Abdominal Aortic Aneurysm Genetic Associations: Mostly False? A Systematic Review and Meta-analysis

Bradley, Declan; Badger, Stephen A.; McFarland, Marie; Hughes, A E

doi:10.1016/j.ejvs.2015.09.006

Cited by 42 publications

(43 citation statements)

References 114 publications

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“…It is no surprise that a significant part of the changed gene expression is related to genes involved in inflammatory processes, i.e. genes for chemokines, integrins, and those for T and B cell activation, similarly to the previously published studies (Biros et al 2014, Hinterseher et al 2013, Giusti et al 2009, Butt et al 2016, Tanios et al 2015. Destructive inflammation is the main characteristic of AAA formation and progression; it is therefore understandable that immunological mechanisms are at play.…”

Section: Discussionsupporting

confidence: 69%

“…Taking samples from the same patient represents a possible limitation of the study if the genetic factors played a significant role in the onset of the disease. While in the thoracic aortic aneurysms (TTA), we already know a specific list of genes that are undoubtedly associated with the pathogenesis of TAA, no mutation predicting the occurrence of AAA has yet been found (Carino et al 2018). Therefore, it will certainly not be a monogenic disease.…”

Section: Discussionmentioning

confidence: 99%

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Gene Expression in Patients With Abdominal Aortic Aneurysm – More Than Immunological Mechanisms Involved

et al. 2019

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Abdominal aortic aneurysm (AAA) is a serious condition of unclear pathogenesis and progression. Two samples were collected from 48 patients during AAA surgery. One sample was collected from the aneurysm, the other from the aneurysm proximal neck where the tissue did not exhibit any aneurysmal changes. Subsequently, gene expression profiles using microarrays (Illumina) were compared in RNA extracted from the samples. Overall, 2,185 genes were found to be upregulated and 2,100 downregulated; from which 158 genes had a different expression with FDR<0.05 (False Discovery Rate) and FC≥2 (Fold Change). Of this number, 115 genes were over-expressed and 43 under-expressed. The analysis of the gene list based on their biological pathways revealed that the regulation of inflammation was mediated by chemokine and cytokine signaling pathways, the integrin signaling pathway, and T and B cell activation. Moreover, a change was identified in the expression of genes involved in both intercellular and intracellular signaling systems.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Gene Expression in Patients With Abdominal Aortic Aneurysm – More Than Immunological Mechanisms Involved

et al. 2019

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“…Those differences were confirmed in many different cell types, such as macrophages, smooth muscle cells, and fibroblasts . The MMP3 gene polymorphism 1171dupA has been associated with many cardiovascular diseases such as: CHD, myocardial infarction, instable angina, ischemic stroke, deep venous thrombosis, abdominal aortic aneurysm, coronary artery stenosis, and hypertension . Numerous studies indicate the association between this polymorphism and coronary artery disease; however, the results are inconsistent.…”

Section: Introductionmentioning

confidence: 94%

MMP1 and MMP3 gene polymorphisms in patients with acute coronary syndromes

Pawlik

Plucinska²,

Kopec

et al. 2017

IUBMB Life

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Matrix metalloproteinases (MMPs) are the group of proteolytic enzymes that break down the components of the connective tissue matrix leading to unstable atherosclerotic plaques. The aim of this study was to examine the association between MMP1-1607dupG (rs1799750) and MMP3-1171dupA (rs3025058) gene polymorphisms and acute coronary syndromes (ACS) in the form of unstable angina. This study included 197 patients with ACS in the form of unstable angina confirmed by coronary angiography (defined by >70% stenosis in at least one major coronary artery) and 144 healthy controls. There was no statistically significant difference in the distribution of the MMP1-1607dupG (rs1799750) polymorphism between patients with unstable angina and the control group. With regard to the MMP3-1171dupA (rs3025058) polymorphism, a significant increase in the frequency of the 6A/6A genotype among patients with unstable angina was detected. This association was confirmed in multivariate logistic regression analysis, where male sex and rs3025058 6A/6A genotype were significantly associated with an increased risk of ACS. © 2017 IUBMB Life, 69(11):850-855, 2017.

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“…Future screening studies may also evaluate genetic factors in association with presence of AAA, as it has been suggested that polymorphisms in some genes had strong or moderate association with AAA. 30 While the cost-effectiveness of the current screening programs is obvious, population stratification to identify the most vulnerable based on novel risk factors may further increase their efficacy and reduce costs, especially in consideration with the need for rescreening because of the aging population. Future screening programs may benefit from the inclusion of more targeted criteria in order to increase the number of detected AAAs.…”

mentioning

confidence: 99%

Abdominal Aortic Aneurysm Screening: Do We Need to Shift Toward a Targeted Strategy?

2017

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Several abdominal aortic aneurysm (AAA) screening programs have been developed worldwide, aiming at early identification of individuals with an unknown AAA. 1 This became possible because of the high accuracy (sensitivity and specificity of nearly 100%) of duplex scan, a noninvasive investigation performed by portable scanners. 2 Early detection of AAA allows a timely elective repair leading to a reduced AAA-related mortality and complications associated with an urgent intervention. 3,4 A recent systematic evidence review for the US Preventive Services Task Force suggested that onetime invitation for AAA screening in men aged 65 years or older was associated with decreased AAA rupture and AAA-related mortality rates. 5 Another study highlighted the significant risk of AAA patients for developing cardiovascular (CV) events and thus the identification of those patients even with small AAA may contribute to CV risk reduction. 6 A recent meta-analysis showed that invitation to AAA screening in 64-year-old men significantly reduced both all-cause and AAA-related mortality. 7 The Society for Vascular Surgery (SVS) has recommended onetime duplex scan screening for AAAs in men aged 55 years or older with a family history of AAA, all men aged 65 years or older, and women aged 65 years or older who have smoked or have a family history of AAA. 8 In the United States, Medicare covers 1 ultrasound scan screening of men aged 65 to 75 years who ever smoked in their lifetime or men and women who have a family history of AAA disease as part of a "Welcome to Medicare" package. 9 The European Society for Vascular Surgery has recommended that men should be screened for AAAs with a single duplex scan at the age of 65 years or younger men who may be at increased risk (eg, those who smoke or have a family history). 10 On the other hand, although the American College of Preventive Medicine has recommended onetime screening in men aged 65 to 75 years who have ever smoked, it has not recommended routine screening in women. 11 Recent literature has highlighted the association of clinical factors with the increased incidence of AAA, which are not included in the indications of guidelines for AAA screening.A total of 22 studies involving 13 388 patients concluded that AAA prevalence was significantly higher in patients with coronary artery disease versus patients without (odds ratio [OR] 2.42, 95% confidence interval [CI], 2.08-2.81). 12 Another meta-analysis showed that serum low-density lipoprotein cholesterol is higher in patients with AAA (mean differences [MD], 0.25 mmol/L; 95% CI, 0.08-0.42 mmol/L; P ¼ .004) than control patients while the serum high-density lipoprotein cholesterol is likely lower. 13 Additionally, a significant association between AAA and other factors has been demonstrated, such as body mass index (OR 1.20; 95% CI, 1.17-1.22), 14 chronic obstructive pulmonary disease (adjusted OR 3.0; 95% CI 1.6-5.5, P < .001), 15 primary abdominal wall hernia (OR 2.32; 95% CI, 1.72-3.14; P for effect <.00001; P for heterogeneity <.0...

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Abdominal Aortic Aneurysm Genetic Associations: Mostly False? A Systematic Review and Meta-analysis

Cited by 42 publications

References 114 publications

Gene Expression in Patients With Abdominal Aortic Aneurysm – More Than Immunological Mechanisms Involved

Gene Expression in Patients With Abdominal Aortic Aneurysm – More Than Immunological Mechanisms Involved

MMP1 and MMP3 gene polymorphisms in patients with acute coronary syndromes

Abdominal Aortic Aneurysm Screening: Do We Need to Shift Toward a Targeted Strategy?

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