Non-atherosclerotic Aneurysms Research Articles

Lipidomic signatures of aortic media from patients with atherosclerotic and nonatherosclerotic aneurysms

Aortic aneurysms are associated with fatal aortic rupture. Current therapeutic approaches are limited to implantation of aortic prostheses and stent-grafts; no effective drugs are available because the pathogenic mechanisms of aortic aneurysms remain unclear. Here, we aimed to elucidate the molecular mechanisms of the initiation and progression of aortic aneurysm by lipidomics. We performed lipidomics analyses of lipids in the aortic media of normal, border, and aneurysm areas from patients with thoracic atherosclerotic aortic aneurysm (N = 30), thoracic nonatherosclerotic aortic aneurysm (N = 19), and abdominal atherosclerotic aortic aneurysm (N = 11) and from controls (N = 8) using liquid chromatography and mass spectrometry. Significant alterations were observed in the lipid profiles of patients with atherosclerotic aortic aneurysms and to a lesser extent in those with nonatherosclerotic aneurysms. Increased triacylglycerols (TGs) and decreased ether-type phosphatidylethanolamines (ePEs) were observed throughout the normal, border, and aneurysm areas of thoracic and abdominal atherosclerotic aortic aneurysms. Prostaglandin D2 increased, but ePEs and TGs decreased in normal areas of thoracic atherosclerotic aortic aneurysms and thoracic nonatherosclerotic aortic aneurysms compared with the control tissues. These findings expand our knowledge of metabolic changes in aortic aneurysms and provide insights into the pathophysiology of aortic aneurysms.

Natural history and outcome after treatment of unruptured intradural fusiform aneurysms.

Management of unruptured fusiform intracranial aneurysms is controversial because of the paucity of natural history data. We studied their natural history and outcome after treatment. We reviewed our neurovascular database from January 2000 to October 2013. Inclusion criteria were unruptured, intradural fusiform aneurysms with a diameter of <2.5 cm. Criteria were developed to define atherosclerotic aneurysms. For outcome assessment, we used the modified Ranking Scale and aneurysm measurements on serial imaging. Mann-Whittney (continuous) and Fisher exact (categorical) tests were used for risk factor analysis. For nonatherosclerotic aneurysms (96 patients; 193 person-years follow-up), 1 patient died (rupture) during follow-up (mortality, 0.51% per year) and 8 patients (10%) showed aneurysm progression (risk, 1.6% per year). Risk factors for progression were maximum diameter (>7 mm; odds ratio, 12; 95% confidence interval, 1.4-104) and symptomatic clinical presentation (odds ratio, 16; 95% confidence interval, 3.1-81.4). Of the 23 treated patients, 3 had died (mortality, 12.5%) and 3 had serious disability (modified Ranking Scale, ≥3; 12.5%). For the atherosclerotic aneurysms (25 patients; 97 person-years follow-up), 5 had died (mortality, 5.2% per year) and 13 of 20 (65%) had aneurysm progression (risk, 12% per year). When compared with patients with nonatherosclerotic aneurysms, case fatality (odds ratio, 19.2; 95% confidence interval, 2.1-172) and aneurysm progression (odds ratio, 17.8; 95% confidence interval, 5.3-56) were higher. Nonatherosclerotic fusiform intradural aneurysms have a low risk of adverse outcome within the first few years after diagnosis and remain stable unless symptomatic on presentation or >7 mm in maximum diameter. High risks of treatment should be balanced against this benign natural history. Atherosclerotic aneurysms have a worse natural history and may represent a different disease entity.

Clinical analysis and surgical considerations of atherosclerotic cerebral aneurysms: experience of a single center.

ObjectiveAtherosclerotic cerebral aneurysms are known to increase occurrence of thromboembolic events and occlusion of perforator vessels intraoperatively due to pathological changes in the vessels themselves. In the current study, we analyzed the points to be considered during surgery for atherosclerotic cerebral aneurysms and the postoperative results.Materials and MethodsWe retrospectively reviewed the medical records, radiological results, and surgical records, including intraoperative video recordings and photographs, of 262 patients who underwent cerebral aneurysm surgery. We then performed a detailed analysis of aneurysm features, surgical methods, and clinical outcomes.ResultsAmong 278 aneurysms in 262 patients, 73 aneurysms in 67 patients showed atherosclerotic features (atherosclerotic group, AG), and 205 aneurysms in 195 patients showed no evidence of atherosclerosis (non-atherosclerotic group, NAG). In the AG, clipping with multiple permanent clips was performed in 14 aneurysms, and clip slippage was found in four cases. Six AG cases had a remnant neck after clipping, which was significantly more frequent than in the NAG (p < 0.05). Clinical outcomes and surgery-related complications did not differ significantly between the two groups.ConclusionIn the surgical repair of aneurysms, the incidence of ischemia, which is irreversible or severe, might be greater in atherosclerotic than in non-atherosclerotic aneurysms. In addition, multiple clips might be applied to atherosclerotic aneurysms for effective obliteration and an aneurysm neck might be left to avoid a region of atheroma.

Prolidase Activity in Patients With Coronary Artery Aneurysm

Decreased collagen biosynthesis and increased collagenolysis may induce aneurysmal progress in arterial walls. Prolidase plays a role in collagen synthesis. In this study, we sought to evaluate whether there is a correlation between nonatherosclerotic coronary artery aneurysms (CAAs) and prolidase activity. A total of 174 CAAs were diagnosed in 144 (2.1%) patients among 6845 coronary angiographies performed between 2009 and 2012. In all, 23 (15.9%) patients had nonatherosclerotic aneurysms. Prolidase activity was compared to the results of 19 healthy volunteers with normal coronary arteries. Demographic parameters were similar between the groups. Mean prolidase activity was 241.6 ± 54.4 mU/mL in the coronary aneurysm group and 730.3 ± 243.1 mU/mL in the control group (P < .001). The incidence of CAAs ranges between 0.3% and 5.3% in the general population. Decreased prolidase activity may reduce collagen biosynthesis that may contribute to aneurysm formation.

Imaging of non-atherosclerotic aneurysmal disease

Atherosclerotic aneurysms account for about 95% of all aneurysms. This overview concentrates on the 5% leftover, which however represents a heterogenic group of aneurysms with a wide range of different pathogenesis. Thus, therapy is not exclusively restricted to the exclusion of the aneurysm. In non-atherosclerotic aneurysmal disease various additional therapeutic strategies are included such as chemotherapy, anti-inflammatory therapy and embolisation procedures. Diagnosis, therapeutic decision making and even therapy itself to a growing extent depends on adequate (pretherapeutic) imaging and therefore radiologic expertise. This review describes the most common forms of non-atherosclerotic aneurysms and focuses on their pathogenesis, potential diagnostic approaches and therapy options.

Rupture of vasa vasorum and intramural hematoma of the aorta: a changing paradigm

Dear ladies and gentlemen I would like to congratulate Adamastor Humberto Pereira for his excellent review about rupture of vasa vasorum in 2010. From the vascular histopathologist standpoint of view it is worth emphasising the role of vasa vasorum in acute dissection with and/or without aneurysms. We found lightmicroscipally in 46 of 171 cases a rupture of vasa vasorum as the cause of dissection (Figure 1 and 2)1,2. Furthermore I would like to remark that vasa vasorum in aneurysms of the aorta ascendens presenting a wide morphological spectrum. In atherosclerotic aneurysms nonstenotic vasa vasorum were observed. In contrast to these findings non-atherosclerotic aneurysms showed concentric and excentric stenosis causing leiomyomatous hyperplasia3.

Is the surgical repair of unruptured atherosclerotic aneurysms at a higher risk of intraoperative ischemia?

Background The incidence of ischemia might be increased in the surgical repair of atherosclerotic unruptured aneurysms compared to non-atherosclerotic aneurysms. The atherosclerotic wall might increase the occurrence of thrombembolic events or its rigidity might endanger the occlusion of perforators within the aneurysm vicinity. Methods 87 patients (53 patients without and 34 patients with atherosclerotic unruptured aneurysms, 50.5 ± 9.7 years) were analyzed for severity of atherosclerosis within the aneurysm and the aneurysm bearing vessel, surgical maneuvers, intraoperative alterations in evoked potentials and clinical and neuroradiological results. Results Temporary vessel occlusion (25% vs. 50%, p = 0.021), repositioning of a permanent clip (21% vs. 56%, p = 0.001) and aneurysm remnants (2% vs. 18%, p = 0.012) occurred more often in patients with atherosclerotic aneurysms. At 6 months, 3/34 patients with atherosclerosis (8.8%) had an unfavorable outcome, all patients without atherosclerosis had a favorable outcome ( p = 0.056). Conclusion The surgical repair of unruptured aneurysms is safe but patients with atherosclerotic altered vessels and aneurysms accounted to a minor increase in unfavorable outcome and an increased risk of morbidity at 6 months postoperatively. This factor should be taken into consideration when performing surgery of atherosclerotic, unruptured aneurysms.

Aneurysmata der Aorta ascendens und des Truncus pulmonalis

A case of two non-atherosclerotic aneurysms localised in the ascending aorta and in the pulmonary trunk is presented. Histopathologically, a severe granulomatous inflammation affecting the whole aneurysms wall was documented. To the best of our knowledge it is the second ever documented case of simultaneous occurrence of aneurysms in the aorta and the pulmonary artery.

Matrix Metalloproteinase and Tissue Inhibitor Expression in Atherosclerotic and Non-Atherosclerotic Thoracic Aortic Aneurysm

Conclusion: Tissue inhibitor/metalloproteinase phenotypes of atherosclerotic thoracic aneurysms (TA) are similar to those of abdominal aortic aneurysms (AAA). Summary: It is felt an imbalance of the equilibrium between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) can contribute to the formation of an AAA. Whereas atherosclerotic TAs have similar histologic features as AAAs, many TAs are not atherosclerotic in origin and are characterized more by extensive cystic medial necrosis rather than the chronic, inflammatory cell infiltrate more commonly found in atherosclerotic aneurysms. It is known altered expressions of MMPs and their TIMPs influence formation of atherosclerotic aneurysms in the abdominal aorta. In this study, the authors sought to determine the expression of MMPs and TIMPs in both nonatherosclerotic and atherosclerotic TAs. Comparisons were also made with a set of age-matched controls. MMP-2 and -9 activities were measured with antibody capture, and TIMP-1 and -2 levels were measured by enzyme-linked immunosorbent assay. There were 24 atherosclerotic aneurysms studied, 63 nonatherosclerotic aneurysms, and 17 controls. Gene expression was assessed with reverse transcriptase polymerase chain reaction. All data are expressed in nanograms per milligram of protein. MMP levels in controls, atherosclerotic, and nonatherosclerotic groups were 80 ± 7, 49 ± 50, and 35 ± 44, (P = .002). In the atherosclerotic group, MMP-9 activity was greater than in the nonatherosclerotic group and controls (11.7 ± 15.7 vs 2.5 ± 2.2 vs 1.7 ± 1.9, P = .001). In the control group, TIMP-1 and -2 levels were greater than in either aneurysm group. TIMP-1 levels were 376 ± 192 vs 234 ± 233 vs 174 ± 148 (P = .003), and TIMP-2 levels were 143 ± 74 vs ± 13 vs 27 ± 43 in the control, atherosclerotic, and nonatherosclerotic groups, respectively (P < .001). MMP messenger RNA was expressed to a greater degree in atherosclerotic aneurysms than in controls. Comment:Not surprisingly, MMP-9 levels were higher in atherosclerotic TAs than in controls and nonatherosclerotic TAs. The authors also noted regional differences in MMP activity levels, with ascending atherosclerotic TAs having higher total MMP-2 activity than descending atherosclerotic TAs. They postulate reduced MMP-2 activity and TIMP protein gene expression in nonatherosclerotic TAs compared with controls may reflect dysfunction of smooth muscle cells with respect to their ability to compensate for age-related hemodynamic stresses.

Renal artery aneurysm in a cadaveric kidney transplantation

A 44-year-old haemodialysis patient was admitted for a cadaveric renal transplant. The donor renal artery (from a 38-year-old female who died of a subarachnoid haemorrhage) was found on dissection to have a thinwalled saccular aneurysm, measuring approximately 10mm in diameter (Figure 1) which was ressected with end-to-end branch reanastomosis. The kidney functioned well, with no complications at the time of writing. There was no suggestion that this was either an inflammatory or mycotic aneurysm. Saccular non-atherosclerotic aneurysms have been reported occasionally in the literature and do not present a contraindication to transplants if they can be successfully resected [1,2]. In Japan, where marginal kidneys are used for live donations, atherosclerotic renal arteries, including those with aneurysms, have been reconstructed with varying success prior to renal transplantation [3,4]. Further investigation of donor details are underway to determine if there was any underlying reason for the presence of the renal artery aneurysm.

Matrix metalloproteinase and tissue inhibitor expression in atherosclerotic and nonatherosclerotic thoracic aortic aneurysms

The altered expression of matrix metalloproteinases and their inhibitors influences the formation of atherosclerotic abdominal aortic aneurysms. Their association with thoracic aneurysms is less clear. This study describes the expression of metalloproteinases and their inhibitors in atherosclerotic and nonatherosclerotic thoracic aneurysms, and compares these with age-matched controls. Matrix metalloproteinase-2 and 9 activity were measured by antibody capture, and tissue inhibitor-1 and 2 levels were measured by enzyme-linked immunosorbent assay in 24 patients with atherosclerotic aneurysms and in 63 patients with nonatherosclerotic aneurysms. Gene expression was assessed with reverse transcriptase polymerase chain reaction. The results were compared with 17 controls. Data are in nanograms per milligram of protein. Matrix metalloproteinase-2 activity was greater in controls than in the atherosclerotic and nonatherosclerotic groups (80 +/- 67 vs 49 +/- 50 and 35 +/- 44, P = .002). Matrix metalloproteinase-9 activity was greater in the atherosclerotic group than in the nonatherosclerotic group and controls (11.7 +/- 15.7 vs 2.5 +/- 2.2 and 1.7 +/- 1.9, P = .001). Tissue inhibitor-1 and 2 levels were greater in controls than in either aneurysm group (tissue inhibitor of metalloproteinase-1: 376 +/- 192 vs 234 +/- 233 and 174 +/- 148, P = .003; tissue inhibitor of metalloproteinase-2: 143 +/- 74 vs 14 +/- 13 and 27 +/- 43, P < .001). Atherosclerotic aneurysms expressed more matrix metalloproteinase mRNA than controls. The metalloproteinase/tissue inhibitor phenotype of atherosclerotic thoracic aneurysms is similar to that of abdominal aneurysms. The diminished expression of metalloproteinases and tissue inhibitors in nonatherosclerotic thoracic aneurysms relative to aged controls may represent a loss of smooth muscle cells.

Matrix metalloproteinases 2 and 9 in human atherosclerotic and non‐atherosclerotic cerebral aneurysms

Matrix metalloproteinases 2 and 9 (MMP 2 and -9) have been implicated in the pathogenesis of atherosclerosis and aneurysm formation. The goal of the study was to establish the role of these metalloproteinases in both human atherosclerotic and non-atherosclerotic cerebral aneurysms. Eleven cerebral aneurysms (four atherosclerotic, seven non-atherosclerotic) were immunohistochemically stained for MMP 2 and -9. As controls, atherosclerotic and normal Circle of Willis arteries were similarly immunostained. All specimens were retrieved at autopsy and were paraffin-embedded. In order to evaluate the real MMP 2 and -9 activities, gelatin zymography was also performed in only two available specimens of non-atherosclerotic intracranial aneurysms, because of the relative unavailability of fresh intracranial aneurysm tissue (i.e. reluctance to excise the aneurysm fundus at surgery). Our data establish that MMP 2 and -9 were expressed minimally or not at all in normal Circle of Willis arteries but were strongly expressed in medial smooth muscle cells of atherosclerotic Circle of Willis arteries. In the aneurysm group, both MMP 2 and -9 were strongly expressed in the atherosclerotic aneurysms, but MMP 2 alone was detected in the non-atherosclerotic aneurysms. Zymography revealed a weak enzyme activity correlating to MMP 9 standard recombinant protein. MMP 2 activity was not demonstrated in either specimen. This study shows that the expression of MMP 2 and -9 is associated with atherosclerosis, be it in aneurysmal or non-aneurysmal cerebral vessels but MMP 2 appears to be specifically expressed in aneurysms devoid of atherosclerosis perhaps suggesting a pathogenic role for MMP 2 in the alteration of the extracellular matrix of cerebral arteries during aneurysm formation.

Giant Left Anterior Descending Artery Aneurysm in a Patient with Behcet's Disease

Coronary artery aneurysm is a rare coronary abnormality nearly half of which originates from atherosclerotic lesions. The major causes of non-atherosclerotic coronary aneurysms include coronary ectasia, Kawasaki disease, Takayasu aortitis, thoracic trauma and complicated angioplasty; however, it has been rarely reported associated with Behcet's disease.

Spontaneous carotid artery aneurysms

Spontaneous carotid artery aneurysms are infrequently reported, and are almost always non-atherosclerotic. The records of 29 patients with a spontaneous carotid aneurysm treated in an academic vascular unit between 1990 and 1998 were reviewed. All 29 patients were black South Africans; three had bilateral aneurysms. There were 24 men and five women, of mean age 35 (range 13-62) years. Some 25 aneurysms involved the common carotid artery, 12 of which affected the bifurcation, and seven were located in the internal carotid artery. Twenty-five aneurysms were managed surgically, four of which were ligated owing to sepsis. Histo- logical evaluation showed human immunodeficiency virus-related arteritis in four, tuberculous aneurysms in ten, Takayasu's arteritis in two, atherosclerosis in three and non-specific chronic inflammation in four patients. Microbiological examination was negative in all but one patient who had Salmonella sp. cultured. Outcome was generally favourable, but one patient died from massive hemispheric infarction. There were no other new neurological deficits. Carotid aneurysms pose a considerable surgical challenge but are amenable to operative intervention with good result. Ligation appears to be well tolerated in this group of predominantly non-atherosclerotic aneurysms.

Proposed classification of nonatherosclerotic cerebral fusiform and dissecting aneurysms.

The aim of this study is to classify nonatherosclerotic aneurysms unrelated to the branching zones (including fusiform aneurysms and dissecting aneurysms). Damage to the internal elastic lamina (IEL) is often an associated factor in the pathogenesis of aneurysm formation. In this study, 85 nonatherosclerotic aneurysms arising from an arterial trunk unrelated to the branching zones were classified into four different types, based on the lesional patterns of the IEL and the state of the intima. Type 1 corresponded to classic dissecting aneurysms, the pathogenesis of which was characterized by acute widespread disruption of the IEL without intimal thickening. Patients with Type 1 aneurysms had an ominous clinical course, and many presented with sudden subarachnoid hemorrhage with frequent rebleeding. Type 2 aneurysms were segmental ectasias, which had an extended and/or fragmented IEL with intimal thickening. Weakness of the arterial wall caused by the damaged IEL was assumed to be compensated by the intimal thickening. The luminal surface of the thickened intima was smooth without thrombus formation. The patients with Type 2 aneurysms had a placid clinical course. Type 3 aneurysms were dolichoectatic dissecting aneurysms, pathologically characterized by fragmentation of the IEL, multiple dissections of thickened intima, and organized thrombus in the lumen. Most of them were symptomatic and progressively enlarged over time. Type 4 aneurysms were saccular aneurysms unrelated to the branching zones. They arose in areas with minimally disrupted IEL without intimal thickening, and there was a risk of rupture. There was a strong relationship between the pathological features of the aneurysms and their clinical courses. This classification may provide a rationale for modes of treatment.

Femoral Occlusion in a Young Racing Cyclist and Nonatherosclerotic Aneurysms in the Autogenous Saphenous Vein Graft Used — A Case Report

The authors report and discuss a case of a young male smoker with major vascular problems. He was admitted with a femoral occlusion probably caused by his being an amateur racing cyclist. After reconstruction with a reversed autogenous saphenous vein graft he suffered several thrombophlebites of his lower extremities. Despite intensive investigations no cause was found for his apparent thrombotic tendency. Two years after reconstruction he was operated on for a true aneurysm occurring in his saphenous vein graft. Another two years later the whole saphenous vein graft was exchanged for a prosthesis be cause of multiple nonatherosclerotic aneurysms.