Blood Biomarkers and Serologic Immunological Profiles Related to Periodontitis in Abdominal Aortic Aneurysm Patients

BackgroundPeriodontitis is a chronic inflammatory gum disease associated with systemic diseases such as cardiovascular diseases.AimTo investigate the association of systemic blood biomarkers, C-reactive protein (CRP), levels of lipopolysaccharide (LPS), and IgG levels against periodontal pathogens Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) with the stability, based on the aortic diameter, the growth rate and the eligibility for surgical intervention, of patients with abdominal aortic aneurysm (AAA).MethodsPatients with stable AAA (n = 30) and unstable AAA (n = 31) were recruited. The anti-A. actinomycetemcomitans and anti-P. gingivalis IgG levels were analyzed by ELISA, the LPS analysis was performed by using the limulus amebocyte lysate (LAL) test, and plasma levels of CRP were determined using an immune turbidimetric method. The association between these blood systemic biomarkers, AAA features, periodontal clinical parameters and oral microbial profiles were explored. Regression models were used to test the relationship between variables.ResultsThe presence of antibodies against Pg and Aa, LPS and high CRP concentrations were found in all AAA patients. The IgG levels were similar in patients with stable and unstable AAA (both for Aa and Pg). Among investigated blood biomarkers, only CRP was associated with AAA stability. The amount of LPS in saliva, supra, and subgingival plaque were significantly associated with the systemic LPS (p <0.05).ConclusionsThis post-hoc study emphasizes the presence of antibodies against Pg and Aa, LPS and high CRP concentrations in all AAA patients. The presence of Pg in saliva and subgingival plaque was significantly associated with the blood LPS levels. For further studies investigating periodontitis and systemic diseases, specific predictive blood biomarkers should be considered instead of the use of antibodies alone.

Change in Abdominal Aortic Aneurysm Sac Diameter After Endovascular Repair: A Single-Center Experience From Taiwan

Purpose: The purpose of this study was to investigate the change in the diameter of infrarenal abdominal aortic aneurysm (AAA) sacs after endovascular aortic repair (EVAR) in Taiwanese patients and to depict its association with clinical outcomes. Materials and Methods: This retrospective cohort study was conducted on patients who underwent EVAR for infrarenal AAA between January 2011 and December 2016. All preoperative and follow-up computed tomography (CT) images were reviewed. Postoperative CT angiography was arranged after 1 month and annually thereafter. The maximal diameter on the axial plane and the maximal diameter perpendicular to the centerline on the coronal and sagittal planes were measured. The study examined post-EVAR sac diameter change over time and compared the differences in adverse events (AEs) among groups. Results: The survey included a total of 191 patients with a median follow-up duration of 2.5 (interquartile range: 1.1–2.9) years. Overall survival rates at 1, 2, and 5 years were 92%, 81%, and 76%, respectively. According to their last CT scans, the patients were categorized into 3 groups as follows: shrinkage, stationary, and enlargement, which comprised 58 (30.4%), 118 (61.8%), and 15 (7.9%) patients, respectively. Pre-EVAR characteristics and sac diameters were similar among the groups. Sac shrinkage was exclusively observed in the first 2 years, whereas sac enlargement developed at all follow-up periods. Patients with sac enlargement had higher incidence rates of endoleaks, complications, and reintervention than the other groups. Conclusion: Based on our observations, post-EVAR sac shrinkage only occurs in the first 2 years; however, post-EVAR sacs may enlarge at any point and even after 5 years. In our study, patients with sac enlargement had higher rates of adverse events and reintervention.

The Role and Mechanism of SIRT6 in Regulating Phenotype Transformation of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm

Background. Data mining of current gene expression databases has not been previously performed to determine whether sirtuin 6 (SIRT6) expression participates in the pathological process of abdominal aortic aneurysm (AAA). The present study was aimed at investigating the role and mechanism of SIRT6 in regulating phenotype transformation of vascular smooth muscle cells (VSMC) in AAA. Methods. Three gene expression microarray datasets of AAA patients in the Gene Expression Omnibus (GEO) database and one dataset of SIRT6-knockout (KO) mice were selected, and the differentially expressed genes (DEGs) were identified using GEO2R. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of both the AAA-related DEGs and the SIRT6-related DEGs were conducted. Results. GEO2R analysis showed that the expression of SIRT6 was downregulated for three groups and upregulated for one group in the three datasets, and none of them satisfied statistical significance. There were top 5 DEGs (KYNU, NPTX2, SCRG1, GRK5, and RGS5) in both of the human AAA group and SIRT6-KO mouse group. Top 25 ontology of the SIRT6-KO-related DEGs showed that several pathways including tryptophan catabolic process to kynurenine and negative regulation of cell growth were enriched in the tissues of thickness aortic wall biopsies of AAA patients. Conclusions. Although SIRT6 mRNA level itself did not change among AAA patients, SIRT6 may play an important role in regulating several signaling pathways with significant association with AAA, suggesting that SIRT6 mRNA upregulation is a protective factor for VSMC against AAA.

Fibrates: A Possible Treatment Option for Patients with Abdominal Aortic Aneurysm?

Abdominal aortic aneurysm (AAA) is a life-threatening disease; however, there is no established treatment for patients with AAA. Fibrates are agonists of peroxisome proliferator-activated receptor alpha (PPARα) that are widely used as therapeutic agents to treat patients with hypertriglyceridemia. They can regulate the pathogenesis of AAA in multiple ways, for example, by exerting anti-inflammatory and anti-oxidative effects and suppressing the expression of matrix metalloproteinases. Previously, basic and clinical studies have evaluated the effects of fenofibrate on AAA. In this paper, we summarize the results of these studies and discuss the problems associated with using fenofibrate as a therapeutic agent for patients with AAA. In addition, we discuss a new perspective on the regulation of AAA by PPARα agonists.