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Joint control of low-density lipoprotein cholesterol, lipoprotein(a), and high-sensitivity C-reactive protein in relation to risk of cardiovascular disease in adults with steatotic liver disease

Zhang, Shunming LU ; Borné, Yan LU ; Ma, Le ; Huang, Tao and Qi, Lu (2026) In Nutrition, Metabolism and Cardiovascular Diseases
Abstract

Background and aims: We examined whether the excess cardiovascular disease (CVD) risk among adults with steatotic liver disease (SLD) subtypes could be reduced or eliminated through joint control of low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) [Lp(a)], and high-sensitivity C-reactive protein (hs-CRP). Methods and results: This prospective cohort study included 291,995 participants from the UK Biobank, comprising 77,187 with metabolic dysfunction-associated steatotic liver disease (MASLD), 22,190 with metabolic dysfunction and alcohol-associated liver disease (MetALD), 5474 with alcohol-associated liver disease (ALD), and 187,144 without SLD. Cox proportional hazards models were used to assess CVD risk associated with... (More)

Background and aims: We examined whether the excess cardiovascular disease (CVD) risk among adults with steatotic liver disease (SLD) subtypes could be reduced or eliminated through joint control of low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) [Lp(a)], and high-sensitivity C-reactive protein (hs-CRP). Methods and results: This prospective cohort study included 291,995 participants from the UK Biobank, comprising 77,187 with metabolic dysfunction-associated steatotic liver disease (MASLD), 22,190 with metabolic dysfunction and alcohol-associated liver disease (MetALD), 5474 with alcohol-associated liver disease (ALD), and 187,144 without SLD. Cox proportional hazards models were used to assess CVD risk associated with numbers of LDL-C, Lp(a), and hs-CRP controlled within the target range. During 12 years of median follow-up, 24,251 CVD events were documented, with 19,661 coronary heart disease and 5600 stroke. Among individuals with various SLD subtypes, those with all three factors controlled had the lowest risks of CVD, with HRs (95% CIs) of 0.65 (0.58, 0.72) in MASLD, 0.61 (0.49, 0.76) in MetALD, and 0.57 (0.35, 0.93) in ALD when comparing to zero-factor control. In addition, among individuals with SLD subtypes achieving all three factors within target ranges, the HRs (95% CIs) of CVD were 0.97 (0.88, 1.07) in MASLD, 0.90 (0.75, 1.08) in MetALD, and 0.63 (0.42, 0.95) in ALD, as compared with non-SLD controls. Similar association patterns were observed for coronary heart disease and stroke. Conclusions: Participants with various SLD subtypes who had optimally controlled LDL-C, Lp(a), and hs-CRP showed no excess or even lower risk of CVD as compared with the general population. Trial registered: Not available.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
in press
subject
keywords
Cardiovascular disease, High-sensitivity C-reactive protein, lipoprotein(a), Low-density lipoprotein cholesterol, Steatotic liver disease
in
Nutrition, Metabolism and Cardiovascular Diseases
article number
104722
publisher
Elsevier
external identifiers
  • scopus:105036302294
  • pmid:41997799
ISSN
0939-4753
DOI
10.1016/j.numecd.2026.104722
language
English
LU publication?
yes
additional info
Publisher Copyright: © 2026 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University
id
b4d9e736-5705-400c-8349-56283f2f246e
date added to LUP
2026-04-27 17:48:17
date last changed
2026-05-25 19:33:35
@article{b4d9e736-5705-400c-8349-56283f2f246e,
  abstract     = {{<p>Background and aims: We examined whether the excess cardiovascular disease (CVD) risk among adults with steatotic liver disease (SLD) subtypes could be reduced or eliminated through joint control of low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) [Lp(a)], and high-sensitivity C-reactive protein (hs-CRP). Methods and results: This prospective cohort study included 291,995 participants from the UK Biobank, comprising 77,187 with metabolic dysfunction-associated steatotic liver disease (MASLD), 22,190 with metabolic dysfunction and alcohol-associated liver disease (MetALD), 5474 with alcohol-associated liver disease (ALD), and 187,144 without SLD. Cox proportional hazards models were used to assess CVD risk associated with numbers of LDL-C, Lp(a), and hs-CRP controlled within the target range. During 12 years of median follow-up, 24,251 CVD events were documented, with 19,661 coronary heart disease and 5600 stroke. Among individuals with various SLD subtypes, those with all three factors controlled had the lowest risks of CVD, with HRs (95% CIs) of 0.65 (0.58, 0.72) in MASLD, 0.61 (0.49, 0.76) in MetALD, and 0.57 (0.35, 0.93) in ALD when comparing to zero-factor control. In addition, among individuals with SLD subtypes achieving all three factors within target ranges, the HRs (95% CIs) of CVD were 0.97 (0.88, 1.07) in MASLD, 0.90 (0.75, 1.08) in MetALD, and 0.63 (0.42, 0.95) in ALD, as compared with non-SLD controls. Similar association patterns were observed for coronary heart disease and stroke. Conclusions: Participants with various SLD subtypes who had optimally controlled LDL-C, Lp(a), and hs-CRP showed no excess or even lower risk of CVD as compared with the general population. Trial registered: Not available.</p>}},
  author       = {{Zhang, Shunming and Borné, Yan and Ma, Le and Huang, Tao and Qi, Lu}},
  issn         = {{0939-4753}},
  keywords     = {{Cardiovascular disease; High-sensitivity C-reactive protein; lipoprotein(a); Low-density lipoprotein cholesterol; Steatotic liver disease}},
  language     = {{eng}},
  publisher    = {{Elsevier}},
  series       = {{Nutrition, Metabolism and Cardiovascular Diseases}},
  title        = {{Joint control of low-density lipoprotein cholesterol, lipoprotein(a), and high-sensitivity C-reactive protein in relation to risk of cardiovascular disease in adults with steatotic liver disease}},
  url          = {{http://dx.doi.org/10.1016/j.numecd.2026.104722}},
  doi          = {{10.1016/j.numecd.2026.104722}},
  year         = {{2026}},
}