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PubMed1999

[Behavior of soft tissue structures in surgical leg lengthening].

Experimental animal studies and clinical investigations show three processes going on during extremity lengthening with the Ilizarov-method. At first degenerative changes including cell necroses in the muscles, the nerves and the tendons [corrected] occur as well as denervation of muscle fibers resulting in neurogenous muscle atrophies. These alterations are followed by reperative and regenerative processes as well as the reinnervation of the denervated muscle fibers. Secondly histoneogenesis occur which leads to a high increase of tissue-specific cells and a growth of the muscles, tendons and vessels. Therefore tensile-stress is an important factor of tissue growth. Thirdly adaptive processes proceed during leg lengthening. For example the high biosynthetic activity during tissue growth seems to indicate an increase of vasa vasorum.

Animals↗
PubMed2001

Fatal hemorrhage in stented esophageal carcinoma: tumor necrosis of the aorta.

We report a case of fatal hematemesis in a patient with an esophageal stent for palliation of malignant dysphagia. Post-mortem examination showed tumor thrombi in the vasa vasorum of the aorta causing aortic wall necrosis and perforation. Massive delayed hemorrhage is reported as a complication of metallic esophageal endoprostheses but in the majority of cases there have been no post-mortem examinations. In this case the post-mortem examination demonstrated that the cause of death was not stent-related. We feel that this case report adds important information to the current literature regarding the delayed complications seen in patients with esophageal carcinoma who have been palliated with metallic stents.

Aged↗
PubMed1998

[Intramural hemorrhage of the thoracic aorta: diagnosis, therapy and prognosis of 209 in vivo diagnosed cases].

Aortic dissection with no entry or false lumen flow was recently identified as intramural hemorrhage of the aortic wall (IMH). Analysis of the literature revealed 209 cases of in vivo diagnosed IMH reflecting 17% of all dissections, whereas in postmortem studies this condition is found in 4-13%. Transesophageal echocardiography, computed tomography, magnetic resonance imaging and aortography (to rule out dissection) have been applied for diagnosing IMH in 57, 49, 43 and 38% of the cases, respectively. However, diagnostic accuracy of each modality is not available to date. In 34%, IMH involves the ascending aorta (type A). The average age of patients with IMH ranges between 55 and 65 years; 65% are males. In 12%, IMH was associated with abdominal aortic aneurysm. With 87%, arterial hypertension is the predominant risk factor for IMH irrespective of its location. As suggested by the term "mediastinal apoplexy" IMH may--similar to cerebral apoplexy--result from hypertensive rupture of the vasa vasorum in the aortic media. With 97%, the majority of patients present with acute chest or back pain similar to classic dissection. Mediastinal widening is found in 83%; signs of hemothorax/pleural effusion are present in 38%, acute aortic regurgitation in 26%, pericardial effusion in 23%, acute neurologic deficits in 12%, and pulse deficits in 5%. In 18%, IMH progresses to dissection and in another 15% to rupture. In 25% and 28%, respectively, dissection and rupture occur in the ascending aorta and in 12% and 9%, respectively, in the descending thoracic aorta. The 30-day mortality of IMH is 24% (36% with type A and 12% with type B IMH; p < 0.05). With surgical repair, mortality of type A IMH is lowered to 18% compared to 60% with medical treatment (p < 0.01). In contrast, with 8% mortality associated with medical treatment, prognosis of type B IMH is more favorable without surgical intervention, the latter associated with a 30-day mortality of 33% (p < 0.05). Thus, IMH is a potential precursor of dissection and should be managed like dissection with undelayed surgical intervention in patients with type A IMH and with medical treatment in type B IMH.

Aortic Dissection↗
PubMed2001

Expression of cell adhesion molecule T-cadherin in the human vasculature.

Alterations in expression of surface adhesion molecules on resident vascular and blood-derived cells play a fundamental role in the pathogenesis of cardiovascular disease. Smooth muscle cells (SMCs) have been shown to express T-cadherin (T-cad), an unusual GPI-anchored member of the cadherin family of adhesion molecules. Particular relevance for T-cad in cardiovascular tissues is indicated by our present screen (immunoblotting) of human tissues and organs whereby highest expression of T-cad was found in aorta, carotid, iliac and renal arteries and heart. To explore the (patho)physiological role for T-cad in the vasculature we performed an immunohistochemical analysis of T-cad expression in normal human aorta and atherosclerotic lesions of varying severity. T-cad was present both in the intima and media and was expressed in endothelial cells (ECs), SMCs and pericytes, but not in monocytes/macrophages, foam cells and lymphocytes. In the adventitia T-cad was present in the wall of vasa vasorum and was expressed in ECs, SMCs and pericytes. T-cad was differentially expressed in SMCs from distinct vascular layers of normal aorta (for example, high in the subendothelial (proteoglycan) layer of the intima, low in the musculoelastic intimal layer and in the media), as well as at different stages of lesion progression. In SMCs there was an apparent inverse relationship between the intensities of T-cad and smooth muscle alpha-actin expression, this being most prominent in lesions. The findings suggest a phenotype-associated expression of T-cad which may be relevant to control of the normal vascular architecture and its remodelling during atherogenesis.

Aorta↗
PubMed2001

Aortic lesions in aspergillosis: histopathological study of two autopsy cases.

The involvement of the aorta in aspergillosis is relatively rare, and its histopathological features have not been described in detail. In two autopsy cases of invasive aspergillosis in immunologically compromised patients with hematological disorders, the aspergillotic lesions of the aorta showed different characteristic histopathological features depending on the three layers of aortic wall. Intimal lesions were formations of the mural thrombus composed of aggregates of numerous fungal hyphae arranged perpendicularly to the aortic wall. In the media, smooth muscle cells were completely necrotic (anemic infarct of the media), while the framework of elastic fibers was well preserved, with only a few fungal hyphae detected. In the adventitia, an intense, partly granulomatous chronic inflammatory change with fibrosis was observed in association with mycotic embolic occlusion of the vasa vasorum. These histopathological changes were considered to represent one of the typical tissue reaction patterns in the wall of an elastic artery in aspergillosis.

Aorta, Thoracic↗
PubMed1998

[Detection of extracellular matrix protein (laminin) in experimental arterial anastomoses].

AIM: To investigate the distribution of Laminin in experimental microvascular surgery. MATERIAL AND METHODS: Autografts (4 mm) of the left common carotid artery in 20 Wistar rats were harvested after 4 weeks. The specimens were investigated immunohistochemically for the demonstration and distribution of Laminin. RESULTS: The demonstration and distribution pattern of Laminin was a function of the accuracy of each single suture. In the intima, the organisation and amount of Laminin was directed to the lumen and dependent from the distance and vitality of the vessel segments' cells. The media had in its axis direction the lowest reparative potency to regenerate the continuity break. The adventitia formed a thick cuff around the anastomosis, which was circularly grown through with Laminin-positive vasa vasorum. The marked myointimal hyperplasia in the area around the anastomosis and in the entire autograft was constituted of Laminin-positive extracellular matrix. CONCLUSIONS: Our results support the demand for a careful and atraumatic suture technique in microvascular surgery.

Anastomosis, Surgical↗
PubMed2001

The effect of supplemental oxygen on the transarterial wall oxygen gradients at a prosthetic vascular graft to artery anastomosis in the rabbit.

Artery wall hypoxia has been proposed to contribute to many kinds of artery wall pathology, including atherosclerosis and intimal hyperplasia. The purpose of this study was to determine the effect of supplemental oxygen on the transarterial wall oxygen gradients at a prosthetic vascular device (PVG)-to-artery anastomosis. The transarterial wall oxygen gradient in the infrarenal aorta of New Zealand White rabbits housed for 42 days in a 40% supplemental oxygen was measured with an oxygen microelectrode 2 mm distal to a PVG-to-artery anastomosis. Oxygen tensions were significantly increased throughout the artery wall at all time points in the supplemental oxygen groups compared to those in non-oxygen-supplemented groups. Within the oxygen-supplemented groups, the outer artery wall had diminished oxygen tensions immediately following creation of the anastomosis, with a slow return to control oxygen tensions on postanastomosis day 42 which correlated with a return of the vasa vasorum. These changes were noted without differences in blood pressure or arterial blood oxygen concentrations within the oxygen-supplemented group. Artery wall hypoxia noted following the creation of a PVG-to-artery anastomosis can be eliminated and artery wall oxygen tensions significantly increased by the administration of supplemental oxygen.

Animals↗
PubMed1998

Internal carotid artery dissection in a patient with Behçet's syndrome.

The authors report a case of internal carotid artery dissection in a young woman with Behçet's syndrome. The authors postulate that a vasculitis of the vasa vasorum already suspected as the basis of aneurysm formation in course of Behçet's syndrome can account for occurrence of arterial dissection in this inflammatory condition.

Aortic Dissection↗
PubMedDate not supplied

Cardiac, aortic, and pulmonary arteriopathy in HIV-infected children: the Prospective P2C2 HIV Multicenter Study.

Arteriopathy in human immunodeficiency virus (HIV)-infected patients is being increasingly recognized, especially in children. However, few studies have histologically evaluated the coronary arteries in HIV-infected children, and none have systematically assessed the aorta and pulmonary arteries. The coronary arteries, thoracic aorta, and the main and branch pulmonary arteries from the postmortem hearts of 14 HIV-infected children were systematically reviewed for vasculopathic lesions and compared with 14 age-matched controls. Findings from the HIV-infected children were compared with clinical, laboratory, and other postmortem findings. Coronary arteriopathy, seen in seven (50%) of the HIV-infected children, was primarily calcific, and it was associated with decreased CD3 and CD4 peripheral blood counts. Large vessel arteriopathy, seen in 9 (64%) of the 14 HIV-infected children, was primarily centered on the vasa vasorum and consisted mainly of medial hypertrophy and chronic inflammation. Large vessel lesions were associated with increased left ventricular mass z-scores (P = 0.02), and 78% of patients with large vessel arteriopathy had postmortem cardiomegaly. Coronary and large vessel arteriopathies are common in pediatric HIV-infection and have different clinicopathologic features suggesting different pathogenesis.

Aorta↗
PubMed2001

Plaque angiogenesis and atherosclerosis.

Therapeutic angiogenesis trials refer to the stimulation of collateral arterioles and new vascular conduits to perfuse ischemic myocardium and limbs. Atherosclerotic lesions responsible for vascular occlusions themselves are associated with angiogenesis within the vessel wall. Plaque neovascularization is comprised of a network of capillaries that arise from the adventitial vasa vasorum and extend into the intimal layer of atherosclerotic lesions and other types of vascular injury. The functions of these plaque capillaries are proposed to be important regulators of plaque growth and lesion instability. The development of agents that are positive and negative regulators of angiogenesis may have potential therapeutic implications in the progression and acute manifestations of atherosclerosis. This review focuses on the role of plaque angiogenesis in atherosclerosis and discusses the potential therapeutic applications of angiogenesis inhibitors in this disease.

Angiogenesis Inhibitors↗
PubMed2004

Aortic Intramural Hematoma: Current Diagnostic and Therapeutic Recommendations.

Aortic intramural hematoma (IMH) is an acute, potentially lethal disorder that is similar to but pathologically distinct from acute aortic dissection. Although hemorrhage into the aortic media occurs in both disorders, an intimal tear with resultant false lumen is not present in IMH. Instead, hemorrhage occurs within the aortic wall either due to rupture of the vasa vasorum or, less commonly, because of an atherosclerotic penetrating aortic ulcer. The most common risk factors associated with IMH are hypertension, atherosclerosis, and advanced age. IMH is life-threatening because the hematoma may extend along or rupture through the aorta, leading to hemothorax, cardiac tamponade, stroke, mesenteric ischemia, or renal insufficiency. Optimal treatment is still somewhat controversial; however, there is no question that hypertension must be treated effectively and immediately. This is usually best accomplished by intravenous infusion of beta-blocking agents, with or without the addition of sodium nitroprusside. Recent studies support surgical treatment (ie, aortic root replacement) for IMH involving the ascending aorta, although some subsets of this population may be at lower risk and may benefit from medical therapy alone. In patients with IMH involving only the descending aorta, medical therapy alone is recommended (unless impending rupture, aortic aneurysm, or end-organ ischemia occurs). Patients who survive the acute event require intensive treatment of hypertension and frequent follow-up examinations. Because this population (especially the subset with penetrating aortic ulceration) is at high risk for aortic aneurysm and rupture, serial imaging studies of the aorta are essential.

Journal Article↗
PubMed2005

Infectious Aortitis.

Infection of the aorta usually results from septic embolization to the vasa vasorum, hematogenous seeding of an existing aneurysm, or extension from a contiguous site of infection. The diagnosis should be considered in patients, often men over the age of 50 years with atherosclerosis, who present with fever, abdominal pain, palpable abdominal mass, and leukocytosis, with or without positive blood cultures. In the pre-antibiotic area, infectious aortitis was largely a complication of infective endocarditis, and was usually caused by group A streptococci, Streptococcus pneumoniae, or Haemophilus influenzae. Now a diverse array of bacteria and fungi has been associated, most commonly Salmonella species, which comprise nearly one third of the abdominal aortic infections and Staphylococcus aureus. Computed tomography is the most useful imaging modality. Medical treatment alone carries a high mortality, whereas the mortality with surgery combined with antimicrobial treatment is lower. Empiric antibiotics effective against S. aureus and gram-negative rods, such as Salmonella, should be initiated in cases identified before microbiologic diagnosis. Surgical debridement and revascularization should be completed early because delay may lead to aneurysm rupture, which increases mortality. The intent of surgery is to 1) control hemorrhage, if the aneurysm has ruptured; 2) confirm the diagnosis; 3) control sepsis; and 4) reconstruct the arterial vasculature. The patient should remain on parenteral or oral antibiotics for at least 6 weeks, perhaps longer, to assure full eradication of the pathogen and prevent recurrent infection. Close medical follow-up is indicated and includes serial blood cultures and computed tomography scans.

Journal Article↗
PubMed1991

Complete left main coronary artery occlusion: angiographic evaluation of collateral vessel patterns and assessment of hemodynamic correlates.

An angiographic study of eight patients with total occlusion of the left main coronary artery identified six patients with chronic occlusion and two with acute complete occlusion. In each of six patients, there were two to six different intercoronary collateral pathways. Altogether, a total of 13 specific collateral channels were recognized. One patient had evidence of unique homocollaterals represented by enlarged vasa vasorum, which created a vascular cuff that surrounded a totally obstructed left main artery. The ventricular function and hemodynamic parameters in these patients not only depend on the collateral vessels but may also be affected by the severity of coronary artery disease in the artery that supplies collaterals.

Aged↗
PubMed1987

Aortic distensibility abnormalities in coronary artery disease.

Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.

Adult↗
PubMed1982

Effects of particle size and perfusate composition on the uptake of colloidal gold by the rabbit thoracic aorta perfused in situ.

The influence has been investigated of particle size on the uptake of radioactive gold colloid by the rabbit thoracic aorta perfused in situ. Particles ranging in diameter from 14 nm to 40 nm were suspended in 0.9% NaCl and infused either at a pressure of 15 mm Hg for times of between 2 1/2 and 60 min or at pressure of between 15 and 160 mm Hg for 5 min. Uptake by the whole intima-media increased with perfusion time and hydrostatic pressure but did not depend on particle size. Radioactive assay of serial sections across the aortic wall also showed that particle size did not influence the distribution of tracer. An effect of perfusate composition on uptake was demonstrated in further experiments in which particles either 14 or 40 nm in diameter were suspended in pooled rabbit serum and infused at pressures of between 15 and 140 mm Hg for 5 min. Uptake and transmural distribution were again independent of particle size, but uptake was 4-5-fold less than when the particles were perfused in saline. Under all perfusion conditions radioactivity fell steeply across the intima and then rose gradually across the media and adventitia. Radioactivity in the outer media and adventitia increased with perfusion time but little change could be detected in intimal activity. In transmission electron micrographs, particles in the intima were not seen to penetrate the internal elastic lamella and in the outer media particles remained extracellular and did not enter collagen bundles. Autoradiographs showed that particles in the intima were uniformly distributed around the circumference of the vessel but in the outer media and adventitia particles usually clustered close to the vasa vasorum.

Animals↗
PubMed1986

Lectin binding to distinguish cell types in fixed atherosclerotic arteries.

In order to assess the possible utility of lectin binding to identify the cellular components of fixed arterial lesions we studied lectin binding in experimental rabbit and monkey vessels, as well as in human atherosclerotic arteries obtained at surgery. The avidin-biotin-peroxidase technique was used to localize the binding of the following biotinylated lectins: Concanavalin A (Con A), Dolicho biflorus agglutinin (DBA), soybean agglutinin (SBA), peanut agglutinin (PNA), Phaseolus vulgaris agglutinin (PHA), Ricinus communis agglutinin (RCA), wheat germ agglutinin (WGA), and Ulex europaeus agglutinin (UEA). PHA demonstrated specific cytoplasmic staining of macrophages in rabbit, monkey, and human tissues and differentiated macrophages from other cell types in atherosclerotic lesions. When morphometric comparisons were made between lesion PHA staining and another macrophage marker, acid lipase, very similar results were obtained. Con A, RCA, and WGA stained macrophages intensely and differentiated them from other cell types in normal reticuloendothelial tissues and lesions, but also stained smooth muscle cells and endothelial cells when these cells developed lipid vacuoles. UEA stained the endothelium of vasa vasorum consistently in human arteries, but staining of artery lumen endothelium was variable. Endothelial cells of rabbit or monkey vessels did not stain with UEA. DBA, PNA, and SBA did not consistently stain any cellular structures in arteries. PHA was found to be an excellent marker to differentiate and quantify macrophages in glutaraldehyde or formalin-fixed, paraffin-embedded experimental and human atherosclerotic lesions. Con A, RCA and WGA merit further detailed study in conjunction with other histochemical tests as possible markers of functional changes in arterial cells during lesion development.

Animals↗
PubMed1989

A surgical model to study in vivo efflux of cholesterol from porcine aorta. Evidence for cholesteryl ester transfer through the aortic wall.

We describe a surgical procedure in pigs which makes it possible to follow the influx into, the penetration through and the efflux from the arterial wall of labeled lipoproteins. After 4 h exposure of the luminal side of the arterial wall to labeled lipoproteins, labeled esterified cholesterol was found in all layers of the aortic wall, whereas labeled free cholesterol gained access only to the most luminal layer. The data suggest that at least 40%, if not 80-90%, of the cholesteryl ester that enters the aortic wall from the luminal side, passes through the entire wall and leaves the aortic wall through vasa vasorum and lymphatics. They also suggest that free cholesterol in the lipoproteins exchanges extensively with cellular free cholesterol while the lipoproteins penetrate through the most luminal layer. More than 90% of the labeled cholesteryl ester disappeared from the arterial wall during a cold chase period of 4 days. By the simultaneous use of [3H]cholesterol and [14C]cholesterol it was shown that only 10-20% of this disappearance can be explained by cholesteryl ester hydrolysis in the arterial wall.

Animals↗
PubMed1992

Adrenaline increases the uptake of low-density lipoproteins in carotid arteries of rabbits.

The uptake of low-density lipoprotein was compared in carotid arteries of anaesthetized male New Zealand rabbits after infusing alternate carotids with adrenaline, or with saline as a control. The infusions were at approximately 2% of the carotid blood flow, the adrenaline being at approximately 10 nM in the carotid blood. Human low density lipoprotein, methylated to prevent recognition by the high affinity receptor (m-LDL), was labelled with 125I and injected intravenously. Adrenaline infusions for 2 or 4 h significantly increased m-LDL radioactivity in the carotid walls. The radioactivity of reinjected red cells labelled with 51Cr was the same in the walls of both carotids. This excluded the possibility that the excess LDL radioactivity in adrenaline infused carotids was accounted for by increased amounts of blood in the arterial wall. It also made it improbable that the excess LDL resulted from decreased elimination through a vasoconstriction effect of adrenaline on the vasa vasorum, which should have decreased the amount of radioactivity due to red cells. The results, therefore, suggest that adrenaline at its pathophysiological blood concentrations accelerates the uptake of LDL by large arteries in rabbits.

Animals↗