Serum fatty acids profile and association with early-onset coronary artery disease.

docosahexaenoic acid docosapentaenoic acid early-onset coronary artery disease eicosapentaenoic acid fatty acids

Journal

Therapeutic advances in chronic disease
ISSN: 2040-6223
Titre abrégé: Ther Adv Chronic Dis
Pays: United States
ID NLM: 101532140

Informations de publication

Date de publication:
2021
Historique:
received: 03 02 2021
accepted: 21 06 2021
entrez: 19 8 2021
pubmed: 20 8 2021
medline: 20 8 2021
Statut: epublish

Résumé

Fatty acids (FAs) play crucial roles in modulating and preventing diseases in humans, including early-onset coronary artery disease (EOCAD). In this study, we aimed to provide a profile of FAs in the serum of EOCAD patients and identify potential EOCAD-associated FAs. In the first stage, we analyzed the FAs profiles in pooled samples of patients with EOCAD using gas chromatography-mass spectrometry. In the second stage, the serum levels of the candidate FAs were validated in EOCAD patients. A total of 128 EOCAD patients and 64 controls were included in the study. Forty-nine serum FAs were quantified in pooled samples; three ω-3 FAs were identified to be associated with EOCAD. Moreover, results from the validation stage indicated that serum levels of docosahexaenoic acid (DHA) were significantly lower in EOCAD patients (55.43 ± 33.86 µg/ml) and myocardial infarction (MI) patients (47.49 ± 28.44 μg/ml) than those in the controls (70.65 ± 43.56 µg/ml). Multivariate regression analysis revealed that elevated serum DHA level was an independent protective factor for EOCAD [odds ratio (OR) = 0.8917, 95% confidence interval (CI): 0.879-0.957] and MI (OR = 0.835, 95% CI: 0.799-0.862). Decreased serum levels of docosapentaenoic acid (DPA) and eicosapentaenoic acid (EPA) were observed in the early-onset MI group. The study provided the serum FAs profile of EOCAD and confirmed that the decrease in serum levels of DHA, DPA, and EPA was associated with EOCAD. These findings might contribute to understanding the cardiovascular effects of FAs, particularly the protective effects of ω-3 polyunsaturated FAs.

Sections du résumé

BACKGROUND BACKGROUND
Fatty acids (FAs) play crucial roles in modulating and preventing diseases in humans, including early-onset coronary artery disease (EOCAD). In this study, we aimed to provide a profile of FAs in the serum of EOCAD patients and identify potential EOCAD-associated FAs.
METHODS METHODS
In the first stage, we analyzed the FAs profiles in pooled samples of patients with EOCAD using gas chromatography-mass spectrometry. In the second stage, the serum levels of the candidate FAs were validated in EOCAD patients.
RESULTS RESULTS
A total of 128 EOCAD patients and 64 controls were included in the study. Forty-nine serum FAs were quantified in pooled samples; three ω-3 FAs were identified to be associated with EOCAD. Moreover, results from the validation stage indicated that serum levels of docosahexaenoic acid (DHA) were significantly lower in EOCAD patients (55.43 ± 33.86 µg/ml) and myocardial infarction (MI) patients (47.49 ± 28.44 μg/ml) than those in the controls (70.65 ± 43.56 µg/ml). Multivariate regression analysis revealed that elevated serum DHA level was an independent protective factor for EOCAD [odds ratio (OR) = 0.8917, 95% confidence interval (CI): 0.879-0.957] and MI (OR = 0.835, 95% CI: 0.799-0.862). Decreased serum levels of docosapentaenoic acid (DPA) and eicosapentaenoic acid (EPA) were observed in the early-onset MI group.
CONCLUSION CONCLUSIONS
The study provided the serum FAs profile of EOCAD and confirmed that the decrease in serum levels of DHA, DPA, and EPA was associated with EOCAD. These findings might contribute to understanding the cardiovascular effects of FAs, particularly the protective effects of ω-3 polyunsaturated FAs.

Identifiants

pubmed: 34408821
doi: 10.1177/20406223211033102
pii: 10.1177_20406223211033102
pmc: PMC8366202
doi:

Types de publication

Journal Article

Langues

eng

Pagination

20406223211033102

Informations de copyright

© The Author(s), 2021.

Déclaration de conflit d'intérêts

Conflict of interest statement: The authors declare that there is no conflict of interest.

Références

Atherosclerosis. 2013 Jun;228(2):306-15
pubmed: 23518178
J Biomed Sci. 2017 Jul 27;24(1):50
pubmed: 28750629
Biosci Rep. 2020 Sep 30;40(9):
pubmed: 32808654
Eur J Prev Cardiol. 2016 Mar;23(5):502-10
pubmed: 25956428
Eur J Nutr. 2019 Oct;58(7):2639-2647
pubmed: 30167851
Nutr J. 2015 Oct 29;14:111
pubmed: 26514181
Biochimie. 2019 Apr;159:36-48
pubmed: 30716358
Circulation. 1957 Aug;16(2):227-45
pubmed: 13447167
Curr Atheroscler Rep. 2010 Nov;12(6):384-90
pubmed: 20711693
Am J Clin Nutr. 2008 Nov;88(5):1232-41
pubmed: 18996857
Eur J Intern Med. 2010 Dec;21(6):511-5
pubmed: 21111936
Nat Genet. 2009 Mar;41(3):334-41
pubmed: 19198609
Clin Chim Acta. 2017 Jan;464:195-199
pubmed: 27884754
Dis Markers. 2018 Oct 23;2018:1236837
pubmed: 30425752
Eur J Clin Nutr. 2020 Apr;74(4):651-656
pubmed: 31896827
J Clin Lipidol. 2015 Sep-Oct;9(5):703-8
pubmed: 26350818
Am J Clin Nutr. 1995 May;61(5):1129-39
pubmed: 7733039
JAMA Cardiol. 2018 Mar 1;3(3):225-234
pubmed: 29387889
Vascul Pharmacol. 2019 Jan;112:54-71
pubmed: 30115528
Proteomics Clin Appl. 2019 May;13(3):e1800079
pubmed: 30411527
Curr Diabetes Rev. 2012 Jan;8(1):2-17
pubmed: 22414056
Angiology. 2018 Aug;69(7):630-637
pubmed: 29241351
J Nutr. 1998 Feb;128(2 Suppl):444S-448S
pubmed: 9478045
Ann Nutr Metab. 2011;59(2-4):176-86
pubmed: 22142965
J Am Coll Cardiol. 2003 Feb 19;41(4):521-8
pubmed: 12598059
Nutrition. 2010 Oct;26(10):915-24
pubmed: 20888548
Biomolecules. 2020 Jul 30;10(8):
pubmed: 32751513
Nutrients. 2012 Dec 11;4(12):1989-2007
pubmed: 23363996
Ther Adv Chronic Dis. 2019 Dec 6;10:2040622319891539
pubmed: 31839921
Trends Cardiovasc Med. 2001 Apr-May;11(3-4):131-8
pubmed: 11686002
Lancet. 1999 Aug 7;354(9177):447-55
pubmed: 10465168
Biochem Genet. 2020 Apr;58(2):245-256
pubmed: 31552564
Aging Clin Exp Res. 2013 Aug;25(4):357-63
pubmed: 23824826
Biomedicines. 2020 Aug 25;8(9):
pubmed: 32854210
JAMA. 2016 Feb 2;315(5):457-8
pubmed: 26746707
Curr Opin Lipidol. 2003 Jun;14(3):337-9
pubmed: 12840665
Atherosclerosis. 2013 Jan;226(1):178-85
pubmed: 23206978
J Clin Lipidol. 2012 May-Jun;6(3):216-34
pubmed: 22658146
Diabetes Care. 2009 Feb;32(2):215-20
pubmed: 18957534
Nutr Rev. 2009 May;67(5):273-83
pubmed: 19386031
Lancet. 1989 Sep 30;2(8666):757-61
pubmed: 2571009
Circulation. 2019 Mar 26;139(13):1593-1602
pubmed: 30586733

Auteurs

Chao Xuan (C)

Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, No.1677, Wutai Mountain Road, Qingdao (West Coast), 266500, China.

Qing-Wu Tian (QW)

Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.

Hui Li (H)

Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.

Jun-Jie Guo (JJ)

Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, China.

Guo-Wei He (GW)

Center for Basic Medical Research & Department of Cardiovascular Surgery, TEDA International Cardiovascular Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.

Li-Min Lun (LM)

Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, No.1677, Wutai Mountain Road, Qingdao (West Coast), 266500, China.

Classifications MeSH