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      ABO gene polymorphisms are associated with acute coronary syndrome and with plasma concentration of HDL-cholesterol and triglycerides

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          Abstract

          The role of ABO gene polymorphisms in acute coronary syndrome (ACS) and lipid metabolism is increasingly recognized. We investigated whether ABO gene polymorphisms are significantly associated with ACS and the plasma lipid profile. Six ABO gene polymorphisms (rs651007 T/C, rs579459 T/C, rs495928 T/C, rs8176746 T/G, rs8176740 A/T, and rs512770 T/C) were determined by 5’exonuclease TaqMan assays in 611 patients with ACS and 676 healthy controls. The results demonstrated that the rs8176746 T allele was associated with a lower risk of ACS under the co-dominant, dominant, recessive, over-dominant, and additive models ( P ═ 0.0004, P ═ 0.0002, P ═ 0.039, P ═ 0.0009, and P ═ 0.0001, respectively). Furthermore, under co-dominant, dominant, and additive models, the rs8176740 A allele was associated with a lower risk of ACS ( P ═ 0.041, P ═ 0.022, and P ═ 0.039, respectively). On the other hand, the rs579459 C allele was associated with a lower risk of ACS under the dominant, over-dominant, and additive models ( P ═ 0.025, P ═ 0.035, and P ═ 0.037, respectively). In a subanalysis performed with the control group, rs8176746 T and rs8176740 A alleles were associated with low systolic blood pressure and with both high high-density lipoprotein-cholesterol (HDL-C) and low triglyceride plasma concentrations, respectively. In conclusion, ABO gene polymorphisms were associated with a lower risk of ACS, and lower systolic blood pressure and plasma lipid levels, suggesting a causal relationship between ABO blood groups and the incidence of ACS.

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          Most cited references35

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          2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes

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            Haploview: analysis and visualization of LD and haplotype maps.

            Research over the last few years has revealed significant haplotype structure in the human genome. The characterization of these patterns, particularly in the context of medical genetic association studies, is becoming a routine research activity. Haploview is a software package that provides computation of linkage disequilibrium statistics and population haplotype patterns from primary genotype data in a visually appealing and interactive interface. http://www.broad.mit.edu/mpg/haploview/ jcbarret@broad.mit.edu
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              Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage.

              Observational studies of necrotic core progression identify intraplaque hemorrhage as a critical factor in atherosclerotic plaque growth and destabilization. The rapid accumulation of erythrocyte membranes causes an abrupt change in plaque substrate characterized by increased free cholesterol within the lipid core and excessive macrophage infiltration. Neoangiogenesis is associated closely with plaque progression, and microvascular incompetence is a likely source of intraplaque hemorrhage. Intimal neovascularization is predominantly thought to arise from the adventitia, where there are a plethora of pre-existing vasa vasorum. In lesions that have early necrotic cores, the majority of vessels invading from the adventitia occur at specific sites of medial wall disruption. A breech in the medial wall likely facilitates the rapid in-growth of microvessels from the adventitia, and exposure to an atherosclerotic environment stimulates abnormal vascular development characterized by disorganized branching and immature endothelial tubes with "leaky" imperfect linings. This network of immature blood vessels is a viable source of intraplaque hemorrhage providing erythrocyte-derived phospholipids and free cholesterol. The rapid change in plaque substrate caused by the excessive accumulation of erythrocytes may promote the transition from a stable to an unstable lesion. This review discusses the potential role of intraplaque vasa vasorum in lesion instability as it relates to plaque rupture.
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                Author and article information

                Journal
                Biomol Biomed
                Biomol Biomed
                Biomolecules and Biomedicine
                Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina
                2831-0896
                2831-090X
                1 December 2023
                1 December 2023
                : 23
                : 6
                : 1125-1135
                Affiliations
                [1 ]Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, México
                [2 ]Departamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, México
                [3 ]Unidad Coronaria, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, México
                [4 ]Unidad de Medicina Experimental, Hospital General de Mexico, Dr. Eduardo Liceaga, Mexico City, México
                [5 ]Unidad de Investigación en Epidemiologia y Servicios de Salud-Área de Envejecimiento. Centro Médico Nacional Siglo XXI. Instituto Mexicano del Seguro Social, Mexico City, México
                Author notes
                [* ]Correspondence to José Manuel Fragoso: mfragoso1275@ 123456yahoo.com.mx
                [#]

                Gilberto Vargas-Alarcón and Oscar Pérez-Méndez contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-7916-5163
                https://orcid.org/0000-0002-6977-1829
                https://orcid.org/0000-0001-8467-3488
                https://orcid.org/0000-0002-4370-9963
                https://orcid.org/0000-0002-5942-4102
                https://orcid.org/0000-0002-9224-7400
                https://orcid.org/0000-0002-9442-3471
                https://orcid.org/0009-0000-5476-4020
                https://orcid.org/0000-0003-3137-7815
                Article
                BB-23-1125
                10.17305/bb.2023.9244
                10655879
                37334748
                84b1cbc6-61ff-4d94-ae8f-5f40ae9930a3
                © 2023 Vargas-Alarcón et al.

                This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

                History
                : 2 May 2023
                : 19 June 2023
                : 10 June 2023
                Categories
                Research Article

                polymorphisms,acute coronary syndrome (acs),human abo blood group system

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