Progression to Cirrhosis Leads to Improvement in Atherogenic Milieu.
Atherosclerosis
Cardiovascular disease
Cirrhosis
Lipoprotein
Nonalcoholic steatohepatitis
Journal
Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
08
11
2019
accepted:
05
03
2020
pubmed:
20
3
2020
medline:
23
4
2021
entrez:
20
3
2020
Statut:
ppublish
Résumé
The prevalence of coronary artery disease (CAD) is high among patients with cirrhosis; however, the impact of it on cardiovascular disease (CVD) is not known. The aim of the current study was to evaluate CVD events in patients with cirrhosis and impact of cirrhosis on biomarkers of atherogenesis. The study included 682 patients with decompensated cirrhosis referred for liver transplantation (LT) evaluation between 2010 and 2017. All patients were followed until they experienced a CVD event, non-cardiac death, liver transplantation or last follow-up. To evaluate mechanistic link, patients with NASH cirrhosis were propensity matched 1:2 to non-cirrhosis NASH patients and biomarkers of atherogenic risk were compared. The composite CVD outcome occurred in 23(3.4%) patients after a median follow-up period of 585 days (IQR 139, 747). A strong association between presence of any CAD and CVD event was noted (HR = 6.8, 95% CI 2.9, 15.9) that was independent of age, gender, BMI, and MELD score. In competing risk model, the combined rate of LT and non-cardiac was significantly higher when compared to the rate of CVD events. Marker of insulin resistance and inflammation-related markers were similar in patients with and without cirrhosis. Patients with cirrhosis were more likely to have reduced VLDL, sdLDL-C, LDL-C, and triglycerides. Interestingly, patients with cirrhosis had an increase in serum HDL-2, the anti-atherogenic lipoprotein, and adiponectin, a protective serum adipokine. The risk of CVD events in patients with cirrhosis is low and may potentially be due to improvement in markers of atherogenic risk.
Identifiants
pubmed: 32189102
doi: 10.1007/s10620-020-06196-4
pii: 10.1007/s10620-020-06196-4
doi:
Substances chimiques
Inflammation Mediators
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
263-272Subventions
Organisme : BLRD VA
ID : I01 BX000197
Pays : United States
Commentaires et corrections
Type : CommentIn
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