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Introduction: The aim of this study was to assess the efficacy of choline and DHA or exposure to environmental enrichment in obese adult and aging rats on alterations in body mass index, serum lipid profile and arterial wall changes, despite stopping high fat diet consumption and interventions during adulthood. Methods: 21 day old male Sprague Dawley rats were assigned as Experiment-1 & 2 - PND rats were divided into 4 groups with interventions for 7 months (n = 8/group). NC– Normal control fed normal chow diet; OB- Obese group, fed high fat diet; OB + CHO + DHA- fed high fat diet and oral supplementation of choline, DHA. OB + EE- fed high fat diet along with exposure to enriched environment . Experiment-2 had similar groups and interventions as experiment 1 but for next 5 months were fed normal chow diet without any interventions. Body mass index was assessed and blood was analyzed for serum lipid profile. Common Carotid Artery (CCA) was processed for Haematoxylin and eosin, Verhoff Vangeison stains. Images of tissue sections were analyzed and quantified using image J and tissue quant software. Results: In experiment.1, mean body mass index (p < 0.001), serum lipid profile (p < 0.01), thickness of tunica intima (p < 0.05), tunica media (p < 0.01) and percentage of collagen fibers (p < 0.01) of CCA were significantly increased in OB compared to NC. These were significantly attenuated in OB + CHO + DHA and OB + EE compared to OB. In experiment.2, mean body mass index (p < 0.01), serum lipid profile (p < 0.05) and thickness of tunica media of CCA (p < 0.01) were significantly increased in OB compared to NC. In OB + CHO + DHA and OB + EE, significant attenuation was observed in mean body mass index and mean thickness of tunica media compared to same in OB. Conclusion: Adult obesity has negative impact on body mass index, serum lipid profile and arterial wall structure that persists through aging. Supplementation of choline and DHA or exposure to enriched environment during obesity attenuates these negative impacts through aging.

Highlights • Angioleiomyoma is a rare benign tumor comprised of smooth muscle cells. • Other than biopsy, no modality of investigation can conclude the diagnosis. • Favorable prognosis can be obtained by simple local excision. • This case report presents a condition in which this tumor emerged from hand’s artery - An extraordinary observation., Introduction With the rarity and benign nature, angioleiomyoma is a tumor of disputed etiology that originates from the tunica media of the blood vessels. Lacking any characteristic clinical or radiological features, often leading to preoperative misdiagnosis, it is only diagnosed confidently on the basis of histopathology; for this reason combined with the rarity, angioleiomyoma would not be usually found at the top of the differential diagnosis list. Local excision is usually curative with excellent prognosis. Case This report discusses a case of a 60-year-old healthy lady who complained of a chronic painless mass in the right 2nd digit. Originating from the proper ulnar digital artery, it was excised with no complications. Histopathology results confirmed the diagnosis of angioleiomyoma. No recurrence was observed 6 months following the procedure. Discussion Out of the handful published papers concerned with angioleiomyoma in hands, few report the origin to be the digital artery. Conclusion Further awareness about this tumor is required and it should be included in the differential diagnoses list of the treating surgeon.

Objective: Synchrotron radiation-based X-ray phase-contrast tomography (XPCT) imaging is an innovative modality for the quantitative analysis of three-dimensional morphology. XPCT has been used in this study to evaluate ascending aorta specimens from patients with acute type A aortic dissection (ATAAD) and to analyze the morphologic structure of the aortic wall in patients with this condition. Methods: Aortic specimens from 12 patients were obtained during repairs for ATAAD and were fixed with formalin. Five patients had Marfan syndrome (MFS), and seven did not. In addition, six normal aortas were obtained from autopsies. Using XPCT (effective pixel size, 12.5 μm; density resolution, 1 mg/cm3), the density of the tunica media (TM) in each sample was measured at eight points. The specimens were subsequently analyzed pathologically. Results: The density of the TM was almost constant within each normal aorta (mean, 1.081 ± 0.001 g/cm3). The mean density was significantly lower in the ATAAD aortas without MFS (1.066 ± 0.003 g/cm3; P < .0001) and differed significantly between the intimal and adventitial sides (1.063 ± 0.003 vs 1.074 ± 0.002 g/cm3, respectively; P < .0001). The overall density of the TM was significantly higher in the ATAAD aortas with MFS than those without MFS (1.079 ± 0.008 g/cm3; P = .0003), and greater variation and markedly different distributions were observed in comparison with the normal aortas. These density variations were consistent with the pathologic findings, including the presence of cystic medial necrosis and malalignment of the elastic lamina in the ATAAD aortas with and without MFS. Conclusions: XPCT exhibited differences in the structure of the aortic wall in aortic dissection specimens with and without MFS and in normal aortas. Medial density was homogeneous in the normal aortas, markedly varied in those with MFS, and was significantly lower and different among those without MFS. These changes may be present in the TM before the onset of aortic dissection.

To evaluate by Doppler ultrasound (DUS) the venous intima-media thickness (vIMT) in patients with or without great saphenous vein (GSV) incompetence.A prospective vIMT measurement was performed by DUS in an outpatient cohort. Patients were divided in two groups: group A, patients without GSV reflux; and group B, patients with at least one refluxing GSV. Group B was further divided in group B1, patients with monolateral refluxing GSV; and group B2, patients with bilateral GSV reflux. The vIMT was measured in the femoral vein (FV), 3 to 5 cm distal to the saphenofemoral junction (vIMT[FV]), and in the GSV, 3 to 5 cm from saphenofemoral junction (vIMT[R-] or vIMT[R+]) in the case of a nonrefluxing or a refluxing GSV, respectively. Only one limb per patient was considered for vIMT analysis: in group A, the limb with the greater vIMT(R-), in subgroup B1 the limb with a refluxing GSV, and in subgroup B2 the limb with the lower vIMT(R+). The primary outcome was the difference of vIMT of GSV between groups A and B. Secondary outcomes were differences in vIMT(FV) among groups and the correlation between vIMT of GSV and demographic or clinical parameters. A subgroup analysis of vIMT in GSV was conducted in B1 patients, describing vIMT variations in both limbs.Forty-four patients were enrolled. In the group A (26 patients), vIMT of the GSV was lower than in the group B (18 patients; 0.31 ± 0.01 mm vs 0.49 ± 0.02 mm; P .001). The difference was significant also for vIMT(FV) (group A, 0.67 ± 0.02 mm vs group B, 0.77 ± 0.03 mm; P .014). No statistical correlation between age, body mass index, family history, or use of elastic stockings and vIMT(FV) or vIMT(R+ or R-) was detected. Considering the whole population, vIMT of GSV was higher in patients with Clinical, Etiology, Anatomy and Pathophysiology (CEAP) class C of 2 or greater than in classes C 0 and 1 (0.43 ± 0.02 mm vs 0.32 ± 0.02 mm; P .0002). The difference was significant also for vIMT(FV) in patients with class a class C of 2 or greater and C of 0 to 1 (0.77 ± 0.02 mm vs 0.64 ± 0.03 mm; P .0008, respectively). In group B1, vIMT(R+) was higher than vIMT(R-) (0.50 ± 0.02 mm vs 0.32 ± 0.02 mm, respectively; P .0001). The difference was not significant for vIMT(FV).vIMT seems to be an indirect marker of saphenous insufficiency. In GSV incompetence, an augmented wall thickening is visible in the FV as well. Further studies are needed to assess the accuracy of DUS measurements of vIMT. Longitudinal studies are also needed to evaluate possible GSV and FV vIMT variations related to disease progression or treatment.

Graphical abstract, Diabetes is strongly associated with cardiovascular disease, but the mechanisms, structural and biomechanical consequences of aberrant blood vessel remodelling remain poorly defined. Using an experimental (streptozotocin, STZ) rat model of diabetes, we hypothesized that diabetes enhances extracellular protease activity in the aorta and induces morphological, compositional and localized micromechanical tissue remodelling. We found that the medial aortic layer underwent significant thickening in diabetic animals but without significant changes in collagen or elastin (abundance). Scanning acoustic microscopy demonstrated that such tissue remodelling was associated with a significant decrease in acoustic wave speed (an indicator of reduced material stiffness) in the inter-lamellar spaces of the vessel wall. This index of decreased stiffness was also linked to increased extracellular protease activity (assessed by semi-quantitative in situ gelatin zymography). Such a proteolytically active environment may affect the macromolecular structure of long-lived extracellular matrix molecules. To test this hypothesis, we also characterized the effects of diabetes on the ultrastructure of an important elastic fibre component: the fibrillin microfibril. Using size exclusion chromatography and atomic force microscopy, we isolated and imaged microfibrils from both healthy and diabetic aortas. Microfibrils derived from diabetic tissues were fragmented, morphologically disrupted and weakened (as assessed following molecular combing). These structural and functional abnormalities were not replicated by in vitro glycation. Our data suggest that proteolysis may be a key driver of localized mechanical change in the inter-lamellar space of diabetic rat aortas and that structural proteins (such as fibrillin microfbrils) may be biomarkers of diabetes induced damage.

Localization of cyclooxygenase-2 (COX-2) in rat aortae was investigated. In endothelium-intact aortic strips stimulated with interleukin-1 β (IL-1 β ), COX-2 was detected in adventitial fibroblasts and macrophages but not in tunica media. IL-1 β−induced COX-2 expression was also detected in medial smooth muscle cells of endothelium-denuded aortae and cultured rat aortic smooth muscle cells. IL-1β−induced COX-2 expression in all of the above cells was abolished in the presence of U0126, an inhibitor of extracellular signal-regulated kinases (ERK). Thus, IL-1β induces COX-2 through the ERK-mediated pathway in adventitial fibroblasts and macrophages of healthy aortae; and in addition, medial smooth muscle cells are also responsible for COX-2 expression in remodeled aortae. Keywords:: cyclooxygenase-2, remodeling, vascular smooth muscle

To investigate the relationship between thyroid function and carotid intima-media thickness (CIMT) in a relatively large general population with euthyroid status we initially enrolled 1772 Japanese adults (421 men and 1351 women) who participated in a medical screening program for the general population over 40 years old. To evaluate only euthyroid subjects without vascular diseases and/or its major risk factors, 1129 were excluded and 643 participants (175 men and 468 women) were included for further analysis. Simple and multivariate linear regression analyses were performed to evaluate free thyroxine (fT4) and thyroid-stimulating hormone (TSH) levels and other existing parameters, including carotid intima-media thickness. By multivariate linear regression analysis adjusted for age and sex, free thyroxine was significantly correlated with triglycerides (beta=0.07, p=0.015), carotid intima-media thickness (beta=-0.091, p=0.049), and thyroid-stimulating hormone (beta=-0.091, p=0.003). Thyroid-stimulating hormone was significantly correlated with high-density lipoprotein cholesterol (HDL-C) (beta=-0.001, p=0.015), HbA(1c) (beta=0.038, p=0.045), carotid intima-media thickness (beta=0.27, p=0.001), and free thyroxine (beta=-0.15, p=0.003). When adjusted for confounding factors, free thyroxine was significantly correlated only with carotid intima-media thickness (beta=-0.13, p=0.043) and thyroid-stimulating hormone was significantly correlated with HDL-C (beta=-0.001, p, Atherosclerosis. 204(2), pp e77-e81

Objective Observational studies have reported inverse associations between adherence to the Mediterranean diet (MedDiet) and atherosclerotic disease. We tested the effect of two types of MedDiet on progression of subclinical carotid atherosclerosis. Methods We randomized 187 high-cardiovascular-risk asymptomatic subjects (51% women, mean age 67 years) to three treatment arms: MedDiet with supplemental virgin olive oil (VOO), n = 66; MedDiet with supplemental nuts, n = 59; and control diet, n = 62. Participants received nutrition behavioral counseling in quarterly group and individual educational sessions. Free supplemental foods were provided to the MedDiet groups. Changes in mean intima-media thickness (IMT) were measured ultrasonographically in the far wall of bilateral common carotid arteries after 1 year. Results Overall, no significant between-group differences in IMT progression were observed after 1-year. However, a significant interaction (p = 0.03) between baseline IMT and treatment effect was apparent. Among participants with baseline IMT ≥ 0.9 mm, 1-year IMT changes versus control showed significant differences of −0.079 mm (95% confidence interval, −0.145 to −0.012) for the MedDiet with VOO and −0.072 mm (−0.140 to −0.004) for the MedDiet with nuts. No IMT changes occurred in any intervention group among participants with lower baseline IMT values (, Spanish Government (FIS-ISCIII, PI050976, PI070240, PI081943, PI1002293, RTIC 06/0045, CIBERobn, and CNIC/06); Government of Navarra (PI41/2005, PI36/2008). RTIC 06/0045 and CIBERobn are initiatives of ISCIII, Spanish Government.

To examine whether individuals with normal glucose tolerance (NGT), whose 1-h post-load plasma glucose isor=155 mg/dl, or with impaired glucose tolerance (IGT) have an increased carotid intima-media thickness (IMT), as compared with NGT individuals with 1-h post-load plasma155 mg/dl.Atherosclerosis risk factors, oral glucose tolerance test (OGTT), and ultrasound manual measurement of IMT were analyzed in 400 non-diabetic Caucasians.As compared with individuals with a 1-h post-load plasma glucose155 mg/dl, NGT individuals with a 1-h post-load plasma glucoseor=155 mg/dl exhibited higher hsCRP (2.0+/-1.5 vs. 1.5+/-1.0, P=0.008), and IMT (0.82+/-0.20 vs. 0.71+/-0.16; P=0.006), and lower insulin sensitivity (71+/-39 vs. 105+/-57; P0.0001), and IGF-1 levels (214+/-88 vs. 176+/-49; P0.03). No significant differences were observed in metabolic and cardiovascular risk factors between IGT and NGT subjects with a 1-h post-load glucoseor=155 mg/dl. Of the three glycemic parameters, 1-h and 2-h post-load glucose, but not fasting glucose, were significantly correlated with IMT. In a stepwise multivariate regression analysis in a model including age, gender, and a variety of atherosclerosis risk factors, the three variables that remained significantly associated with IMT were age (P0.0001), BMI (P0.0001), and 1-h post-load glucose (P=0.02) accounting for 20.2% of its variation.NGT subjects with a 1-h post-load glucoseor=155 mg/dl have an atherogenic profile similar to IGT individuals. These data suggest that a cutoff point of 155 mg/dl for the 1-h post-load glucose during OGTT may be helpful in the identification of NGT subjects at increased risk for cardiovascular disease.

Epidemiological and autopsy studies suggest a close link between aging and the clinical manifestation of atherosclerosis. Several experiments show increased arterial susceptibility to atherogenetic stimuli in aged subjects. All together, these findings support the concept that aging represents an independent atherogenetic risk factor, intimately associated to other parietal, microenvironmental and systemic noxae. Smooth muscle cells (SMCs) represent the major arterial cell population. As aging occurs, SMCs progressively migrate from the tunica media and accumulate into the tunica intima. Myointimal thickening may represent the site where low-grade atherogenic stimuli cause early development and more severe lesion progression. Intimal SMC accumulation is characterized from a switch, from a differentiated to a synthetic phenotype, with reduced myocytic cytoskeletal markers and the expression of new proteins. Aging also associates to changes of SMC proliferative and apoptotic behavior and response to growth factors, such as transforming growth factor-beta1. The alteration of SMC properties represents a crucial event in the pathobiology of arterial wall, since it contributes to the vascular remodeling and decline of function with aging and favors the progression of atherosclerosis. Increased knowledge of biomolecular mechanisms regulating these events helps to develop new strategies aimed at contrasting the adverse effect of vascular aging.

Objective To determine the relationship between carotid intima-media thickness (IMT), carotid wall shear stress (WSS) and restenosis after femoro-popliteal percutaneous transluminal angioplasty (PTA). Patients and methods Thirty-one subjects (18 men, 13 women, median age 69 years) treated with femoro-popliteal PTA for symptomatic peripheral arterial occlusive disease were enrolled. On admission, IMT, internal diameter and blood velocity of the common carotid artery (CCA) were assessed by high-resolution ultrasonography. Blood viscosity was measured and carotid WSS was calculated. Patients were followed up for 6 months for the occurrence of significant restenosis (>50%) as documented by duplex ultrasonography. Two patients were lost to follow-up. Results Fourteen patients (48%) developed restenosis at 6 months. IMT and WSS were not different in patients without and with restenosis (IMT: 0.90 (0.85–0.97) vs. 0.89 (0.84–0.93) mm, p=0.51; WSS: 14.1 (11.9–19.2) vs. 15.9 (12.8–21.5) dyne/cm2, p=0.48). The hazard ratio of incident restenosis as estimated by Cox regression analysis was 0.04 for IMT (p=0.23; 95% CI 0.0001–8.22) and 1.07 for WSS (p=0.10; 95% CI 0.98–1.17). Conclusions In this pilot study involving a limited number of patients, carotid IMT and carotid WSS are not significantly related to restenosis at 6 months after femoro-popliteal PTA. This might be the result of different underlying pathophysiology for atherosclerosis and restenosis.

Publisher Summary This chapter discusses the anatomical heterogeneity and physiology of blood vessels, also the physiology of heart. Blood vessels of different anatomical origin have various functions in the circulation. Based on histologically defined criteria, the vessel wall of conduit arteries can be divided into three main layers. From the abluminal to the luminal side these consist of the outer tunica adventitia, the central tunica media, and the inner tunica intima. The physiological control mechanisms operated to maintain arterial blood pressure can be exerted through remote control or local control. Remote control is exerted by neural and humoral factors, while local regulation involves mechanical and metabolic factors such as carbon dioxide, pH and endothelium-derived factor. The circulation of the blood is maintained by the pump function of the heart. It can be divided into four chambers, that is left and right atrium and left and right ventricle. Under normal physiological conditions, the baroreceptor reflex regulates blood pressure and heart activity. Chronic hypertension results in a resetting of the baroreceptors so that they exert less inhibition of the vasomotor centers.

Rupture of a saccular aneurysm is the cause of hemorrhage in approximately 80% of patients with nontraumatic subarachnoid hemorrhage (SAH). SAH results from rupture of nonsaccular aneurysms including fusiform or atherosclerotic aneurysms, mycotic aneurysms, and traumatic aneurysms. Histological sections of saccular aneurysm demonstrate fragmentation and loss of the internal elastic membrane and loss of the smooth muscle of the tunica media. These pathologic changes of the arterial walls are not congential in nature as once surmised, but rather are acquired because of hemodynamic stresses. The diagnosis of SAH begins with the recognition of signs and symptoms as described and is confirmed primarily with computed tomography of the head. Four-vessel cerebral angiography in at least two projections is required for localization and anatomic definition of cerebral aneurysms. Close medical surveillance is essential to prevent and/or treat potential complications, including deep venous thrombosis, pulmonary embolism, infections, and delayed hydrocephalus.

This chapter discusses the surgical management of aneurysms in the pediatric age groups. The most common aneurysm site in pediatrics is the internal carotid artery bifurcation. There is a change in the pathology in children under 2 to 5 years old. The most common locations become the middle cerebral artery and the basilar artery bifurcation. Middle cerebral aneurysms are equally distributed between proximal and distal sites, the latter by contrast being very uncommon in adults. Most aneurysms in children are saccular aneurysms. These are likely acquired through hemodynamically induced degeneration of the internal elastic membrane at arterial bifurcations. Defects in the tunica media are much more common than aneurysms and probably do not directly contribute to aneurysm formation. It is likely that factors such as clinical grade, amount of subarachnoid blood on computed tomographic scan, day of admission after hemorrhage, and associated intracerebral and intraventricular hemorrhage that are important in adults are also important in children. Aneurysm site and size, hypertension, and associated medical illnesses were prognostic factors for outcome in multivariate analysis in adults but may be less important in pediatrics.

Human omental veins have a rich supply of sympathetic nerves which penetrates deep into the tunica media with terminals located 100–500 nm from adjacent muscle cells. The terminals contain large dense cored (LDV; 87.5 nm), small dense cored (SDV; 51 nm) and small clear vesicles (SCV). Electrical stimulation increases the number of small vesicles 30% and exo/endocytotic profiles 6-fold. With phentolamine present, stimulation decreases the numbers of large and small vesicles, and there is an increased frequency of vesicles closely associated with the terminal membrane.

Publisher Summary This chapter presents a study that discusses the relationship between the geometry of ventral interventricular branch (VIB) and its function. Five mongrel dogs of both sexes were used for the experiment. The chapter discusses the geometry, structure, and relative amounts of the structural component of VIB. The geometry of the vessel is characterized by the conspicious thinness of its wall, which is evident not only from the results of measurements but also from direct visual observation. The thinness is caused by a reduction of the number of smooth muscle cell layers in the media of the VIB. With a decrease of intravascular pressure, the vessel wall becomes slender and gives the impression of a vein. The VIB originates as a continuation of the left coronary artery and has three layers clearly differentiated at its beginning: (1) tunica adventitia, (2) tunica media, and (3) tunica intima. The artery is located directly below the epicardium. The chapter also illustrates the quantitative proportions of the two important components of the vascular wall, namely, elastic tissue and smooth muscle.