Aortic Wall In Patients Research Articles

SAT0051 Vitamin D Levels and Inflammation in the Aortic Wall of Patients with Inflammatory Rheumatic Disease and Coronary Artery Disease

BackgroundVitamin D is involved in immune reactions, and vitamin D deficiency is associated with autoimmune diseases and with cardiovascular diseases (CVDs). In Feiring Heart Biopsy Study (FHBS), we previously demonstrated...

Is there any difference in aortic wall quality between patients with aortic stenosis and those with regurgitation?†

The interaction between aortic valve (AV) and aortic wall pathology is currently unclear. No intraoperative examination or investigation is able to predict postoperative dissection or aneurysm formation in patients operated on for primary AV pathology. The aim of the present study was therefore to evaluate the mechanical and histological properties of the aortic wall in patients operated on for aortic stenosis (AS) or regurgitation (AR). The aortic walls of 229 patients (age 67.5 ± 11.0 years) operated on for AS (n = 135, Group 1) or AR (n = 94, Group 2) were subjected to mechanical stress testing and postoperative histological examination. Ascending aortic diameter was ≥50 mm in 46/229 patients and 40-49 mm in 52/229 patients. AR was associated with an increased tendency to aortic media disruption (P < 0.001) and with media degeneration (P < 0.001) compared with AS patients. The incidence of aortic aneurysm (≥50 mm) was increased in AR patients (35 in AR and 11 in AS, P < 0.01). The aortic wall cohesion was better in patients with an aortic diameter of <40 mm compared with those with moderate dilatation of 40-49 mm (P = 0.009) or an aortic aneurysm (P = 0.002). Our study proves that patients presenting for AV replacement with AR have a poorer quality of the ascending aorta despite a superior thickness compared with patients with AS. In addition, patients with a slightly dilated aorta (40-49 mm) have a poorer cohesion of the aortic wall than those with normal aortic dimensions.

Toll-Like Receptor-2 Plays a Fundamental Role in Periodontal Bacteria-Accelerated Abdominal Aortic Aneurysms

Periodontopathic bacteria are detected at a high rate in specimens obtained from the aortic walls of patients with abdominal aortic aneurysm (AAA) and are involved in AAA development. The purpose of this study was to clarify the role of Toll-like receptors (TLRs), which are key receptors of virulence factors of many periodontal bacteria, on periodontopathic bacteria-accelerated AAA progression. AAA was produced by peri-aortic application of 0.25 mol/L CaCl2, with NaCl used as a control. The mice were inoculated with live Porphyromonas (P.) gingivalis or vehicle once weekly. At 4 weeks after the application of CaCl2, the aortic diameter of the P. gingivalis-infected wild-type mice showed a significant increase in comparison with vehicle control mice (P<0.05). The P. gingivalis-infected TLR-2 deficient mice showed no statistical increase in aortic diameter over the same period. The aortic diameter of the P. gingivalis-infected TLR-4 deficient mice statistically increased. Immunohistochemically, the levels of matrix metalloproteinase-2 and -9 in the aneurysmal samples from wild-type mice were higher than in TLR-2 deficient mice. P. gingivalis accelerated the progression of experimental AAA through TLR-2 signaling.

急性大動脈解離後の大動脈外膜の張力と伸びに関する研究

Objective: To our knowledge, no previous study has described the measurement of the tensile strength of the human aortic adventitia. In the present study, we examined the relationship between the tension and length of the aortic adventitia resected from the aortic wall of patients with acute aortic dissection. Methods: We obtained rectangular specimens from the aortic adventitia that was resected in patients with acute aortic dissection during surgery. The specimens were placed on a tension meter (Digital Force Gauge FGS-10, SHIMPO, Kyoto, Japan) within 15 min after resection and stretched until they were pulled apart, and the tension and length were recorded. Results: We obtained 18 specimens during surgery from 11 cases of acute aortic dissection. When the specimen was being pulled apart, the mean tension recorded was 10.2 ± 4.9 N/cm specimen width, whereas the mean elongated length recorded was 4.2 ± 1.1 mm/cm specimen length. Discussion: We determined that the aortic adventitia is elastic and expandable up to 140% of its original length. This indicates that dilation of the aorta to >4.2 cm in diameter may result in a rupture if the original aortic diameter prior to dissection was 3 cm. (*English translation of J Jpn Coll Angiol 2013; 53: 77-81)

The elusive link between aortic wall histology and echocardiographic anatomy in bicuspid aortic valve: implications for prophylactic surgery

Prediction of aortic dissection or rupture is extremely difficult in patients with bicuspid aortic valve. We aimed to identify clinical and echocardiography predictors of histological abnormalities of the aortic wall in patients with bicuspid aortic valve undergoing aortic surgery. We assessed the histology of the aortic wall and clinical and echocardiography variables in a cohort of patients with bicuspid aortic valve (n = 127) and a wide spectrum of valvar disease who underwent replacement of the ascending aorta (with or without aortic valve surgery). Histology was classified using a 5-grade system developed by Larson and Edward. Histological alterations of the aortic wall were absent/mild (grade 0-1) in 77 patients (61%) and moderate/severe (grade 2-3) in 50 (39%). Patients with moderate/severe histological alterations were younger (47 ± 17 vs 53 ± 16; p = 0.042). Eighteen patients out of 48 (38%) with an ascending aorta diameter ≤ 4.5 cm had grade 2-3 aortic wall disease as did 8 out of 18 (44%) with a diameter ≤ 4 cm. Nineteen out of 46 (41%) patients with a maximal ascending aortic area/height ratio < 10 cm(2) m(-1) had moderate/severe histological alterations. Multivariate logistic regression analysis showed that the indexed diameter of the aortic annulus was significantly associated with grade 2-3 aortic wall disease (odds ratio (OR): 12.22, 95% confidence interval (CI): 1.65-90.38, p = 0.014). A high proportion of patients with bicuspid aortic valve and mild to moderate aortic dilatation have severe histological abnormalities of the aortic wall that are not predictable by clinical and echocardiographic findings. These observations suggest that risk stratification for aortic dissection or rupture in patients with bicuspid aortic valve is so far quite suboptimal and future investigations are warranted.

Elastic Properties of Aortic Wall in Patients With Bicuspid Aortic Valve by Magnetic Resonance Imaging

Bicuspid aortic valve (BAV) is frequently associated with aortic wall abnormalities, including dilation of the ascending aorta and even dissection. We propose 2 new indexes of aortic wall biophysical properties, the maximum rates of systolic distension and diastolic recoil (MRSD and MRDR, respectively), in patients with BAV and matched control subjects. We evaluated 53 consecutive young patients with BAV (36 males, mean age 16 ± 4 years) with mild aortic valve disease and a control group of 22 age- and gender-matched healthy volunteers. All subjects underwent a cardiac magnetic resonance imaging study that included phase velocity mapping and cine acquisition at several aortic levels. The MRSD and MRDR were measured in the ascending aorta in both patients with BAV and controls. Of the 53 patients with BAV, 26 had enlarged ascending aortas (dilated BAV), and 27 had a normal aortic diameter (nondilated BAV). Compared to controls, the MRSD was significantly lower in the whole BAV group (4.37 ± 1.1 vs 9.1 ± 2.1), in patients with dilated BAV (4.5 ± 1.1 p <0.0001), and in those with nondilated BAV (4.3 ± 1.0, p <0.0001). The MRDR was greater in the whole BAV group (-4 ± 1.2 vs -7.6 ± 2.7, p <0.0001), in the dilated BAV group (-3.9 ± 1.3, p <0.0001), and in the nondilated BAV group (-4.1 ± 1.2, p <0.0001). A receiver operating characteristic curve analysis of MRSD distinguished BAV from controls with 100% sensitivity and 95% specificity. In conclusion, MRSD and MRDR were slower in the patients with BAV than in the controls, regardless of the dimensions of the ascending aorta.

Pleiotropic Effects of ARB in Vascular Metabolism - Focusing on Atherosclerosis-Based Cardiovascular Disease

The renin-angiotensin system (RAS) plays an essential role in fluid and electrolyte homeostasis and the regulation of vascular tone; however, dysregulation and over-activation of the RAS lead to the pathogenesis of various cardiovascular diseases. The RAS is closely associated with NADPH oxidase, a major enzymatic source of reactive oxygen species (ROS) in vasculature, and angiotensin II, the final effecter of the RAS, is a potent stimulator of this oxidase. There are accumulating evidences to support the significance of NADPH oxidase in the pathogenesis of atherosclerosis. We demonstrated that the expression of NADPH oxidase is markedly enhanced in human atherosclerotic coronary arteries, and the distribution of oxidized oxidized low-density lipoprotein (LDL) in vasculature is closely associated with NAPDH oxidase and ROS. Our series of observations indicate there is a vicious circle consisting of vascular NADPH oxidase, the RAS, ROS, and oxidized LDL. Furthermore, we demonstrated that angiotensin II type 1 receptor blockers (ARBs) significantly suppressed the expression of NADPH oxidase p22(phox) in the aortic walls of patients with thoracic aortic aneurysm. ARBs, widely used for treatment of hypertension and hypertension-related organ damage, have succeeded in reducing the onset of cardiovascular diseases, preventing organ damage, and cardiac death. These beneficial effects of ARBs are largely dependent upon their primary effects of blood pressure lowering. However, this group of agents exerts a wide variety of biological effects on vascular metabolism, including antioxidative and anti-inflammatory actions. These pleiotropic actions play a role in cardiovascular protection. From a viewpoint of oxidative stress, we discuss pleiotropic effects of ARBs on vascular metabolism focusing on pathogenesis of atherosclerosis-based cardiovascular diseases.

Porphyromonas gingivalis promotes murine abdominal aortic aneurysms via matrix metalloproteinase-2 induction

Abdominal aortic aneurysm (AAA) is a common and lethal disorder, and MMPs are highly expressed in AAA lesions. Large numbers of periodontopathic bacteria have been reported to be present in specimens obtained from the aortic walls of patients with an AAA. The purpose of this study was to analyze the influence of periodontopathic bacteria on AAA dilatation. AAAs were produced in mice by the periaortic application of 0.25 M CaCl(2), and NaCl was used as a control. The mice were inoculated once weekly with live Porphyromonas gingivalis, live Aggregatibacter actinomycetemcomitans or vehicle. Four weeks after the periaortic application of either CaCl(2) or NaCl, a significant increase was observed in the aortic diameter of P. gingivalis-challenged mice compared with the vehicle control mice (p < 0.05), whereas there was no statistically significant increase in the aortic diameter of the A. actinomycetemcomitans-challenged mice. Immunohistochemical analysis found significantly higher numbers of CD8-positive and MOMA2-positive cells and significantly higher levels of MMP-2 in the aneurysmal samples of P. gingivalis-challenged mice compared with control mice. Live P. gingivalis promoted a significant proliferation of splenocytes in comparison with P. gingivalis-lipopolysaccharide and live A. actinomycetemcomitans (p < 0.05). These findings demonstrate that challenge with P. gingivalis, but not with A. actinomycetemcomitans, can accelerate, or even initiate, the progression of experimental AAA through the increased expression of MMPs.

Bicuspid aortic valve and aortic dilation: The current understanding

Aim: The bicuspid aortic valve (BAV) is one of the most common congenital heart disorders affecting 1–2% of the population. Individuals with a BAV tend to develop ascending aortic dilation, and are believed to be at high risk of aortic rupture and dissection. The association between the BAV and aortic stenosis, aortic regurgitation or infective endocarditis has been previously described, leading to the hypothesis of a common developmental anomaly incorporating both the aortic valve and thoracic aorta, and requires genetic solutions. The present article aims to make a comprehensive review of the possible determinants of this congenital defect entity. Methods: A literature retrieval was made by using the search terms ‘bicuspid aortic valve’ and ‘aortic dilation’ or ‘aortic aneurysm’ in major medical databases, including EMBASE, Cochrane Library, LILACS, MEDLINE and ADOLEC. A total of 496 articles were obtained. Relevant studies in the aetiologies of the BAV on the basis of clinical observations and basic research were selected and analysed. Results: Results from clinical observations have taken a haemodynamically resultant aortic dilation in the presence of a BAV into consideration. The two pathogenetic factors, haemodynamic and genetic, might coexist. Each of them could in turn prevail in different clinical pictures or anatomical forms. The presence of medial degeneration, elastic fragmentation and changes in smooth muscle cells was found to be much more severe in patients with a BAV than in those with a tricuspid aortic valve. Determination of the apoptotic index showed significantly increased numbers of dead smooth muscle cells in aneurysmal sections when compared with the normal aorta. Mean endothelial nitric oxide synthase levels in the endothelial cells of the aortic wall in patients with a BAV were significantly lower compared with those with a tricuspid aortic valve. Of importance are the novel findings of extracellular matrix degradation in terms of matrix metalloproteinase and their inhibitors, as well as mutations of variable genes, including Notch1, NKX2.5, ubiquitin fusion degradation 1-like gene and KCNJ2, that have drawn particular attention in the hope of offering an evolutionary explanation of this disorder. Conclusion: The development of the BAV might have diverse molecular triggers, thus it might be difficult to characterize the inciting events that result in a BAV and aortic wall disorders. Extracellular matrix dysregulation and cell death pathways are regarded as important molecular mechanisms of the aortopathy. Matrix degradation and gene mutations are the preferred hypotheses accounting for the development of this congenital lesion.

Glucose Metabolism in the Vessel Wall Correlates With Mechanical Instability and Inflammatory Changes in a Patient With a Growing Aneurysm of the Abdominal Aorta

It has been shown by our group and by others1,2 that increased glucose metabolism in the aortic wall of patients with aneurysms of the abdominal aorta (AAA) can be visualized in vivo by 18F-fluorodeoxyglucose positron emission tomography (FDG-PET). Interestingly, an increased glucose metabolism in AAA wall was strongly associated with rapid progression or acute symptoms and therefore increased rupture risk. Moreover, the PET signal was correlated with histopathological changes such as activation of MMP-9, collagen, and elastic fibers as well as macrophage infiltration in the AAA wall. (It is well documented by preclinical studies that increased activity of MMP9 facilitates aneurysm rupture). However, the true prognostic value of increased FDG uptake for AAA progression and rupture risk still remains uncertain. To provide clear evidence, surveillance of small AAA by multiple PET scans would be necessary over a long period. However, PET studies are not routinely performed in patients with AAA for practical and ethical reasons and therefore an increase in glucose metabolism in AAA wall was not directly observed until now. Further, it is …

Proteomic identification of differentially expressed proteins in aortic wall of patients with ruptured and non-ruptured abdominal aortic aneurysms

Proteomic identification of differentially expressed proteins in aortic wall of patients with ruptured and non-ruptured abdominal aortic aneurysms

Proteomic identification of differentially expressed proteins in aortic wall of patients with ruptured and nonruptured abdominal aortic aneurysms

To compare the basic proteomic composition of abdominal aortic aneurysm (AAA) wall tissue in patients with nonruptured and ruptured aneurysms. A proteomic approach with two-dimensional gel electrophoresis (2D-PAGE) and mass spectrometry (MS) was used to identify differentially expressed proteins in AAA tissue from nine patients with nonruptured and eight patients with ruptured AAA. Computerized image analysis was used to detect protein spots. Differentially expressed protein spots were in-gel digested and identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Western blot analysis was used to confirm differential expression. Seven differentially expressed proteins were detected among 745 protein spots, selecting spots whose average relative volumes differed more than twofold between the nonruptured and the ruptured group. Four protein spots were up-regulated in the ruptured group, and three were down-regulated. Five of the spots were identified. Among the upregulated spots, No. 605 was identified as peroxiredoxin-2. The up-regulation was confirmed by Western blotting. No. 381 was identified as an actin fragment. Two spots, Nos. 719 and 499, could not be identified. Among the down-regulated protein spots, No. 130 contained two peptides; one reliably determined peptide, FEDGVLDPDYPR, is found in vitronectin. Another peptide, QIDNPDYK, was borderline significant and found in calreticulin. The down-regulation of vitronectin was confirmed by Western blotting. Spot Nos. 193 and 199 both contained peptides from albumin with actin also present in No. 199. The identified proteins suggest that the aortic wall of ruptured aneurysms responds to a stressful condition and that proteolytic degradation of the cytoskeleton and connective tissue may be part of the response.

Cysteine protease activity in the wall of abdominal aortic aneurysms

Cysteine proteases are potent elastolytic enzymes and together with their inhibitor, cystatin C, have been linked with the growth of abdominal aortic aneurysms (AAAs). These enzymes and their inhibitors have previously been studied in AAAs, but comparisons have always been made with wall from normal aorta. Atherosclerosis is a feature of aneurysmal disease and may therefore confound comparisons with normal wall. This study compared the expression and activity of cysteine proteases and their inhibitors in aneurysm wall with their expression in the aortic wall of patients with aortic occlusive disease (AOD). Aortic wall was obtained from 82 patients with AAA and 13 with AOD. Protein expression and activity of cathepsin B, H, K, L and S, and cystatins A, B, and C were measured by enzyme-linked immunosorbent assay and specific fluorogenic substrate assays. Matrix metalloproteinase 9 (MMP-9) activity was measured by quantitative bioimmunoassay in the same extracts. AAA wall had 330% more cathepsin H protein (P = .007) and >30% less cystatin C (P = .03) than the aortic wall from patients with AOD. The activity of cathepsins B, H, L, and S was significantly greater in AAA than AOD (376%, [P < .0001], 191%, [P = 0.019], 223%, P = 0.002, and approximately 20% [P = 0.045] respectively). MMP-9 activity was also increased in AAA compared with AOD (P<0.0001) and levels in the wall of AAA correlated positively with cathepsin L activity (r = 0.42, P<.0001) and negatively with cystatin C (r = -0.75, P<.0001). The activity of four cathepsins B, H, L, and S was higher in the aneurysm wall than in aortic wall of patients with occlusive disease. This was associated with a reduced level of cystatin C in the aneurysmal wall. Cathepsin H was the only protein in which there was a correlation between protein level and activity, which suggests that post-translational modifications were responsible for activation of the other cathepsins. Increased cathepsin activity may influence the activity of MMP-9, which is thought to have an important role in aneurysm development.

Abstract 2677: Reduction In Tie-2+/flk-1+ Vascular Stem Cells In Thoracic Aortic Aneurysm With Dissections: A Novel Contributor To Acellular Lesion Development

Background. Ascending thoracic aortic aneurysms leading to type A dissections (TAAD) are a life-threatening disease triggered by a complex interactions between environmental and genetic factors. Pathologically, this disease is characterized by a progressive loss of vascular smooth muscle cells (SMCs) and extracellular elastic fibers in the aortic media. Apoptosis, a form of programmed cell death, has been shown to contribute to the loss of medial SMCs. However, little is known about the role of vascular progenitor or stem cells in the pathogenesis of aortic aneurysms. Methods and Results. In this study we examined expression of Tie-2 (receptor for angiopoietin) and Flk-1 (receptor for vascular endothelial cell growth factor), two receptors critical for regulation of vascular stem cell survival and growth in the aortic lesions of patients with TAAD. Immunohistochemistry with specific antibodies against Tie-2 and Flk-1 showed a marked reduction in the numbers of Tie+/Flk+ cells in TAAD when compared to control aortas. There was also a change in the distribution pattern of vascular progenitor cells positive for both Tie-2 and Flk-1 in TAAD patients’ aortic tissues. Compared to normal control aortas, the Tie-2 and Flk-1 immunostained cells were much lower in intensity and scattered. In the regions with paucity of Tie-2+/Flk-1+ cells, there was an increased number of apoptotic cells as determined by in situ DNA end-labeling (TUNEL). Many of the Tie-2 and Flk-1 positive cells in TAAD showed poor morphology with nuclear degeneration and cytoplasmic fragmentation and disarray. Conclusion . These results indicate a paucity of Tie-2+/Flk-1+ vascular stem cells in the aortic wall of patients with TAAD, implying that the stem cell capacity to regenerate SMCs is exhausted. Similar loss of stem cells is observed with Duchenne muscular dystrophy, where the regenerated capacity is significantly compromised. Stem cells loss may similarly impair the capacity of SMCs in aortic tissue in repair and regeneration, and ultimately lead to TAAD formation.

721 eTracking of carotid arteries as a new tool in evaluation of early functional vascular remodeling

s S119 Eur J Echocardiography Abstracts Supplement, December 2006 ness index (6.04±2.2 vs 4.08±1.6, p=0.045), slope S (1.12±0.2 vs 0.8± ±0.14 m/sec2, p=0.002) and early diastolic velocity of upper aortic wall E (3.5±1 vs 6±0.6 cm/sec, p=0.0001). Aortic distensibility had a significant positive correlation with early diastolic velocity of aortic wall E (r=0.534, p=0.015) but not with slope S and aortic stiffness index was correlated positively only with slope S (r=0.396, p=0.046). Conclusions: Elastic properties of the aorta can be evaluated by using color tissue doppler imaging of the upper aortic wall in patients with end-stage renal disease. In our study the slope of systolic velocity and the early diastolic velocity of upper aortic wall are associated with alteration in aortic wall properties.

Abdominal Aortic Aneurysm Is a Specific Antigen‐Driven T Cell Disease

To determine whether monoclonal/oligoclonal T cells are present in abdominal aortic aneurysm (AAA) lesions, we amplified beta-chain T cell receptor (TCR) transcripts from these lesions by the nonpalindromic adaptor (NPA)-polymerase chain reaction (PCR)/V-beta-specific PCR followed by cloning and sequencing. Sequence analysis revealed the presence of substantial proportions of identical beta-chain TCR transcripts in AAA lesions in 9 of 10 patients examined, strongly suggesting the presence of oligoclonal populations of alphabeta TCR+ T cells. We have also shown the presence of oligoclonal populations of gammadelta TCR+ T cells in AAA lesions. Sequence analysis after appropriate PCR amplification and cloning revealed the presence of substantial proportions of identical VgammaI and VgammaII TCR transcripts in 15 of 15 patients examined, and of Vdelta1 and Vdelta2 TCR transcripts in 12 of 12 patients. These clonal expansions were very strong. All these clonal expansions were statistically significant by the binomial distribution. In other studies, we determined that mononuclear cells infiltrating AAA lesions express early- (CD69), intermediate- (CD25, CD38), and late- (CD45RO, HLA class II) activation antigens. These findings suggest that active ongoing inflammation is present in the aortic wall of patients with AAA. These results demonstrate that oligoclonal alphabeta TCR+ and gammadelta TCR+T cells are present in AAA lesions. These oligoclonal T cells have been clonally expanded in vivo in response to yet unidentified antigens. Although the antigenic specificity of these T cells remains to be determined, these T cells may play a significant role in the initiation and/or the propagation of the AAA. It appears that AAA is a specific antigen-driven T cell disease.

Thromboses aortiques « isolées » : analyse rétrospective de 10 observations

Introduction Thrombi of the aorta are mostly linked to atheromatous plaques on the aortic wall of patients with classical risk factors for cardiovascular disease. The thrombus rarely appears on sound arteries and in this case is called « isolated ». Methods We present a retrospective study of ten patients with « isolated » thrombi of the aorta treated between 1995 and 2004 at the Hospital of Grenoble. The following parameters were considered in this analysis: age of the patient when the thrombosis appeared, gender, cardiovascular risk factors, revealing mode of the thrombus, its anatomic location, biological and morphological exploration results and the treatment performed. Patients with atheromatous plaques on the aortic wall were excluded. Results In eight out of ten cases the clinical presentation of the aortic thrombus is an acute ischemia of a limb. In all of the cases the diagnosis was confirmed by an injected thoraco-abdominal scan apart from one case where the primary diagnosis was made using an arterial echo-Doppler. The search for the thrombophilia can be considered to have been exhaustive in seven cases. For the search of an anti-phospholipid antibody syndrome this has been achieved in eight cases. Two etiologic diagnoses could be placed. The first one revealed during the aortic thrombosis a neoplasia of adenocarcinomic type without any primary identified. The second case was an essential thrombocythemia diagnosed one year after the thrombosis. The eight other cases remained « isolated » after an average 2.5 years follow-up. Discussion Less than one hundred cases of aortic thromboses could be identified in the literature. The cases developing on a sound artery are difficult to quantify and the word « isolated » thrombus may be sometimes used by default. The hypothesis of an isolated focal atheromatous plaque or of inflammatory pathologies inducing a thrombus can be an example. The biological and morphological explorations have to be exhaustive even if in most of the cases they are not sufficient for the diagnosis. Therapy calls for anti-coagulation but is not standardized. The clinical follow-up appears to be essential since pathological conditions can possibly develop after the event of the thrombosis. It also enables refinement of the actions to be taken especially regarding long-term use of anticoagulants. (J Mal Vasc 2005; 30: 280-90)

Aortic Organ Disease Epidemic, and Why Do Balloons Pop?

As children, we learned that a balloon blown up to its limit of elasticity would pop. For similar aortic ballooning, we hardly know more. Furthermore, in the 21st century, with a nascent epidemic of aortic-related deaths, there have been no consequential advances in preventing the loss of aortic elasticity or in describing the etiology or injury that causes aortic disease. Nor is there an explanation as to why, in some people the aorta “pops” and in others, the aorta dissects. See p 1098 In the United States between 1999 and 2001, at least 129 533 people died from diseases of the aorta and its branches, excluding carotid and coronary disease—an average of 43 199/year, according to the Centers for Disease Control and Prevention ICD-10 codes (Table). The upper limit could potentially exceed 46 817 per year. This number is greater than the ≈40 000 people who die annually from breast cancer, homicides, pancreatic cancer, colon cancer, prostate cancer, or motor vehicle accidents.1 Despite this, little research and even less funding have been allocated to aortic disease research, possibly because disease of a supposedly utilitarian pipe that conveys blood to a pantheon of organs engenders less interest or sympathy in comparison with, for example, cancer. Furthermore, the dismal prognosis of aortic disease, a marker of systemic problems despite successful surgery, has not roused much concern, with a 5-year average survival rate of only 60% in most patients.2 This figure does not differ much from that of stage IB lung cancer. Even the aortic disease–related deaths of media figures such as Albert Einstein, Lucille Ball, Conway Twitty, and John Ritter have fomented little interest. As Western populations age, this most common cause of deaths including sudden death will become an increasing factor in long-term survival. View this table: Deaths Related to Aortic Disease …

E‐SAR‐94010 (LipoEsar®): A Pleiotropic Lipoprotein Compound with Powerful Anti‐atheromatous and Lipid Lowering Effects

E-SAR-94010 (LipoEsar) is a natural product extracted from the marine species S. pilchardus, by means of non-denaturing biotechnological procedures. The main chemical ingredient of LipoEsar is a lipoprotein (60–80%) whose micelle structure probably mimics that of physiological lipoproteins involved in lipid metabolism. In preclinical studies LipoEsar has shown to be effective in (a) reducing blood cholesterol (Cho), triglyceride (TG), uric acid (UA), and glucose (Glu) levels, as well as liver alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activity; (b) enhancing immunological function by regulating both lymphocyte and microglia activity; (c) inducing antioxidant effects mediated by superoxide dismutase activity; and (d) improving cognitive function. Clinical studies have revealed that LipoEsar reduces blood total cholesterol (T-Cho) (20–30%), Glu (5–10%), UA (10–15%), TG (30–50%), ALT and AST, after 1–3 months of treatment at a daily dose of 250–500 mg (t.i.d.). The effect on T-Cho is the result of decreasing LDL-Cho levels and increasing HDL-Cho levels in parallel with an improvement in hepatic protection reflected by reduction in ALT, AST, and GGT activity. Most of these therapeutic effects on the regulation of lipid metabolism tend to show an age-dependent pattern and are also associated with specific genomic profiles in the population. In addition, LipoEsar diminishes the size of xanthelasma plaques by 30–60% after 6–9 months of treatment. Similar effects can be observed on atheromatous plaques on the aortic wall of patients with familial and sporadic hypercholesterolemia. LipoEsar is the first marine biotechnological product with lipoprotein structure displaying hypolipemic activity in blood and tissues acting as a potential neuroprotectant in cerebrovascular disorders and arteriosclerosis. Preliminary studies indicate that the biological activity of LipoEsar is genotype-dependent. Since genetic defects in the APOE gene result in familial dysbetalipoproteinemia or type III hyperlipoproteinemia (HLP-III) with increased plasma Cho and TG as a consequence of impaired clearance of chylomicron and VLDL remnants, in the present paper we have investigated the influence of different APOE genotypes on the therapeutic response of LipoEsar in patients with chronic dyslipemia. The study has been performed in 419 patients (age: 55.24 ± 17.71 years; range: 9–96 years) of both sexes (females: N = 212; age: 57.04 ± 17.68 years; range: 15–96 years; males: N = 207; age: 53.38 ± 17.58

Lack of association between serum immunoreactivity and Chlamydia pneumoniae detection in the human aortic wall.

Only a few studies have focused the attention on the relation between elevated anti-Chlamydia pneumoniae (CP) antibodies and the detection of CP in the arterial wall. The aim of our study is thus to investigate the relationship between immune response to CP and detection of CP in the aortic walls of patients with abdominal aortic aneurysm. A specimen of aortic wall was obtained from 102 consecutive patients who underwent abdominal aneurysm repair. The possible presence of CP was studied by polymerase chain reaction and confirmed by nonradioactive DNA hybridization. Antibody response to CP was studied (IgG, IgA titers). We found 33 patients (32.4%) with CP DNA+. No correlation between CP DNA detection and antibody titers was found (IgG P=0.52, IgA P=0.66). High correlation between IgG and IgA titer was observed (P<0.01). Endovascular presence of CP and antibody titers was not related to the age of the patient. CP antibody titers are not associated with the presence of CP in the aortic wall of patients with abdominal aortic aneurysm.