and SES-specific transition rates for each transition. Next, the baseline prevalence of lifestyle levels was calculated by every 10-year
age bracket and by SES among participants without VHD
at baseline and those with VHD during follow-up. Then,
we used SES-specific hazard ratios by lifestyle, and the
proportions of lifestyle categories, to weight transition

Wei et al. BMC Medicine(2024) 22:367

rates as described in previously published methods [27].
Finally, using the weighted age-specific and SES-specifictransition rates, we constructed life tables for people withand without VHD [28, 29]. We assumed that individuals currently without VHD could develop the conditionin the future. Our life tables concluded at 100 years, withmethodological details provided in the supplemental
method in Additional file 1. Years of life gained due tohealthier lifestyles was calculated by subtracting the life
expectancies of participants with ideal and moderate lifestyles from those with a poor lifestyle of the same age and
SES. The 95% confidence interval for the life expectancy
was estimated by conducting 2000 Monte Carlo simulations. To account for gender-specific differences in life
expectancy, all analyses were conducted separately formen and women.
We confirmed the robustness of our analyses by performing sensitivity analyses in which (1) the continuous
lifestyle score was considered rather than categoricalvariable; (2) the five lifestyle factors were analyzed separately, instead of being aggregated into a single score;(3) additional adjustments were made for potential confounders in the lifestyle-VHD relationship, such as coronary artery disease, atrial fibrillation, cardiomyopathy,
heart failure, chronic kidney disease, and cancer; (4) the
Cardiovascular Health (CVH) metric, introduced by theAmerican Heart Association (AHA), was used instead oflifestyle; (5) aortic stenosis and mitral regurgitation wereconsidered separately, instead of being aggregated into a
general VHD category; (6) low socioeconomic status wasindicated by a TDI percentile above 40, rather than 60th
percentile; (7) individual-level measures of SES, such as
household income and educational attainment, wereused; (8) participants who developed VHD or died within
the first 2 years of follow-up were excluded; (9) for the
analysis of VHD patients (transition 3), we made additional adjustments to account for any operations related
to VHD; (10) participants without VHD were assumed
to be immune to the disease, and their expected lifetimes
were recalculated.; (11) multiple imputation was conducted to impute all missing independent variables andtest the influence of missing data.
All statistical analyses were performed using the R software 4.0. All P values were two-sided and considered statistically significant when less than 0.05.

Results
Cohort characteristics

There are a total of 164,775 participants with data available for analysis after excluding 115,688 participants due
to missing data on lifestyle factors (n = 115,215) and the
TDI (n = 473) as well as excluding 221,905 participants
who were younger than 60 years old (Additional file 1: Fig.

Page 4 of 12

S1). Of the 164,775 participants in the final analysis, 997
reported VHD at baseline. The mean follow-up period
was 12.3 years (SD 2.7) for VHD incidence, 6.0 years (SD4.3) for mortality among those with VHD, and 12.5 years(SD 2.5) for mortality among those without VHD. Overthe follow-up period, 5132 incident events and 1418 VHD
deaths, and 17 810 non-VHD deaths occurred.
The baseline characteristics of eligible participants are
outlined in Table 1. For the overall participants, the mean
age was 64.1 years (SD 2.8), and 51.8% were female. There
were 30,006 (18.2%) participants with a poor lifestyle,46,119 (28.0%) with a moderate healthy lifestyle, and88,650 (53.8%) who adopted an ideal lifestyle. A majorityof UK Biobank participants met the healthy criteria foreach lifestyle factor, with no current smoking having thehighest adherence rate (over 90%), while a smaller proportion achieved healthy diet standards (44.8% to 60.2%)
and healthy sleep patterns (55.5% to 58.9%). Participants
with a poor lifestyle exhibited a higher prevalence of
low SES, household income, and educational attainment
compared to those in the ideal lifestyle group.
Incident valvular heart disease and mortality

Participants in both moderate and ideal healthy categories demonstrated lower HRs for all outcomes comparedto those in the poor healthy category, regardless of gender. For women, individuals following an ideal lifestyle
had a 34% and 42% lower rate for incident VHD andmortality from VHD, respectively, compared to thoseadhering to a poor lifestyle. For men, these figures were
23% and 38%, respectively (Table 2). Comparable results
were observed when we repeated the analysis using lifestyle scores as a substitute for lifestyle categories, after
additional adjustment for coronary artery disease, atrial
fibrillation, cardiomyopathy, heart failure, chronic kidneydisease, and cancer and by using AHA’s cardiovascular
health metrics. Analyses for each lifestyle component
showed that, overall, five factors contributed to lower
risk of VHD events and mortality in both women andmen (Additional file 1: Table S3-S4). When the analysis
was carried out separately for aortic stenosis and mitral
regurgitation, a similar pattern was observed, indicatingthat both better health outcomes of aortic stenosis andmitral regurgitation were significantly associated withhealthier lifestyle levels (Additional file 1: Tables S5).
When socioeconomic status and lifestyle categories
were combined, a monotonic association was observed;
participants with higher SES and healthier lifestyles
had better health outcomes in VHD. Those with highSES and an ideal lifestyle had a lower risk of incident
VHD and mortality than their counterparts with low
SES and a poor lifestyle. There was no significant interaction between lifestyle level and SES in terms of VHD

Wei et al. BMC Medicine(2024) 22:367

Page 5 of 12

Table 1 Baseline characteristics by lifestyle level
Characteristicsa

Women

Men

Lifestyle ­levelb

Lifestyle ­levelb

Poor

Moderate

Ideal

All

Poor

Moderate

Ideal

All

(N = 13 221)

(N = 22 369)

(N = 49 821)

(N = 85 411)

(N = 16 785)

(N = 23 750)

(N = 38 829)

(N = 79 364)

Age (years)

63.9 ± 2.83

64.0 ± 2.83

64.0 ± 2.83

64.0 ± 2.83

64.0 ± 2.82

64.2 ± 2.85

64.3 ± 2.86

64.2 ± 2.85

White ethnicity

12 902 (97.59) 21 735 (97.17) 48 454 (97.26) 83 091 (97.28) 16 381 (97.59) 23 077 (97.17) 37 610 (96.86) 77 068 (97.11)

SES ­categorycLow6424 (48.60)

9355 (41.82)

High6795 (51.40)

13 014 (58.18) 31 109 (62.44) 50 918 (59.62) 8899 (53.0)

18 712 (37.56) 34 493 (40.38) 7886 (47.0)

9631 (40.6)

14 015 (36.1)

31 532 (39.7)

14 119 (59.4)

24 814 (63.9)

47 832 (60.3)

Household ­incomed
Low

7986 (60.40)

12 694 (56.75) 26 512 (53.21) 47 192 (55.25) 9701 (57.80)

12 833 (54.0)

19 672 (50.66) 42 206 (53.18)

High2358 (17.84)

4729 (21.14)

12 367 (24.82) 19 454 (22.78) 5089 (30.32)

8110 (34.15)

14 750 (37.99) 27 949 (35.22)

Missing data

2877 (21.76)

4946 (22.11)

10 942 (21.96) 18 765 (21.97) 1995 (11.893)

2807 (11.82)

4407 (11.35)

12 188 (31.39) 28 477 (35.88)

9209 (11.60)

Education ­attainmenteLow7288 (55.12)

10 912 (48.78) 20 870 (41.89) 39 070 (45.74) 7282 (43.38)

9007 (37.92)

High5775 (43.68)

11 189 (50.02) 28 346 (56.90) 45 310 (53.05) 9303 (55.42)

14 442 (60.81) 26 182 (67.43) 49 927 (62.91)

Missing data

158 (1.20)

268 (1.20)

301 (1.27)

605 (1.21)

1031 (1.21)

200 (1.19)

459 (1.18)

960 (1.21)

Healthy lifestyle factors
No current smoking

10 391 (78.59) 20 616 (92.16) 49 039 (98.43) 80 046 (93.72) 12 305 (73.31) 21 355 (89.92) 38 113 (98.16) 71 773 (90.44)

No obesity4542 (34.35)

14 674 (65.60) 45 925 (92.18) 65 141 (76.27) 6403 (38.15)

16 815 (70.80) 36 114 (93.01) 59 332 (74.76)

Regular physicalactivity

3980 (30.10)

13 680 (61.16) 44 697 (89.72) 62 357 (73.01) 5907 (35.19)

16 416 (69.12) 35 710 (91.97) 58 033 (73.12)

Healthy diet2324 (17.58)

9207 (41.16)

39 919 (80.12) 51 449 (60.24) 1714 (10.21)6509 (27.41)

Healthy sleep pattern 2178 (16.47)

9831 (39.93)

39 189 (78.66) 50 298 (58.89) 2845 (16.95)

10 155 (42.76) 31 042 (79.95) 44 042 (55.49)

27 352 (70.44) 35 575 (44.83)

History of disease
Hypertension

5718 (43.25)

7832 (35.01)

13 546 (27.19) 27 096 (31.72) 8185 (48.76)

9640 (40.59)

12 966 (33.39) 30 791 (38.80)

Dyslipidemia

2805 (21.22)

3848 (17.20)

6912 (13.87)

13,565 (15.88) 4439 (26.45)

5493 (23.13)

7589 (19.54)

17 521 (22.08)

Diabetes

1033 (7.81)

1073 (4.80)

1197 (2.40)3303 (3.87)

2128 (12.68)

1986 (8.36)

2010 (5.18)

6124 (7.72)

935 (7.07)

1008 (4.51)

1546 (3.10)

3489 (4.08)

2578 (15.36)2756 (11.60)

3713 (9.56)

9047 (11.40)

Coronary arterydiseaseAtrial fibrillation

119 (0.90)

170 (0.76)

323 (0.65)

612 (0.72)

301 (1.79)

388 (1.63)

619 (1.59)

1308 (1.65)

Heart failure

22 (0.17)

10 (0.04)

15 (0.03)

47 (0.06)

26 (0.15)

24 (0.10)30 (0.08)

80 (0.10)

Cardiomyopathy

13 (0.10)

15 (0.07)

19 (0.04)

47 (0.06)

23 (0.14)

23 (0.10)

34 (0.09)

80 (0.10)

Chronic kidneydisease

9 (0.07)21 (0.09)

17 (0.03)

47 (0.06)

20 (0.12)

22 (0.09)

13 (0.03)

55 (0.07)8154 (10.27)

1911 (14.45)

3112 (13.91)

6774 (13.60)

11,797 (13.81) 1768 (10.53)

2493 (10.50)

3893 (10.03)

Lip lower medication 3935 (29.76)

Cancer5189 (23.20)

8595 (17.25)

17 719 (20.75) 7144 (42.56)

8547 (35.99)

11 618 (29.92) 27 309 (34.41)

Anti-hypertension
medication

4973 (37.61)

6668 (29.81)

11 066 (22.21) 22 707 (26.59) 7675 (45.73)

8827 (37.17)

11 777 (30.33) 28 279 (35.63)

Age at diagnosisof ­VHDf

71.5 ± 5.17

72.0 ± 5.00

71.9 ± 5.05

71.8 ± 5.07

71.2 ± 5.11

71.4 ± 5.02

71.6 ± 5.12

71.4 ± 5.09

127 (23.39)

161 (24.88)

332 (27.74)

620 (25.97)

306 (30.51)367 (33.09)

565 (34.66)

1238 (33.08)

Operation for ­VHDf

SES socioeconomic status, VHD valvular heart diseaseaData were mean ± standard deviation or count (percentage) for continuous and categorical variablesb

Lifestyle level was determined as poor (meeting zero to two Healthy lifestyle factors), moderate (meeting three factors), and ideal (meeting four to five factors)c

Low socioeconomic status referred to individuals above the 60th percentile on the Townsend Deprivation Indexd

Low household income was classified as less than £31,000 family income levelse

Low education was defined as an individual who has attained a level of equal to or lower than levels/GCSEs/CSEs or equivalentf

Age at diagnosis of VHD and whether an operation for VHD was performed were measured in participants with prevalent VHD at baseline and those who developed
incident VHD during follow-up

Wei et al. BMC Medicine(2024) 22:367

Page 6 of 12

Table 2 Incident VHD and death by lifestyle level
Gender Transition

Poor ­lifestylea

Moderate ­lifestylea

Ideal ­lifestylea

No. of cases/
person-years

HR (95% CI) No. of cases/
person-years

HR (95% CI)

Women Incident VHD

458/162789.0

1 [reference]

566/278847.3

0.74 (0.66–0.83) 1007/624752.7

0.66 (0.59–0.73) 0.82 (0.78–0.86)

Mortality
among those
without VHD

1594/159142.2

1 [reference]

1957/274364.2

0.74 (0.69–0.79) 3399/616731.5

0.59 (0.56–0.63) 0.77 (0.75–0.80)

Mortality
among thosewith ­VHDb

109/2161.6

1 [reference]

97/2882.9

0.70 (0.54–0.90)

147/5186.3

0.58 (0.46–0.74) 0.77 (0.68–0.86)

Incident VHD

860/196691.0

1 [reference]

917/285349.2

0.81 (0.75–0.89) 1324/473617.7

0.77 (0.71–0.83) 0.88 (0.85–0.92)

Mortality
among those
without VHD

3183/190093.8

1 [reference]

3433/278191.7

0.76 (0.73–0.80) 4244/463114.3

0.58 (0.56–0.61) 0.76 (0.75–0.78)

Mortality
among thosewith ­VHDb

283/3927.3

1 [reference]

247/4306.9

0.70 (0.57–0.87)

0.62 (0.48–0.79) 0.79 (0.73–0.85)

Men

No. of cases/
person-years

274/6421.3

HR (95% CI)

HR for trend(95% CI)

VHD valvular heart disease, HR hazard ratio, CI confidence interval
Multistate survival analysis with the Gompertz distribution was used to compute HRs (and 95% CI) for the association of lifestyle with incident VHD and mortality. HRs
for trend were calculated treating the lifestyle level as a continuous variablea

Hazard ratios were calculated using a poor lifestyle as the reference. The analysis was adjusted for age, ethnicity, socioeconomic deprivation status, history of
hypertension, dyslipidemia, and diabetes, as well as the use of medication for managing cholesterol and blood pressure. For transition 3, age at diagnosis of VHD was
further adjustedb

The participants with VHD in transition 3 included those with prevalent VHD at baseline (n = 997) and incident VHD (n = 5132) during follow-up

incidence or mortality in those with VHD (Fig. 1). Similar results were obtained in analyses using the reclassified
TDI or individual-level measures of SES and when analyzed separately for aortic stenosis and mitral regurgitation (Additional file 1: Table S6-S7).
Further stratification by SES confirmed that a favorable lifestyle is associated with a lower risk of developing
VHD and reduced mortality. Across various SES groups,
the role of lifestyle on VHD incidence and post-VHD
mortality remained similar (Table 3). The pattern of thisassociation remained consistent after excluding healthoutcomes that occurred during the first 2 years of followup, imputing missing data, reclassifying the TDI, andconsidering individual-level SES measures (Additional
file 1: Table S8-S9). Additionally, lifestyle’s effect on mortality among VHD patients was unchanged after adjustment for VHD operations (Additional file 1: Table S10). A
similar pattern was also observed when the analysis was
conducted separately for aortic stenosis and mitral regurgitation (Additional file 1: Table S11).

Life expectancy with or without VHD

At age 60 within the low-SES group, women with VHD
had expected lifespans from 21.5 (95% CI, 20.9–22.2)
years with a poor lifestyle up to 25.7 (25.2–26.4) years
with an ideal one. Without VHD, the range was 27.4
(26.8–28.0) to 31.8 (31.4–32.4) years. Men with VHD
had projections of 15.9 (15.2–16.8) to 21.0 (20.2–21.7)
years and without VHD, 23.3 (22.7–24.0) to 28.6 (28.0–
29.2) years. Conversely, in the high-SES group, womenwith VHD had life expectancies of 21.2 (20.6–21.9) to25.9 (25.3–26.5) years and men from 18.8 (18.2–19.5)
to 23.0 (23.3–23.6) years. For those without VHD,
women could anticipate living 29.7 (29.2–30.3) to 32.8
(32.3–33.2) years and men from 26.2 (25.6–26.9) to
29.6 (29.0–30.2) years. These life expectancy ranges allcorresponded to poor and ideal lifestyles. Consistentpattern of results was also observed across different age
groups and when presuming that both women and men
without VHD were resistant to the disease (Fig. 2 andAdditional file 1: Fig. S2).

(See figure on next page.)
Fig. 1 The association of the combination of lifestyle and socioeconomic status with health outcomes of valvular heart disease. VHD, valvular
heart disease; HR, hazard ratio. Multistate survival analysis with the Gompertz distribution was used to compute HRs (and 95% CI) to assess
the combined effect of socioeconomic status and lifestyle—which were grouped into six categories, with low socioeconomic status and poor
lifestyle as the reference—on the incidence of VHD and mortality. P for interaction was calculated by additionally including a product termof the socioeconomic and lifestyle factors in the modelWei et al. BMC Medicine(2024) 22:367

Fig. 1 (See legend on previous page.)

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Wei et al. BMC Medicine(2024) 22:367

Page 8 of 12

Table 3 Incident VHD and death by lifestyle level stratified by socioeconomic status
Gender Transition

SES

Poor lifestyle
No. of cases/
person-years

Women Incident VHD

Men

Moderate lifestyle
HR (95% CI) No. of cases/
person-years

HR (95% CI)

Ideal lifestyle
No. of cases/
person-years

HR (95% CI)

HR for trend(95% CI)Low

247/78496.1 1 [reference]

253/116325.3

0.68 (0.58–0.81) 401/233655.8

0.62 (0.54–0.72) 0.80 (0.74–0.86)

High211/84293.0 1 [reference]

313/162521.9

0.80 (0.68–0.94) 606/391096.9

0.69 (0.60–0.80) 0.84 (0.78–0.90)

Mortality
among those
without VHD

Low

883/76492.5 1 [reference]

944/114269.1

0.73 (0.67–0.80) 1342/230475.5

0.54 (0.49–0.59) 0.73 (0.70–0.77)High711/82649.7 1 [reference]

1013/160095.2

0.76 (0.69–0.83) 2057/386256.1

0.65 (0.59–0.71) 0.81 (0.78–0.85)

Mortality
among thosewith VHD

Low

56/1163.6 1 [reference]

44/1233.9

0.81 (0.62–0.97)

58/2083.2

0.63 (0.45–0.89) 0.79 (0.67–0.94)

High53/998.1 1 [reference]

53/1649.0

0.70 (0.50–0.86)

89/3103.1

0.60 (0.49–0.74) 0.74 (0.63–0.87)

Incident VHD

Low

424/90726.2 1 [reference]

395/114154.6

0.82 (0.72–0.93)

481/22504.5

0.77 (0.67–0.87) 0.88 (0.83–0.93)

High436/105964.8 1 [reference]

522/171194.6

0.81 (0.72–0.91) 843/304169.3

0.76 (0.69–0.85) 0.88 (0.84–0.93)

Mortality
among those
without VHD

Low

1806/87487.7 1 [reference]

1636/111104.1

0.73 (0.68–0.78) 1696/165533.7

0.52 (0.48–0.55) 0.72 (0.69–0.74)

High1377/102606.1 1 [reference]

1797/167087.7

0.81 (0.76–0.87) 2548/297580.6

0.65 (0.61–0.70) 0.81 (0.78–0.83)

Mortality
among thosewith VHD

Low

150/1880.3 1 [reference]

113/1822.8

0.80 (0.64–0.99)

109/2196.4

0.61 (0.48–0.76) 0.78 (0.70–0.87)

High133/2046.9 1 [reference]

134/2484.1

0.85 (0.79–0.96)

165/4224.8

0.64 (0.52–0.79) 0.80 (0.72–0.89)

VHD, valvular heart disease; SES, socioeconomic status; HR, hazard ratio; CI, confidence interval
Multistate survival analysis with the Gompertz distribution was used to compute HRs (and 95% CI), using a poor lifestyle as the reference. HRs for trend were
calculated treating the lifestyle level as a continuous variable. The analysis was adjusted for age, ethnicity, history of hypertension, dyslipidemia, and diabetes, as wellas the use of medication for managing cholesterol and blood pressure. For transition 3, age at diagnosis of VHD was further adjusted

Table 4 presents differences in life expectancy by lifestyle level. Life expectancy increased with higher levelsof a healthy lifestyle in participants, both with and without VHD, after adjusting for covariates. For those with
VHD in the low socioeconomic status group at age 60,

life expectancy was 4.2 (95% CI 3.8–4.7) years longer for
women and 5.1 (4.5–5.6) years longer for men when comparing an ideal lifestyle to a poor lifestyle. In the samegroup without VHD, the gains with an ideal lifestyle were
4.4 (4.0–4.8) years for women and 5.3 (4.8–5.7) years forFig. 2 Life expectancy for women and men with and without valvular heart disease according to lifestyle level, stratified by socioeconomic
status. Life expectancy classified by lifestyle level was calculated using weighted transition rates, adjusted for age, ethnicity, socioeconomic
deprivation status, histories of hypertension, dyslipidemia, and diabetes, as well as medication use for cholesterol and blood pressure management.
For individuals with VHD, age at diagnosis of VHD was further adjusted. Each bar represents the life span of participants, with lifestyle level denotedby labels situated between the bars for women and men. The lighter shades at the ends of each bar depict the 95% confidence intervals

Wei et al. BMC Medicine(2024) 22:367

Page 9 of 12

Table 4 Years of life gained by lifestyle level stratified by socioeconomic status
SES

Low

Age

60

70

High

60

70

Lifestyle level

With VHD

Without ­VHDa

Years of life gained (95% CI)

Years of life gained (95% CI)

Women

Women

Men

Men

Poor

Reference

Reference

Reference

Reference

Moderate

1.9 (1.5–2.4)

2.2 (1.7–2.7)

2.4 (2.0–2.8)

2.6 (2.1–3.0)

Ideal

4.2 (3.8–4.7)

5.1 (4.5–5.6)

4.4 (4.0–4.8)

5.3 (4.8–5.7)

Poor

Reference

Reference

Reference

Reference

Moderate

1.6 (1.2–2.0)

1.8 (1.3–2.3)

2.1 (1.7–2.5)

2.2 (1.8–2.6)

Ideal

3.5 (3.1–3.9)

4.0 (3.5–4.5)

4.0 (3.6–4.4)

4.6 (4.1–5.0)

Poor

Reference

Reference

Reference

Reference

Moderate

3.3 (2.8–3.7)

1.5 (1.0–2.0)

2.0 (1.6–2.4)

1.7 (1.3–2.2)

Ideal

4.7 (4.3–5.1)

4.1 (3.7–4.6)

3.1 (2.8–3.5)

3.4 (3.0–3.8)

Poor

Reference

Reference

Reference

Reference

Moderate

2.7 (2.3–3.1)

1.2 (0.7–1.6)

1.8 (1.4–2.2)

1.5 (1.1–1.9)

Ideal

3.9 (3.5–4.3)

3.4 (2.9–3.8)

2.8 (2.5–3.2)

3.0 (2.6–3.4)

VHD valvular heart disease, SES socioeconomic status, CI confidence intervalYears of life gained were computed by subtracting the life expectancy of participants with ideal and moderate lifestyles from those with a poor lifestyle at the sameage, stratified by socioeconomic statusa

We assumed that participants without valvular disease at a given age can acquire the disease later onmen. In the high socioeconomic status group with VHD,
women had a life expectancy increase of 4.7 (4.3–5.1)
years and men gained 4.1 (3.7–4.6) years; for those without VHD, women gained 3.1 (2.8–3.5) years and men 3.4(3.0–3.8) years. A similar pattern of results was observed
when assuming that both women and men without VHD
were immune to the disease and after imputing missing
data (Additional file 1: Table S12-S13).

Discussion
Our analysis of a large cohort study of UK elderly participants suggested that a healthier lifestyle is associatedwith a lower risk of major VHD as well as a lower risk ofmortality in the presence or absence of the disease. Whenconsidering SES together, participants with a favorable
lifestyle and high SES had a significantly lower risk ofincident VHD and mortality compared to those with anunfavorable lifestyle and low SES. We found no evidenceof a significant interaction between lifestyle and SES
in influencing VHD incidence or death following VHD.
Stratified analyses by SES revealed that a healthy lifestyleis associated with a lower risk of incident VHD, reduced
mortality, and increased life expectancy for individuals
with and without VHD across different SES levels.
Our findings are consistent with the EPIC-Norfolk
study [12], the Atherosclerosis Risk in Communities
Study [13], and another UK Biobank study [15], which
reported that a healthier lifestyle can protect against
incident VHD. Our work suggested that healthy living
not only helps prevent VHD initially but also reduces therisk that it will lead to death. Yuting et al. found similar
results in cardiometabolic disease (cardiometabolic disease comprises ischemic heart disease, stroke, and type2 diabetes) that a high-risk lifestyle had negative impacts
on all transitions from healthy to first cardiometabolic
disease, subsequently to cardiometabolic multimorbidity, and then to death [30]. The present results extend theliterature that identified a healthy lifestyle as an effective
way to prevent various types of cardiovascular diseases inolder adults [5, 31], suggesting that it also applies to VHD.
The precise mechanisms by which lifestyle affects the riskof VHD and mortality remain unclear. Research suggeststhat an unhealthy lifestyle can lead to the overstimulationof inflammation, lipid infiltration, oxidative stress, andcellular and organ damage [32, 33]. These pathways contribute to the development of aortic stenosis and mitral
regurgitation [34] and subsequent mortality [35]. Despite
these findings, further studies are needed to elucidate thespecific mechanisms through which lifestyle factors contribute to preventing VHD and mortality.
We confirmed that a healthy lifestyle is associatedwith a reduced risk of incident VHD and mortality
regardless of SES. Furthermore, for the incidence andmortality subsequent to VHD, no significant interaction between lifestyle and SES was observed. Thesefindings support public health efforts that emphasize a healthy lifestyle for everyone. Furthermore, thepresent work and a previous study [36, 37] reported
that participants with a poor lifestyle tend to have alower socioeconomic status, and we found that when

Wei et al. BMC Medicine(2024) 22:367

Page 10 of 12

SES and lifestyle categories were combined, a monotonically increasing association with the risk of VHD
was observed with increasing socioeconomic deprivation and increasingly unhealthy lifestyles. Therefore,
populations with low SES are more vulnerable. To
effectively promote lifestyle practices across diverse
populations, it is essential to allocate increased
resources and investments towards low SES groups.
This strategy seeks to enhance the lifestyle standards across varying SES levels to meet uniform healthbenchmarks, thereby ensuring equitable access to thebenefits of health-promoting interventions across all
socioeconomic segments.
To our knowledge, this is the first study to assess theassociation between lifestyle and life expectancy inindividuals with VHD. We found that a healthy lifestyle
plays a role in increasing life expectancy for people
with and without VHD across various SES. At 60 years
old, an ideal lifestyle increased life expectancy by
4.4 years for women and by 5.3 years for men without
VHD, compared to a poorer lifestyle. Corresponding
estimates for those with VHD were 4.2 years for womenand 5.1 years for men. The present results are consistent with previous findings on the association of thelifestyle with life expectancy with or without diseases.
Chenjie et al. found that ideal cardiovascular health,also referred to as Life’s Simple 7—which incorporates
smoking, diet, physical activity, obesity, blood pressure,cholesterol, and fasting plasma glucose—is associatedwith increased longevity regardless of the presence of
cardiometabolic disease, with an additional 3.9 years
for females and 4.0 years for males with cardiometabolic disease at 65 years old [38]. Yogini et al. showeda survival benefit of about 6.5 years in women and
5.3 years in men for a healthy lifestyle among 65-yearolds with multiple chronic conditions, including cardiovascular diseases. For those without multiple chronic
conditions, the corresponding estimates were 5.9 years
in women and 6.7 years in men [39]. The current study
extends previous findings by demonstrating that adopting a healthier lifestyle is associated with a longer life
expectancy, even for individuals with VHD and in
low-SES groups. Given that both VHD and low socioeconomic status significantly increase mortality burden[40, 41], adopting a healthier lifestyle help counteract
the negative association of VHD and low SES with life
expectancy.

into account potential changes in these factors duringfollow-up. However, this approach provided a more realistic picture of the comparison of health outcomes of
VHD based on the current traits of participants. Nonetheless, future research exploring the long-term trajectories of lifestyle and socioeconomic factors in relation to
VHD outcomes within well-defined cohorts is imperative. Such investigations would deepen our understanding of the influence these variables exert and provide
more precise recommendations for the development ofeffective interventions. Second, although we accounted
for recognized sources of bias, residual confounding
might still exist, and due to the observational nature of
our study, no causal inferences can be made. Third, VHD
was determined from hospital inpatient records in the
UK Biobank, and as prior studies indicate, the prevalenceof undiagnosed VHD among the elderly exists in half ofthe population [4]. This implies that the findings fromthis study are based mainly on symptomatic moderateand severe VHD and may not be applicable to mild conditions. Fourth, this study only included aortic stenosis
and mitral regurgitation. Other subtypes of valvular heartdisease were not included due to their lower incidence inthe UK Biobank, which prevents individual analyses ofthese conditions. Therefore, it is impossible to ensure thatthe conclusions of this study are consistent across different subtypes of valvular heart disease. Consequently, theconclusions of this study can only be applied to aortic
stenosis and mitral regurgitation. Finally, UK Biobank
participants are predominantly white individuals withhigher SES and relatively healthy lifestyles. Despite thelow generalizability of UK Biobank data, research suggests that representativeness of the “target” population
is not crucial for estimating risk factor associations [42].
Nevertheless, caution should be exercised when extrapolating these study results to more diverse populations.

Limitations
Our findings should be interpreted with caution in lightof several limitations. First, SES and lifestyle were measured only at enrollment, which means we did not take

Abbreviations
VHD	Valvular heart disease
SES	Socioeconomic statusHR	Hazard ratio
TDI	Townsend deprivation index

Conclusions
Undertaking a healthy lifestyle helped reduce the progression from health to incident VHD and subsequently
to death and prolonged life expectancy in people withand without VHD across socioeconomic levels. Ourfindings highlighted the importance of comprehensive
healthy lifestyle interventions in preventing VHD, which
can mitigate disease progression and increase life expectancy even among patients with VHD and within lowSES groups.

Wei et al. BMC Medicine(2024) 22:367

Supplementary Information
The online version contains supplementary material available at https://​doi.​
org/​10.​1186/​s12916-​024-​03576-9.
Additional file 1: Table S1-S13. Table S1- [Healthy lifestyle criteria and codesused in UK Biobank]. Table S2- [UK Biobank field codes used for valvular
heart disease definition and follow-up duration]. Table S3- [Associations
between individual lifestyle factors, lifestyle score, and health outcomes invalvular heart disease]. Table S4- [Incident VHD and death by lifestyle level:sensitivity analysis]. Table S5- [Associations between lifestyle level andhealth outcomes in aortic stenosis and mitral regurgitation]. Table S6- [Theassociation of the combination of lifestyle and socioeconomic status withhealth outcomes using reclassified TDI, household income, and education attainment to represent for socioeconomic status]. Table S7- [Theassociation of the combination of healthy lifestyle and socioeconomic
status with health outcomes in aortic stenosis and mitral regurgitation].
Table S8- [Incident VHD and death by lifestyle level stratified by reclassified
TDI, household income, and education attainment]. Table S9- [Incident
VHD and death by lifestyle level stratified by socioeconomic status after
excluding health outcomes within 2 years of recruitment and imputing
missing data]. Table S10- [Mortality among those with VHD by lifestylelevel stratified by socioeconomic status after additionally adjusted for any
operations of VHD]. Table S11- [Association of lifestyle factors with healthoutcomes of aortic stenosis and mitral regurgitation stratified by socioeconomic status]. Table S12- [Years of life gained by lifestyle level stratified bysocioeconomic status for participants immune to valvular heart disease].
Table S13- [Years of life gained by lifestyle level stratified by socioeconomic status after imputing missing data]. Fig. S1-S2. Fig. S1- [Flow chart].
Fig. S2- [Life expectancy for women and men immune to valvular heartdisease according to lifestyle level, stratified by socioeconomic status]
Acknowledgements
This research has been conducted using the UK Biobank Resource underapplications number 86898.
Authors’ contributions
JW, XL, and YW designed the study. YW accessed and verified the data,
conducted the statistical analysis, interpreted the results, and drafted themanuscript with the help of DS. JW, XL, SJ, and YH checked the accuracy of thestatistical analysis. All authors participated in revising the manuscript and haveread and approved the final version. JW, XL, and DS obtained funding for the
study. JW is the guarantor of this work.
Funding
This work was supported by Key Research and development Program(2019YFA0110400 for JW), National Natural Science Foundation of China (No.
81870292 for JW, No. 81570233, 81770252 for XBL, No. 82302479 for DWS), Key
Research and development Program of Zhejiang Province (No.2021C03097,
2018C03084 for JW, No.2022C03063 for XBL), and Zhejiang Research Center of
Cardiovascular Diagnosis and Treatment Technology (JBZX-202001 for JW).
Availability of data and materials
UK Biobank data are available through registration on the UK Biobank (www.​ukbio​bank.​ac.​uk).

Declarations
Ethics approval and consent to participate
The UK Biobank received ethical approval from the NHS National Research
Ethics Service (reference number: 16/NW/0274) and the Swedish Ethical
Review Authority (DNR: 2022–01516-01). All participants of the UK Biobank
provided written informed consent.
Consent for publication
No applicable.
Competing interests
The authors declare no competing interests.

Page 11 of 12

Author details
1
Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China. 2 State Key Laboratoryof Transvascular Implantation Devices, Hangzhou 310009, China. 3 Heart
Regeneration and Repair Key Laboratory of Zhejiang province, Hangzhou 310009, China. 4 Department of Anesthesiology, the Second AffiliatedHospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Received: 15 February 2024 Accepted: 22 August 2024

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