Risk Of Aortic Aneurysm Research Articles

Endothelial cyclin I reduces vulnerability to angiotensin II-induced vascular remodeling and abdominal aortic aneurysm risk.

Retinoblastoma protein (Rb) supports vasoprotective E2F Transcription Factor 1 (E2f1)/Dihydrofolate Reductase (Dhfr) pathway activity in endothelial cells. Cyclin I (Ccni) promotes Cyclin-Dependent Kinase-5 (Cdk5)-mediated Rb phosphorylation. Therefore, we hypothesized that endothelial Ccni may regulate cardiovascular homeostasis, vessel remodeling, and abdominal aortic aneurysm (AAA) formation. Aortic CCNI mRNA expression was analyzed in the Gene Expression Omnibus (GEO) GSE57691 cohort consisting of AAA patients (n=39) and healthy controls (n=10). We employed wild-type (WT) mice and endothelial Ccni knockout (Ccnifl/flTie2-Cre) mice to conduct in vivo and ex vivo experimentation using an Angiotensin (Ang) II hypertension model and a CaCl2 AAA model. Mice were assessed for Rb/E2f1/Dhfr signaling, biopterin (i.e., biopterin [B], dihydrobiopterin [BH2], and tetrahydrobiopterin [BH4]) production, cardiovascular homeostasis, vessel remodeling, and AAA formation. Aortic CCNI mRNA expression was downregulated in AAA patients. Both Ang II- and CaCl2-induced WT mice showed aortic Ccni upregulation coupled with vasculoprotective upregulation of Rb/E2f1/Dhfr signaling and biopterins. Endothelial Ccni knockout downregulated medial Rb/E2f1/Dhfr signaling and biopterins in Ang II-induced hypertensive mice, which exacerbated eNos uncoupling and H2O2 production. Endothelial Ccni knockout impaired in vivo hemodynamic responses and endothelium-dependent vasodilatation in ex vivo mesenteric arteries in response to Ang II. Endothelial Ccni knockout exacerbated mesenteric artery remodeling and AAA risk in response to Ang II and CaCl2. Endothelial Ccni acts as a critical negative regulator of eNos uncoupling-mediated ROS generation and thereby reduces vulnerability to hypertension-induced vascular remodeling and AAA development in mice.

Model-Based Fluid-Structure Interaction Approach for Evaluation of Thoracic Endovascular Aortic Repair Endograft Length in Type B Aortic Dissection.

Thoracic endovascular aortic repair (TEVAR) is a commonly performed operation for patients with type B aortic dissection (TBAD). The goal of TEVAR is to cover the proximal entry tear between the true lumen (TL) and the false lumen (FL) with an endograft to induce FL thrombosis, allow for aortic healing, and decrease the risk of aortic aneurysm and rupture. While TEVAR has shown promising outcomes, it can also result in devastating complications including stroke, spinal cord ischemia resulting in paralysis, as well as long-term heart failure, so treatment remains controversial. Similarly, the biomechanical impact of aortic endograft implantation and the hemodynamic impact of endograft design parameters such as length are not well-understood. In this study, a fluid-structure interaction (FSI) computational fluid dynamics (CFD) approach was used based on the immersed boundary and Lattice–Boltzmann method to investigate the association between the endograft length and hemodynamic variables inside the TL and FL. The physiological accuracy of the model was evaluated by comparing simulation results with the true pressure waveform measurements taken during a live TEVAR operation for TBAD. The results demonstrate a non-linear trend towards increased FL flow reversal as the endograft length increases but also increased left ventricular pulsatile workload. These findings suggest a medium-length endograft may be optimal by achieving FL flow reversal and thus FL thrombosis, while minimizing the extra load on the left ventricle. These results also verify that a reduction in heart rate with medical therapy contributes favorably to FL flow reversal.

Abdominal aortic aneurysm growth rates in patients undergoing local ultrasound surveillance.

Abdominal aortic aneurysm ultrasound surveillance varies between hospitals in the United Kingdom. University Hospitals Bristol and Weston adopt a 6-monthly surveillance interval for 4.5-4.9 cm abdominal aortic aneurysm, which is a deviation from nationally recommended 3-monthly intervals. Assessment of abdominal aortic aneurysm growth rate, and the concurrent impact of abdominal aortic aneurysm risk factors and medications prescribed for risk factors, may inform whether this change in surveillance intervals is safe and appropriate. This analysis was conducted retrospectively. A total of 1312 abdominal aortic aneurysm ultrasound scans from 315 patients between January 2015 and March 2020 were split into 0.5 cm groups, ranging from 3.0 to 5.5 cm. Abdominal aortic aneurysm growth rate was assessed with one-way analysis of variance. The impact of risk factors and risk factor medication on abdominal aortic aneurysm growth rate was analysed using multivariate and univariate linear regression and Kruskal-Wallis tests. Patient cause of death among surveillance patients was recorded. Abdominal aortic aneurysm growth rate was significantly associated with increased abdominal aortic aneurysm diameter (p < 0.001). There was a significant whole-group reduction in growth rate from 0.29 to 0.19 cm/year in diabetics compared to non-diabetics (p = 0.02), supported by univariate linear regression (p = 0.04). In addition, gliclazide patients had lower growth rate compared to patients not on the medication (p = 0.04). One abdominal aortic aneurysm rupture occurred <5.5 cm resulting in death. Abdominal aortic aneurysm measuring 4.5-4.9 cm had a mean growth rate of 0.3 cm/year (± 0.18 cm/year). Therefore, mean growth rate and variability suggest patients are unlikely to surpass surgical threshold of 5.5 cm between the 6-monthly surveillance scans, supported by low rupture rates. This suggests the surveillance interval for 4.5-4.9 cm abdominal aortic aneurysm is a safe and appropriate deviation from national guidance. In addition, it may be pertinent to consider diabetic status when designing surveillance intervals.

High heritability of ascending aortic diameter and trans-ancestry prediction of thoracic aortic disease.

Enlargement of the aorta is an important risk factor for aortic aneurysm and dissection, a leading cause of morbidity in the developed world. Here we performed automated extraction of ascending aortic diameter from cardiac magnetic resonance images of 36,021 individuals from the UK Biobank, followed by genome-wide association. We identified lead variants across 41 loci, including genes related to cardiovascular development (HAND2, TBX20) and Mendelian forms of thoracic aortic disease (ELN, FBN1). A polygenic score significantly predicted prevalent risk of thoracic aortic aneurysm and the need for surgical intervention for patients with thoracic aneurysm across multiple ancestries within the UK Biobank, FinnGen, the Penn Medicine Biobank and the Million Veterans Program (MVP). Additionally, we highlight the primary causal role of blood pressure in reducing aortic dilation using Mendelian randomization. Overall, our findings provide a roadmap for using genetic determinants of human anatomy to understand cardiovascular development while improving prediction of diseases of the thoracic aorta.

New England Congenital Cardiology Association Bicuspid Aortopathy Registry (NECCA BAR): A regional preventive cardiovascular care collaboration

BackgroundBicuspid aortic valve is the most common congenital heart defect, and its association with proximal aortic dilation (aortopathy) increases risk for aortic aneurysm and dissection in adults. Maximal aortic root and ascending aortic dimensions are predictors of adverse cardiovascular outcomes. Recent single center data demonstrate medical therapy with beta or angiotensin II receptor blockers tempers aortic growth rates. Although randomized clinical trials may not be feasible, larger population studies would better inform bicuspid aortic valve preventive cardiovascular care. ObjectiveImprove regional pediatric bicuspid aortopathy collaboration with standardized medical management guidelines and patient care registry. MethodsThe New England Congenital Cardiology Association (NECCA) developed consensus-based prophylactic treatment guidelines for bicuspid aortopathy and designed a regional clinical registry (NECCA BAR) to study cardiovascular practice variation and short-term outcomes in subjects with moderate to severe bicuspid aortopathy. Individuals 6 months to 25 years of age with bicuspid aortic valve (all variants) and body surface area-adjusted aortic root or ascending aorta z score ≥ 4.0 SD, and/or absolute dimension ≥4.0 cm, are eligible for inclusion. Standardized bicuspid aortopathy medical management guidelines were established among New England congenital cardiology practices. The primary aims are to compare cardiovascular practice variation by guideline adherence (medical therapy and athletic participation), and evaluate medication effectiveness by comparing rates of annual change in aortic root and ascending aorta dimensions/z scores over 3 years. Additional endpoints include aortic valve disease progression (stenosis/regurgitation), incidence of aortic dissection, surgery, death, and incidence of adverse drug events. ResultsRecruitment in progress; data analysis pending. ConclusionWe describe the development of regional pediatric clinical care guidelines and a patient care registry designed to refine medical management of bicuspid aortopathy.

Risk of subarachnoid haemorrhages and aneurysms in Danish people with HIV

It remains unclear whether people with HIV (PWH) have increased risk of aneurysms. We aimed to investigate if the risk of subarachnoid haemorrhage, cerebral aneurysm, aortic aneurysm and other arterial aneurysms and dissections is increased in PWH compared with the general population. We performed a nationwide population-based matched cohort study. We compared PWH with age-matched and sex-matched comparison cohort members to calculate incidence rate ratios (IRR) of subarachnoid haemorrhage, cerebral aneurysm, aortic aneurysm and other arterial aneurysms and dissections as well as surgery for these conditions. We included all PWH, who were Danish residents and treated at a HIV healthcare centre between January 1995 and February 2018 ( n = 6935) and an age-matched and sex-matched comparison cohort ( n = 55 480). PWH had increased risk of subarachnoid haemorrhage (IRR 1.7, 95% CI, 1.1-2.6), but no increased risk of surgery for this condition. PWH had no increased risk of cerebral aneurysm or aortic aneurysm or surgery for these conditions. The risk of other arterial aneurysms and dissections was increased in PWH (IRR 2.0, 95% CI, 1.4-2.9), but this only applied for PWH who reported intravenous substance use as a route of HIV transmission (IRR 18.4, 95% CI, 9.3-36.6), and not for PWH without reported injection drug use (IRR 1.2, 95% CI, 0.73-1.7). PWH were not at an increased risk of cerebral, aortic or other arterial aneurysms and dissections. Although PWH were at an increased risk of subarachnoid haemorrhage, subarachnoid haemorrhages were rare among PWH.

Does oral ciprofloxacin affect the structure of thoracic aorta in adult and senile male albino rats? A clue to fluoroquinolones-induced risk of aortic dissection.

In this study, the effect of oral ciprofloxacin on the structure of the thoracic aorta in rats was investigated. Twenty four male albino rats were divided into 4 groups (6 rats/group): group I (adult control), group II (adult rats treated with ciprofloxacin), group III (senile control), and group IV (senile rats treated with ciprofloxacin). Rats in groups II and IV received ciprofloxacin via oral gavage in a daily dose of 3.5 mg/kg/d for 14 days, while control rats received equivalent amount of distilled water used to dissolve the drug. After 2 weeks, all rats were sacrificed, thoracic aortae were dissected, and half of the specimens were processed for paraffin sections and examined by light microscopy. The other half of the specimens were prepared for scanning electron microscopy. Sections from rats treated with ciprofloxacin showed evident damaging effect on aortic wall particularly in (group IV). Aortic intima showed, focal desquamation of the lining epithelium. Tunica media exhibited loss of the normal concentric arrangement and degeneration of the smooth muscle cells. Immune staining for alpha smooth muscle actin showed muscle damage. Interestingly, some sections in (group IV) showed out-pouch (aneurysm like) of the aortic wall. There was dense collagen fibers deposition. Scanning electron microscopic observations of (group IV) revealed uneven intima, adherent blood cells and fibrin filaments to damaged intima, and out-pouch formation. It was concluded that oral ciprofloxacin caused deleterious structural changes in the thoracic aortic wall of rats explaining clinical observations of fluoroquinolones induced risk of aortic dissection and aneurysm.

Does autosomal dominant polycystic kidney disease increase the risk of aortic aneurysm or dissection: a point of view based on a systematic review and meta-analysis

Autosomal Dominant Polycystic Kidney Disease (ADPKD) has several renal and extra-renal manifestations. Studies have reported a higher incidence of aortic aneurysms (AAs)/aortic dissections (ADs) in these patients, and we believe ADPKD should be considered as a risk factor for AA/AD. In order to support our opinion we conducted a systematic review and meta-analysis analyzing the risk of AA/AD in ADPKD patients.We searched MEDLINE, CENTRAL, PsycInfo, Web of Science Core Collection and OpenGrey for observational studies reporting frequency estimates of AA/AD in ADPKD patients compared with controls. We analyzed the odds ratio (OR) of the existence of an AA/AD in patients with ADPKD compared to controls. We also analyzed the odds of having an AA in patients with ADPKD compared to controls, the odds of having an AD in patients with ADPKD compared to controls, differences among subtypes of AA or AD, differences according to age, gender and different study designs.Seven observational studies were included. ADPKD was associated with a higher risk of AA or AD as compared with a population without the disease (OR 4.33; 95% CI 2.69; 6.97, p < 0.001); higher risk of AA (OR 4.18; 95% CI 2.36; 7.40, p < 0.001) and higher risk of AD (OR 9.08; 95% CI 3.11; 26.55, p < 0.001).Our point of view, suggesting the inclusion of aortic aneurysms and aortic dissection in the potential complications of ADPKD, was supported by our systematic review and meta-analysis showing that ADPKD was associated with a significant risk of having/developing an AA/AD. However, the risk of bias of included studies was considered high and these results should be interpreted cautiously. This association should be considered in clinical practice, although further studies are needed to consolidate these findings.

In This Issue

HomeCirculation ResearchVol. 130, No. 5In This Issue Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessIn BriefPDF/EPUBIn This Issue Ruth Williams Ruth WilliamsRuth Williams Search for more papers by this author Originally published3 Mar 2022https://doi.org/10.1161/RES.0000000000000536Circulation Research. 2022;130:691is related toEro1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac ArrhythmiaGLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body InhibitionInhibition of IL11 Signaling Reduces Aortic Pathology in Murine Marfan SyndromeGLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body Inhibition (p 694)Gut hormone receptors in the carotid body may be treatment targets for metabolic syndrome, say Pauza et al.Download figureDownload PowerPointHypertension and diabetes are risk factors for cardiovascular disease (CVD) and yet, for many patients with these two conditions, lowering blood pressure and blood sugar is insufficient for eliminating the risk. Because both hypertension and diabetes are linked to increased sympathetic nerve activation, and because the carotid body (CB)—a clusters of sensory cells in the carotid artery—regulates sympathetic nerve activity, Pauza and colleagues investigated the CB’s possible involvement. They performed a transcriptome analysis of CB tissue from rats with and without spontaneous hypertension and found, among many differently expressed genes, that the transcript encoding glucagon-like peptide-1 receptor (GLP1R) was considerably less abundant in the hypertensive animals. This was of particular interest because the gut hormone GLP1 promotes insulin secretion and tends to be suppressed in type 2 diabetes. Moreover, GLP1R agonists are already used as diabetes treatments. The team now show that treating rat CBs with such an agonist suppresses sympathetic nerve activation and arterial blood pressure, suggesting such drugs may provide benefits in more ways than one, and that the CB could be a novel target for lowering CVD risk in metabolic syndrome.Ero1α-Dependent ERp44 Dissociation from RyR2 Contributes to Cardiac Arrhythmia (p 711)Blocking oxidoreductase Ero1α could reduce arrhythmia risk in cardiovascular disease, say Hamilton et al.Download figureDownload PowerPointThe oxidative stress associated with cardiovascular disease (CVD) can lead to heart arrhythmia and sudden death. At the cellular level, the increased oxidation in the sarcoplasmic reticulum (SR) triggers aberrant release of calcium—via the ryanodine receptor (RyR2) channel—and this in turn ramps up muscle contractions. However, the precise molecular details of the pathology are lacking. Cellular stress is known to raise the level of SR oxidoreductase Ero1α, which interacts with an inhibitor of calcium release called ERp44. Now, Hamilton and colleagues complete the molecular puzzle, showing that ERp44 normally binds and inhibits RyR2 in rat cardiomyocytes. The stress-induced increase in Ero1α expression (in hypertrophic rat cardiomyocytes) causes dissociation of ERp44 from RyR2, they report, thus boosting calcium release. Importantly, the team also showed that inhibiting Ero1α reduced oxidation in the SR, prevented ERp44-RyR2 disassociation and reduced RyR2-mediated calcium release. It also curbed arrhythmia in isolated hypertrophic hearts. Because myocardium from heart failure patients also exhibited increased Ero1α expression compared with controls, the authors say, Ero1α inhibition could be a clinical strategy for preventing CVD-associated arrhythmia.Inhibition of IL11 Signaling Reduces Aortic Pathology in Murine Marfan Syndrome (p 728)Lim et al suggest cytokine IL-11 as a new target for the treatment of Marfan syndrome.Download figureDownload PowerPointPeople with the genetic connective tissue disorder Marfan syndrome (MFS) are typically tall and thin with long limbs, and are prone to skeletal, eye and cardiovascular problems including a life-threatening weakening of the aorta. While MFS patients commonly take blood-pressure lowering treatments to minimize the risk of aortic aneurysm and dissection, there is no cure for MFS nor even a targeted therapy. With the aim of finding novel MFS treatments, Lim and colleagues focused their attention on IL-11. This cytokine is strongly induced in vascular smooth muscle cells (VSMCs) upon treatment with the growth factor TGFβ—itself overactivated in MFS patients and considered a key feature of the syndrome’s molecular pathology. The team now show that IL-11 is indeed strongly upregulated in the aortas of MFS model mice and that genetically eliminating IL-11 in these animals can protect them against the aortic pathology they normally exhibit—including dilation, fibrosis, inflammation, elastin degradation and loss of VSMCs. Furthermore, treating MFS mice with an anti-IL-11 neutralizing antibody had the same beneficial effects. The results therefore suggest that inhibiting IL-11 activity could be a novel approach for protecting the aortas of MFS patients. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesEro1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac ArrhythmiaShanna Hamilton, et al. Circulation Research. 2022;130:711-724GLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body InhibitionAudrys G. Pauza, et al. Circulation Research. 2022;130:694-707Inhibition of IL11 Signaling Reduces Aortic Pathology in Murine Marfan SyndromeWei-Wen Lim, et al. Circulation Research. 2022;130:728-740 March 4, 2022Vol 130, Issue 5Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/RES.0000000000000536 Originally publishedMarch 3, 2022 PDF download Advertisement

Assessment of pleural pressure during sleep in Marfan syndrome.

Patients with Marfan syndrome (MFS) have a high risk for aortic aneurysms. They are also susceptible to sleep-disordered breathing that may expose them to highly negative intrathoracic pressures known to increase aortic transmural pressure, which may accelerate aortic dilatation. Our objective was to quantify overnight intrathoracic pressure changes during sleep in snoring patients with MFS and the therapeutic effect of continuous positive airway pressure (CPAP). We used a questionnaire to identify self-reported snoring patients with MFS. In these patients, we monitored intrathoracic pressure using esophageal pressure (Pes) during overnight baseline and CPAP sleep studies. We defined a peak-inspiratory Pes (Pespeak-insp) < - 5 cm H2O as greater than normal and examined the distribution of Pespeak-insp during baseline and CPAP studies. In our sample of 23 snorers with MFS, we found that 70% of sleep breaths exhibited Pespeak-insp < -5 cm H2O, with apnea/hypopneass accounting for only 12%, suggesting prevalent stable flow-limited breathing and snoring. In a subset (n = 12) with Pes monitoring during a CPAP night, CPAP lowered the mean proportion of breaths with Pespeak-insp < -5 cm H2O from 83.7% ± 14.9% to 3.6% ± 3.0% (P < .001). In addition, contemporaneous aortic root diameter was associated with the mean Pespeak-insp during inspiratory flow-limited breathing and apneas/hypopneas (β = -0.05, r = .675, P = .033). The sleep state in MFS revealed prolonged exposure to exaggerated negative inspiratory Pes, which was reversible with CPAP. Since negative intrathoracic pressure can contribute to thoracic aortic stress and aortic dilatation, snoring may be a reversible risk factor for progression of aortic pathology in MFS. Sowho M, Jun J, Sgambati F, etal. Assessment of pleural pressure during sleep in Marfan syndrome. J Clin Sleep Med. 2022;18(6):1583-1592.

Risk of aortic aneurysm and aortic dissection with the use of fluoroquinolones in Korea: a nested case\u2013control study

BackgroundRecent studies have raised concern about the association of fluoroquinolones with an increased risk of aortic aneurysm and aortic dissection. We aimed to evaluate such risk in a Korean population.MethodsWe conducted a nested case–control study using data from the National Health Insurance Service collected from 2013 to 2017 in Korea. The study cohort included patients older than 40 years and excluded patients who had used fluoroquinolones or been diagnosed with aortic aneurysm, aortic dissection, or related diseases 1 year prior to the cohort entry date. We randomly matched four controls in the risk set with each case of aortic aneurysm and aortic dissection (same sex, age, and cohort entry date). We assessed the risk of aortic aneurysm and aortic dissection from fluoroquinolones and adjusted for potential confounders using a conditional logistic regression model.ResultsA total of 29,638 aortic aneurysm and aortic dissection patients were identified between 2014 and 2017. The use of fluoroquinolones within a year was associated with a 10% increased risk of aortic aneurysm and aortic dissection (adjusted odds ratio: 1.10, 95% CI 1.07–1.14, p < 0.05) compared with nonusers. The risk was higher in patients who had used fluoroquinolones within 60 days (adjusted odds ratio: 1.53, 95% CI 1.46–1.62, p < 0.05). The risk of aortic aneurysm and aortic dissection positively correlated with the cumulative dose and duration of fluoroquinolone therapy (p < 0.001).ConclusionsOur study provides real-world evidence of the risk of aortic aneurysm and aortic dissection from fluoroquinolones in Korea. Patients and medical professionals should be aware that fluoroquinolones can increase the risk of aortic aneurysm and aortic dissection, which may be acerbated by high dosage and duration of use.

Higher Plasma Aldosterone Concentrations Are Associated With Elevated Risk of Aortic Dissection and Aneurysm: a Case-Control Study

Animal models demonstrate circulating aldosterone leads to aortic dissection and aneurysm, whereas data from humans are lacking. Therefore, we aimed to examine the associations of plasma aldosterone concentrations (PAC) with aortic dissection and aneurysm. We identified patients with aortic dissection and aneurysm with assessed PAC before disease onset from hospital-based electronic database and set as case group. Simultaneously, age and gender-matched cohort with PAC measurement whereas without aortic dissection and aneurysm were selected as control group using ratio of 1:4. Multi-variable logistic regression analysis was used to assess the relationship of PAC with aortic dissection and aneurysm. Totally, 133 cases and 531 controls (all hypertensive) were enrolled between 2004 and 2021, with 77.9% men, mean age of 55.5 years and PAC of 13.9 ng/dL. Case group showed significantly higher PAC(14.51 versus 13.65 ng/dL, P=0.012) than did control group. In logistic regression analysis, higher PAC exhibited 1.68-fold higher odds (95% CI, 1.14-2.48, P=0.008) for presence of aortic dissection and aneurysm, significant in adjusted model (odds ratio, 1.69 [95% CI, 1.11-2.57], P=0.015). In stratified analysis, the association between the two was observed in women of all ages and in men with coronary artery disease. Sensitivity analysis by excluding those under interfering agents at PAC measurement and those with primary aldosteronism did not change the relationship of the two. Higher PAC is associated with the increased odd for aortic dissection and aneurysm in patients with hypertension, even in the absence of primary aldosteronism, implying that PAC might be a target for prevention.

Age, smoking, hypertension, and aortic aneurysm: Interactions and risks

Background/Aim: Aortic aneurysm is the bulging of a weakened portion of the aorta. The aorta is the major blood vessel that feeds blood (carrying oxygen, nutrients and water) to the tissues of the body. When a portion of the wall of the aorta becomes weak, blood pushing against the vessel wall can cause it to bulge like a balloon (aneurysm) leading to aortic dissection (a tear in the wall of the aorta that can cause life-threatening bleeding or sudden death). Blood pressure is the force arterial blood exerts on the wall of the artery. When this pressure is consistently high above 140/100 mmHg it is referred to as hypertension. As an individual gets older over time, physiological functions of the body depreciate leading to some abnormalities. Smoking is the consumption of tobacco mostly by inhalation of the smoke that is produced from burning the tobacco. This review article examines the close interactions between age, smoking, hypertension and aortic aneurysm, with a view to understanding mechanisms by which these factors predispose a patient to an aortic aneurism. It is also to observe if these factors interfere with treatment and recovery from aneurysms. Conclusion: After careful review, it is observed that age and smoking are risk factors for hypertension, and together with hypertension, the three factors predispose an individual to high risk for aortic aneurysm.

Prevalence and risk of progressive aortic aneurysm and dissection in adults with conotruncal anomalies.

Conotruncal anomalies share common embryogenic defects of the outflow tracts and great arteries, which result in a predisposition to aortic aneurysms. The purpose of this study was to describe the prevalence and risk of progressive aortic aneurysms in adults with conotruncal anomalies. Retrospective study of adults with conotruncal anomalies that underwent cross-sectional imaging 2003-20. Aneurysm was defined as aortic root/mid-ascending aorta >2.1 mm/m2/>1.9 mm/m2, progressive aneurysm as increase by >2 mm, and severe aneurysm as dimension >50 mm. Of 2261 patients (38 ± 12 years; male 58%), 1167 (52%) had an aortic aneurysm, and 205 (14%) had a severe aortic aneurysm. Mean annual increase in aortic root/mid-ascending aorta was 0.3 ± 0.1 mm/0.2 ± 0.1 mm. The 3-, 5-, and 7-year cumulative incidence of the progressive aortic aneurysm was 4%, 7%, and 9%, respectively. The rate of aneurysm growth decreased with age, with no significant growth after age 40 years. There was an excellent correlation between aortic indices from cross-sectional imaging and echocardiography. Of 950 females, 184 had ≥1 pregnancy, and 81 (44%) of the 184 patients had aortic aneurysm prior to pregnancy. There was no aortic dissection or progression of the aortic aneurysm during pregnancy. Overall, there was no aortic dissection during 7984 patient-years of follow-up. Aortic aneurysm was common in patients with conotruncal anomalies. However, the risk of progressive aneurysm or dissection was low. Collectively, these data suggest a benign natural history and perhaps a less frequent need for cross-sectional imaging. Further studies are required to determine the optimal timing for surgical intervention in this population.

Increased risk of thoracic aortic complications among patients with giant cell arteritis: a nationwide, population-based cohort study.

To assess the risk of aortic aneurysms (AA), aortic dissections (AD) and peripheral arterial disease (PAD) among patients with GCA. In this nationwide, population-based cohort study using Danish national health registries, we identified all incident GCA patients ≥50 years between 1996 and 2018 who redeemed three or more prescriptions for prednisolone. Index date was the date of redeeming the third prednisolone prescription. Case definition robustness was checked through sensitivity analysis. We included general population referents matched 1:10 by age, sex and calendar time. Using a pseudo-observation approach, we calculated 5-, 10- and 15-year cumulative incidence proportions (CIP) and relative risks (RR) of AA, AD and PAD with death as a competing risk. We included 9908 GCA patients and 98204 referents. The 15-year CIP of thoracic AA, abdominal AA, AD and PAD in the GCA cohort were 1.9% (95% CI 1.5, 2.2), 1.8% (1.4-2.2), 1.0% (0.7-1.2) and 4.8% (4.2-5.3). Compared with the referents, the 15-year RR were 11.2 (7.41-16.9) for thoracic AA, 6.86 (4.13-11.4) for AD, 1.04 (0.83-1.32) for abdominal AA and 1.53 (1.35-1.74) for PAD. Among GCA patients, female sex, age below 70 years and positive temporal artery findings were risk factors for developing thoracic AA. The median time to thoracic AA was 7.5 years (interquartile range 4.4-11.2) with a number needed to be screened of 250 (167-333), 91 (71-111) and 53 (45-67) after 5, 10 and 15 years. Patients with GCA have a markedly increased risk of developing thoracic AA and AD, but no increased risk of abdominal AA.

Risk of Aortic Aneurysm and Dissection in Patients with Tuberculosis: A Nationwide Population-Based Cohort Study.

Tuberculosis (TB) can cause chronic inflammation. The occurrence of aortic aneurysm (AA) and aortic dissection (AD) may be associated with chronic inflammatory disease, but whether TB increases the risk of AA and AD remains to be determined. This study aimed to investigate the association between TB and the development of AA and AD. We conducted a population-based cohort study using data obtained from the Taiwan National Health Insurance Database. We selected 31,220 individuals with TB and 62,440 individuals without TB by matching the cohorts according to age, sex, and index year at a ratio of 1:2. Cox regression analysis revealed that the TB cohort had a 1.711-fold higher risk of AA and AD than the non-TB cohort after adjustment for sex, age, socioeconomic status, and comorbidities (adjusted hazard ratio = 1.711; 95% confidence interval = 1.098–2.666). Patients with pulmonary, extrapulmonary, and miliary TB had a 1.561-, 1.892-, and 8.334-fold higher risk of AA and AD, respectively. Furthermore, patients with TB at <6 months, 6–12 months, and 1–5 years of follow-up had a 6.896-, 2.671-, and 2.371-fold risk of AA and AD, respectively. Physicians should consider the subsequent development of AA and AD while treating patients with TB.

Association Between Red Blood Cell Distribution Width-to-Albumin Ratio and Prognosis of Patients with Aortic Aneurysms.

ObjectiveRed blood cell distribution width (RDW) is a predictor of adverse outcomes in aortic aneurysms. Recent recommendations suggest that combining RDW with other biomarkers could yield better results. We, therefore, propose evaluating the biomarker of vascular aging, albumin with RDW to predict the risk of aortic aneurysms. This study aims to explore whether the combination of RDW with albumin can effectively predict the prognosis of aortic aneurysm patients.MethodsThis retrospective cohort study was conducted among adults (age >18) with aortic aneurysms in the Medical Information Mart for Intensive Care Database III V1.4 (MIMIC-III). RAR was measured according to the red blood cell distribution width and albumin. The primary outcome was the 30-day mortality rate, and the secondary outcome was the 90-day and one-year mortality rates. Estimation of hazard ratios (HR) was obtained from Cox regression models for all-cause mortality related to red cell distribution width-to-albumin ratio (RAR) values.ResultsIn total, 312 patients were involved, with an average age of 74.9 ± 10.9 years and an average RAR value of 5.4 ± 1.6 mL/g. In 30 days for all-cause mortality, the HR (95% CI) in the highest RAR group (>5.8 mL/g) in tertiles was 2.54 (1.25, 5.14) in the unadjusted model, with a significant difference compared with the reference group (P < 0.05). After adjusting for race, gender and age, there was still a correlation (P < 0.05), and the HR (95% CI) was 2.51 (1.23, 5.10). Further adjustment of possible covariates showed similar correlation in model 3 (P < 0.05), and HR (95% CI) was 2.66 (1.17, 6.01). Multivariable logistic regression shows that RAR is an independent risk factor for the outcome of aortic aneurysms after adjusting the covariates. In the subgroup analysis, we analyzed the patient’s complications, and no significant interaction was observed.ConclusionRAR is a risk factor for patients with aortic aneurysms. However, more in-depth research is warranted to further analyze and substantiate our findings on the role of RAR in aortic aneurysm patients.

Risk of aortic aneurysm and dissection following exposure to fluoroquinolones, common antibiotics, and febrile illness using a self-controlled case series study design: Retrospective analyses of three large healthcare databases in the US.

Recent observational studies suggest increased aortic aneurysm or dissection (AAD) risk following fluoroquinolone (FQ) exposure but acknowledge potential for residual bias from unreported patient characteristics. The objective of our study is to evaluate the potential association between FQ, other common antibiotics and febrile illness with risk of AAD using a self-controlled case series (SCCS) study design. Retrospective database analysis-SCCS. Primary and Secondary Care. 51,898 patients across 3 US claims databases (IBM® MarketScan® commercial and Medicare databases, Optum Clinformatics). FQ or other common antibiotics or febrile illness. AAD. We studied patients with exposures and AAD between 2012 and 2017 in 3 databases. Risk windows were defined as exposure period plus 30 days. Diagnostic analyses included p-value calibration to account for residual error using negative control exposures (NCE), and pre-exposure outcome analyses to evaluate exposure-outcome timing. The measure of association was the incidence rate ratio (IRR) comparing exposed and unexposed time. Most NCEs produced effect estimates greater than the hypothetical null, indicating positive residual error; calibrated p (Cp) values were therefore used. The IRR following FQ exposure ranged from 1.13 (95% CI: 1.04-1.22 -Cp: 0.503) to 1.63 (95% CI: 1.45-1.84 -Cp: 0.329). An AAD event peak was identified 60 days before first FQ exposure, with IRR increasing between the 60- to 30- and 29- to 1-day pre-exposure periods. It is uncertain how much this pre-exposure AAD event peak reflects confounding versus increased antibiotic use after a surgical correction of AADs. This study does not confirm prior studies. Using Cp values to account for residual error, the observed FQ-AAD association cannot be interpreted as significant. Additionally, an AAD event surge in the 60 days before FQ exposure is consistent with confounding by indication, or increased use of antibiotics post-surgery. NCT03479736.

Risk of aortic dissection or aneurysm in patients with gallstone disease: a retrospective cohort study in Taiwan

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Re: Short-term Ciprofloxacin Prophylaxis for Prostate Biopsy and Risk of Aortic Aneurysm. Nationwide, Population-based Cohort Study

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