Abdominal aortic aneurysm and virus infection: A potential causative role for cytomegalovirus infection?

An abdominal aortic aneurysm (AAA) is a multifactorial disease with a variety of genetic and environmental risk factors, but the exact mechanism of AAA formation and progression is still not well understood. The present study investigated the frequency of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and papillomavirus types 6 and 11 (HPV6 and HPV11), their impact on clinical manifestations of cardiovascular diseases, and their possible association with inflammation in patients with AAA and healthy volunteers. Genotyping of CMV UL75, EBV LMP-1, and HPV6, and HPV11 E6 was performed by polymerase chain reaction (PCR), while the viral DNA loads were measured by quantitative real-time PCR. Cytokine levels were determined by enzyme-linked immunosorbent assays. The CMV UL75 was detected more frequently in the blood of patients with AAA than in the blood of healthy volunteers (32.7% vs. 6.3%, p < .0001). Neither EBV LMP-1 nor HPV6 E6 was found in blood and aortic wall biopsies, while the HPV11 E6 was detected in 36.4% of AAA walls. The CMV infection in patients with AAA was associated with an increased risk of hypertension and coronary artery disease (OR, 9.057; 95% CI, 1.141-71.862; p = .037; and OR, 2.575; 95% CI, 1.002-6.615; p = .049, respectively). Additionally, CMV-infected patients with AAA had higher tumor necrosis factor-α levels compared with noninfected subjects (p = .017). Our findings suggest that CMV infection can stimulate local inflammation in the aorta but is not a direct cause of most abdominal aortic aneurysms.

Ruptured Abdominal Aortic Aneurysm Treated with Endovascular Repair in a Patient with Active COVID-19 Infection during the Pandemic.

We report a patient who presented with acute abdominal pain during the COVID-19 pandemic. His work-up revealed rupture of a 5.8 cm abdominal aortic aneurysm. He also had fever, cough, and shortness of breath and radiologic evidence of COVID-19 infection. After careful consideration, he underwent successful endovascular repair under local anesthesia with good short-term results.

Endovascular Treatment of a Ruptured Pararenal Abdominal Aortic Aneurysm in a Patient With Coronavirus Disease-2019: Suggestions and Case Report.

The aim of this report is to discuss emergent repair for complex aortic diseases in patients affected by novel coronavirus pneumonia (coronavirus disease-2019 [COVID-19]), describing a case of ruptured pararenal aortic aneurysm. An eighty-year-old man with COVID-19 was admitted for ruptured aneurysm of the pararenal aorta and hemorrhagic shock. Endovascular repair was chosen, and a proximal extension of the previous abdominal endograft was performed with parallel stents in the right renal artery and the superior mesenteric artery. Endovascular treatment and early anticoagulation are the key for success for vascular emergencies in patients with COVID-19, despite the risk of late endoleak.

Analysis of host Toll-like receptor 3 and RIG-I-like receptor gene expression in patients with abdominal aortic aneurysm.

OBJECTIVE: Abdominal aortic aneurysm (AAA) is a vascular disease relatively common in the elderly population. Although some events that contribute to the development and progression of AAA are known, there are limited data examining the association of Toll-like receptor 3 (TLR3) and RIG-I-like receptor expression with the pathogenesis of AAAs. In this study, we investigated the gene and protein expression of TLR3 and RIG-I-like receptors (RIG-I and MDA5) in aortic wall and blood of AAA patients and examined the relationship between their expression and immune response. METHODS: Total RNA was extracted from aortic wall tissues and blood samples collected from 20 patients with AAA and blood samples of 17 healthy volunteers without aortic aneurysm. To evaluate the DDX58 (RIG-I), IFIH1 (MDA5), and TLR3 gene expression level, quantitative real-time polymerase chain reaction was used. Extracellular cytokine and pattern recognition receptor levels were quantified by enzyme-linked immunosorbent assays. RESULTS: TLR3, RIG-I, and MDA5 were constitutively expressed in both aortic tissues and blood samples from AAA patients and healthy volunteers. In patients with AAA, higher TLR3 expression in aortic tissues than in blood was found (P = .004). The DDX58 messenger RNA expression was higher in blood of patients with AAA compared with healthy subjects (P = .021). A significantly higher level of plasma interleukin 4 was noticed in patients with AAA than in healthy individuals (P = .008). CONCLUSIONS: This study suggests that RIG-I and TLR3 seem to be important factors in the pathogenesis of AAA.

Association between human parainfluenza virus type 1 and smoking history in patients with an abdominal aortic aneurysm.

Several studies have suggested that infectious agents may induce the development of abdominal aortic aneurysms and/or accelerate their progression. The aim of this study was to evaluate the presence of the respiratory-transmitted viruses such as influenza A and B and parainfluenza type 1 genomes in bioptic fragments of abdominal aortic aneurysms. Furthermore, the association between viral infection and traditional risk factors for aneurysms was investigated employing multivariate logistic regression models. The genome of parainfluenza 1 was detected in 11 out of 57 patients with abdominal aortic aneurysm, influenza A only in one, whereas none of the specimens analyzed resulted positive for influenza B. After adjustment of age, gender, and clinical diagnosis, being current smokers was associated independently with parainfluenza 1 detection in aneurysms. The identification of parainfluenza 1 in aortic aneurysm biopsies supports previous observations of a possible role of viruses in the lesion development. Smoking, by interfering with the respiratory tract's ability to defend itself and predisposing to upper and lower respiratory tract infections may accelerate the onset and progression of abdominal aortic aneurysms.

Rupture of a pseudo aneurysm of the abdominal aorta in a patient with human immunodeficiency virus infection.

Human immunodeficiency virus (HIV) infection has an impact on all systems of the body, including the cardiovascular system. A 54-year-old man presented with abdominal pain. Enhanced computed tomography revealed rupture of a pseudoaneurysm of the abdominal aorta. After surgery, the patient tested positive for HIV. Histological examination of the resected aorta showed leukocytoclastic vasculitis, a characteristic feature of HIV-related vasculitis.

Successful endovascular treatment of an infrarenal aortic aneurysm with leak within the wall in a HIV-positive patient.

We report on a successful endovascular treatment of an infrarenal aortic aneurysm, with leak within the wall, in a HIV-positive patient with CD4 count 130/microL, who presented at the emergency department with abdominal pain.

Active cytomegalovirus infection in aortic smooth muscle cells from patients with abdominal aortic aneurysm.

Cytomegalovirus (CMV) is associated with atherosclerosis and transplant vascular sclerosis. The aim of this study was to explore the hypothesis that active CMV infection in the vessel wall could be associated with abdominal aortic aneurysm (AAA). We examined the prevalence of CMV in AAA specimens from 22 patients undergoing surgery and, in five cases, characterized the function of smooth muscle cells (SMCs) from the aneurysm in vitro. Twenty-one (95%) of the 22 AAA specimens were CMV positive by a polymerase chain reaction assay, in situ hybridization, or a highly sensitive immunohistochemical staining technique. No positive cells were found in aortas from three CMV-seronegative organ donor cadavers. CMV immediate-early and late antigens were expressed in SMCs in the lesions and were associated with 5-lipoxygenase (5-LO) expression. CMV-positive intimal SMCs migrated 6.6 +/- 1.5 times more efficiently than CMV-negative medial SMCs (p < 0.05). In vitro CMV infection of medial SMCs resulted in a 3.2 +/- 1.2 times increase in migration (p < 0.05). The intimal migration was significantly inhibited by antibodies against basic fibroblast growth factor (bFGF; p < 0.05) in a dose-dependent fashion. Antibodies against platelet-derived growth factor (PDGF)-AB, insulin-like growth factor 1, vascular endothelial growth factor (VEGF), RANTES, monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha, or interleukin-1beta did not significantly affect intimal SMC migration. However, intimal and medial SMCs secreted similar amounts of bFGF, MCP-1, MIP-1alpha, RANTES, PDGF-AB, PDGF-BB, epidermal growth factor, and VEGF. CMV infection in vitro of intimal and medial cells did not result in significant changes of bFGF or MCP-1 secretion. Since CMV infection can affect several functional parameters in SMCs, including several key factors in infected SMCs, our findings provide support for the hypothesis that CMV contributes to the pathogenesis of abdominal aortic aneurysm.

Multiple HIV-related aneurysms: open and endovascular treatment.

PURPOSE: To report successful endovascular repair of thoracic aortic aneurysms in 2 patients with human immunodeficiency virus (HIV). CASE REPORTS: Thoracic and abdominal aortic aneurysms (AAA) were found in a 60-year-old woman 1 year after she was diagnosed with HIV. Because of pain and risk of rupture, the AAA was repaired with conventional open techniques in February 1997, while the thoracic aneurysm was excluded in a staged procedure using a homemade endograft delivered through a 10-mm conduit sewn to the aortic tube graft. Two months later, new aneurysms were found in the superficial femoral arteries bilaterally; both were excised and replaced with vein grafts. After 7 years, the patient is well and no longer takes antiretroviral medication. Surveillance imaging shows continued patency of the stent-graft without evidence of leak or migration. In a more contemporary case, a 46-year-old man was found to have 5 focal aneurysms in the aorta; the most proximal descending thoracic aneurysm increased 2 cm in 2 weeks. The two thoracic aneurysms were successfully excluded using 2 Excluder stent-grafts. At 7 months, he was doing well, and the aneurysm had shrunk 11 mm. CONCLUSIONS: Endovascular and open treatment of HIV-related aneurysms is possible, with excellent long-term results. Patients with long-life expectancy should be treated according to the same guidelines as patients without HIV.

A novel hypothesis to explain the hemorrhagic and connective tissue manifestations of Ebola virus infection.

The hemorrhagic and connective tissue complications of infection with Ebola virus are poorly understood. While searching for homologies and motifs of the aortic aneurysm-associated autoantigenic protein 40 kDa (AAAP-40), we have noted some short sequences (possibly shared epitopes) that occur in the envelope glycoprotein (40 kDa) of the Ebola virus. As a first step toward determining whether molecular mimicry of human matrix proteins by the Ebola virus protein might explain some of the severe connective tissue manifestations of infection, we have tested whether immunoglobulin (IgG) purified from the sera of patients with abdominal aortic aneurysm (AAA) are immunoreactive with the 40-kDa protein of the Ebola virus. Immunoblots of soluble Ebola proteins (strain Mayinga/Zaire) were probed with IgG's purified from the sera of eight patients with AAA and two healthy young control volunteers. The proteins were also probed with IgG extracted from the walls of two surgical aneurysm specimens. Serum IgG from eight consecutively studied AAA patients was immunoreactive with an Ebola virus protein of 40 kDa, consistent with the envelope glycoprotein. IgG's extracted from the walls of two AAAs were also reactive. The control sera were not reactive. In addition to the Ebola sequences in AAAP-40, an Ebola sequence also occurs in the microfibril-associated glycoprotein-4 (MAGP-4), which is distributed ubiquitously throughout connective tissue with elastin. We hypothesize that the catastrophic hemorrhagic and connective tissue complications of Ebola virus infection may be the result of these shared epitopes.