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PubMedDate not supplied

Fatal pulmonary arterial dissection and sudden death as initial manifestation of primary pulmonary hypertension: a case report.

We report a rare case of sudden death due to cardiac tamponade following intrapericardial rupture of a main pulmonary artery dissecting aneurysm. On pathology examination, the pulmonary artery showed an intimal tear in an arterial wall area with reduced thickness. However, no degenerative, inflammatory or necrotic processes were evident within the vessel wall. Hypertrophy of the wall of vasa vasorum in the adventitia of the pulmonary artery was found, as well as bilaterally diffuse myointimal arterial hyperplasia of the lung vasculature. According to these findings, we conclude that pulmonary artery rupture occurred in a patient with chronic unrecognized primary pulmonary hypertension.

Aged↗
PubMed2004

Contrast for vascular imaging.

This article discusses the use of standard contrast agents that, when coupled with high-resolution carotid ultrasound, offers the dramatic potential to improve measurement of intimal medial thickness, better defining luminal endothelial surface, improving the determination of plaque ulceration, and offering the dramatic capabilities to visualize directly neovasculature growth of the vasa vasorum. The technique may identify vulnerable plaques and may also show their alterations with therapeutic pharmacologic interventions. In the coronary circulation, use of contrast significantly enhances the ability to image the epicardial coronary arteries to obtain data on coronary flow reserve for the diagnosis of coronary artery disease.

Arteriosclerosis↗
PubMed2004

Effects of different application parameters on penetration characteristics and arterial vessel wall integrity after local nanoparticle delivery using a porous balloon catheter.

Catheter-based local delivery of drug loaded nanoparticles agents offers a potential therapeutic approach to reducing restenosis. However, high delivery pressures and large volumes of infusates may cause severe vascular damage and increase intimal thickening. Therefore, we investigated the penetration pattern and vessel wall integrity of fluorescence-labelled nanoparticles (217 nm in diameter) into the non-atherosclerotic aorta abdominalis of New Zealand white rabbits in dependence of the volume (2.5 and 5 ml) and concentration (0.5 and 1 mg/ml) of the nanoparticle suspension, as well as the infusion pressure (2 and 4 atm) using a channelled balloon catheter (SCIMED REMEDY model RC 20/2.5). The location and penetration characteristics of nanoparticles in the arterial vessel wall were visualized using confocal laser scanning microscopy and transmission electron microscopy (TEM). Catheter design and infusion pressure form a radial particle stream through intima and media into the adventitial layer of the aorta abdominalis. Infusion pressures of 4 atm in combination with high particle concentrations lead to effective nanoparticle delivery without severe vessel wall disruptions. Endothelium of the treated vessel segments was slightly affected during catheter insertion showing partly denudation of the innermost cell layer. TEM micrographs underlines transport functional properties of the vasa vasorum inside the vessel wall. Consequently, local delivery efficiency of nanoparticulate carriers is critically affected by infusion pressure, and concentration of carrier suspensions. These factors need to be taken into consideration for the design of in vivo experiments.

Animals↗
PubMed2006

The complex structure of the smooth muscle layer of spermatic veins and its potential role in the development of varicocele testis.

OBJECTIVES: Varicocele, a dilatation of the pampiniform venous plexus, is considered to cause male infertility. The exact mechanism of varicocele development is not clarified yet. This study focused on the structure of varicocele veins, compared with normal spermatic veins, and its potential role in varicocele development. METHODS: Morphologic and immunohistochemical studies using antibodies against vWF and neurofilament-200 (NF-200) were performed on spermatic vein fragments of 20 varicocele patients and 40 normal spermatic cords. Casting preparation of veins was performed on five normal spermatic cords. RESULTS: Casting preparation frequently revealed circular constrictions of normal spermatic vein lumina. Histologic evaluation showed a strong longitudinal smooth muscle layer in the adventitia of large veins in addition to the circularly organised tunica media. Serial sections showed smooth muscle fibres branching from the outer longitudinal into the inner circular layer. Immunostaining for vWF revealed high vascularisation of this outer layer. Interestingly, the number of nerve fibres marked by NF-200 immunostaining was considerably higher in large veins compared to the testicular artery. The longitudinal smooth muscle layer was significantly degraded in the presence of varicocele grades I and II, and did not even exist in varicocele grade III. Correspondingly, the number of vasa vasorum and nerve fibres was reduced in varicocele veins. CONCLUSIONS: Our data show a complex smooth muscle organisation of spermatic veins, which serves the basis for a contractile mechanism, providing an effective blood transport through pampiniform plexus. This mechanism is obviously damaged in the varicocele. Molecular processes behind this impairment remain to be clarified.

Adolescent↗
PubMed2004

New aspects in the pathogenesis of diabetic atherothrombosis.

Diabetes mellitus is increasing worldwide, resulting from the interaction of obesity, inflammation, and hyperglycemia. Activated immunity and cytokine production lead to insulin resistance and other components of the metabolic syndrome, establishing the link between diabetes and atherosclerosis. Hyperglycemia-induced endothelial dysfunction is mediated by increased oxidative stress, a promoter of adventitial inflammation and vasa vasorum neovascularization in experimental models of diabetic atherosclerosis. Recent studies have documented increased inflammation, neovascularization, and intraplaque hemorrhage in human diabetic atherosclerosis. This inflammatory microangiopathic process is independently associated with plaque rupture, leading to coronary thrombosis. Tissue factor, the most potent trigger of the coagulation cascade, is increased in diabetic patients with poor glycemic control. Circulating tissue factor microparticles are also associated with apoptosis of plaque macrophages, closing the link among inflammation, plaque rupture, and blood thrombogenicity. High-density lipoproteins, responsible for free cholesterol removal, are reduced in patients with insulin resistance and diabetes. High-density lipoprotein therapy leads to a significant decrease in plaque macrophages and increase in smooth-muscle cells. These beneficial effects may be responsible for coronary plaque stabilization in patients treated with recombinant Apolipoprotein A-I Milano/phospholipid complex. Finally, peroxisomal proliferator-activated receptors (PPARs) are now considered the nuclear transcriptional regulators of atherosclerosis. Three subfamilies, including PPAR-alpha, -delta, and -gamma, have been identified with crucial roles in lipid metabolism, plaque inflammation, expression of adhesion molecules and cytokines, and regulation of matrix metalloproteinases. Multiple experimental studies have documented plaque stabilization with PPAR-gamma agonists, a group of medications holding great promise in the treatment of diabetes atherosclerosis.

Arteriosclerosis↗
PubMed2005

Atherothrombosis and high-risk plaque: part I: evolving concepts.

Atherothrombosis is a complex disease in which cholesterol deposition, inflammation, and thrombus formation play a major role. Rupture of high-risk, vulnerable plaques is responsible for coronary thrombosis, the main cause of unstable angina, acute myocardial infarction, and sudden cardiac death. In addition to rupture, plaque erosion may also lead to occlusive thrombosis and acute coronary events. Atherothrombosis can be evaluated according to histologic criteria, most commonly categorized by the American Heart Association (AHA) classification. However, this classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulnerable plaque. Furthermore, the AHA classification does not include plaque erosion. As a result, new classifications have emerged and are reviewed in this article. The disease is asymptomatic during a long period and dramatically changes its course when complicated by thrombosis. This is summarized in five phases, from early lesions to plaque rupture, followed by plaque healing and fibrocalcification. For the early phases, the role of endothelial dysfunction, cholesterol transport, high-density lipoprotein, and proteoglycans are discussed. Furthermore, the innate and adaptive immune response to autoantigens, the Toll-like receptors, and the mechanisms of calcification are carefully analyzed. For the advanced phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaque rupture are systematically evaluated. In the final thrombosis section, focal and circulating tissue factor associated with apoptotic macrophages and circulatory monocytes is examined, closing the link between inflammation, plaque rupture, and blood thrombogenicity.

Atherosclerosis↗
PubMed2005

Aortic dissection in a young man with immune thrombocytopenic purpura.

A 36-year-old man who presented with epigastric and back pain was subsequently diagnosed with aortic dissection. Our patient lacked classic risk factors that would have predisposed him to develop this condition at a young age. He did, however, suffer from untreated, chronic immune thrombocytopenic purpura (ITP) and had a platelet count less than 20,000/mm(3) on admission. We postulate that the thrombocytopenia led to spontaneous hemorrhage within the vasa vasorum of the aorta and the subsequent development of aortic dissection. Chronic ITP has been associated with an increased risk of intracranial hemorrhage but, to our knowledge, has not been reported to be associated with aortic dissection. We encourage clinicians to be aware of this potential risk factor for aortic dissection.

Adult↗
PubMed2006

Characterization of the inflammatory and apoptotic cells in the aortas of patients with ascending thoracic aortic aneurysms and dissections.

OBJECTIVE: The histopathologic abnormality underlying ascending aortic aneurysm and dissection is medial degeneration, a lesion that is described as the noninflammatory loss of smooth muscle cells and elastic fibers. This study sought to determine whether inflammatory cells are present in medial degeneration and assess any possible contribution of these cells to apoptosis of smooth muscle cells. METHODS: Aortic specimens were obtained from patients undergoing prophylactic surgical repair of an ascending aortic aneurysm (n = 9) and type A dissection (n = 7), along with control patients dying of causes unrelated to aortic disease (n = 5). Immunohistochemical staining was performed to evaluate the presence of lymphocytes and macrophages, and markers of apoptosis were assessed in the aortas of patients with ascending aortic aneurysm and dissection. RESULTS: Immunohistochemical study indicated significantly more CD3+ cells in the aortas of patients with aneurysms or dissections than in control aortas (P = .020 and P = .0022, respectively). In addition, aortas of patients with aneurysms or dissections had more CD68+ cells (P = .01 and P = .005, respectively). CD3+ cells were localized in the media and surrounding the vasa vasorum in the adventitia. Cells yielding a positive result on in situ terminal transferase-mediated deoxyuridine triphosphate nick end-labeling were found in increased numbers in the aortas of patients with aneurysms or dissections relative to control aortas (P = .005 and P = .002, respectively). Furthermore, Fas and FasL were increased in the aortic samples from patients with aneurysms and dissections relative to control aortas. CONCLUSION: The coexistence of inflammatory cells with markers of apoptotic vascular cell death in the media of ascending aortas with aneurysms and type A dissections raises the possibility that activated T cells and macrophages may contribute to the elimination of smooth muscle cells and degradation of the matrix associated with thoracic aortic aneurysms and dissections.

Aortic Dissection↗
PubMed2004

Dog peritoneal and pleural cavities as bioreactors to grow autologous vascular grafts.

OBJECTIVE: The purpose of this study was to grow "artificial blood vessels" for autologous transplantation as arterial interposition grafts in a large animal model (dog). METHOD AND RESULTS: Tubing up to 250 mm long, either bare or wrapped in biodegradable polyglycolic acid (Dexon) or nonbiodegradable polypropylene (Prolene) mesh, was inserted in the peritoneal or pleural cavity of dogs, using minimally invasive techniques, and tethered at one end to the wall with a loose suture. After 3 weeks the tubes and their tissue capsules were harvested, and the inert tubing was discarded. The wall of living tissue was uniformly 1-1.5 mm thick throughout its length, and consisted of multiple layers of myofibroblasts and matrix overlaid with a single layer of mesothelium. The myofibroblasts stained for alpha-smooth muscle actin, vimentin, and desmin. The bursting strength of tissue tubes with no biodegradable mesh scaffolds was in excess of 2500 mm Hg, and the suture holding strength was 11.5 N, both similar to that in dog carotid and femoral arteries. Eleven tissue tubes were transplanted as interposition grafts into the femoral artery of the same dog in which they were grown, and were harvested after 3 to 6.5 months. Eight remained patent during this time. At harvest, their lumens were lined with endothelium-like cells, and wall cells stained for alpha-actin, smooth muscle myosin, desmin and smoothelin; there was also a thick "adventitia" containing vasa vasorum. CONCLUSION: Peritoneal and pleural cavities of large animals can function as bioreactors to grow myofibroblast tubes for use as autologous vascular grafts.

Animals↗
PubMed2006

Reduction of myointimal hyperplasia after arterial anastomosis by local injection of transforming growth factor beta3.

BACKGROUND: The transforming growth factor (TGF)-beta family of cytokines exerts pleiotropic actions on vascular smooth muscle cell phenotype, proliferation, and extracellular matrix synthesis. This in vivo study assessed the use of TGF-beta3 in attenuating the development of postanastomotic smooth muscle cell proliferation. METHODS: Under general anesthesia, 10 adult goats underwent transection and reanastomosis of both common carotid arteries. After reanastomosis, one artery was infiltrated with 50 ng of TGF-beta3 in 100 microL of pH buffer around the anastomosis, and the other side was infiltrated with buffer only. After surgery, each animal received 150 mg of aspirin daily. The arteries were explanted after 3 months for histologic examination. RESULTS: Vessel wall thickness surrounding the anastomosis was reduced by 30% after TGF-beta3 treatment compared with placebo (P = .003), with a 20% (P = .002) reduction in cellular content. Although total collagen content was not significantly different between TGF-beta3 and placebo, collagen type VIII content was reduced around the TGF-beta3 anastomoses (P = .011). A reduction in the total elastin content (P = .003) and number of elastic fiber lamellae (P = .042) was found surrounding TGF-beta3-treated anastomoses, but not placebo-treated anastomosis. A 29% increase in vasa vasorum (P = .044) was present around TGF-beta3-treated anastomoses. No differences in inflammatory cell infiltration were seen between sides. CONCLUSIONS: Direct subadventitial infiltration of TGF-beta3 immediately after creation of an arterial anastomosis attenuates cell proliferation, with a reduction in elastin and collagen type VIII content and vessel wall thickness.

Anastomosis, Surgical↗
PubMed2005

Depression and cardiovascular disease: a reciprocal relationship.

Until relatively recently, depression has been considered a purely "mental" disorder and therefore in the natural domain of psychologists and psychiatrists. However, recent epidemiological studies have revealed that aging, physical and psychological stress, chronic pain, several metabolic disorders such as insulin resistance and established diabetes, alcoholism, inflammatory conditions, and vascular disorders such as arterial hypertension all may be associated with depression. The present review examines some of these depression-associated factors and the mechanisms by which they might give rise to vascular disorders such as atherosclerosis, microcirculation endothelial dysfunction, and interstitial disturbances leading to organ damage. A number of disorders involving the circulation can lead progressively and insidiously to large artery rigidity, remodeling of peripheral arteries, and alterations of the microcirculation of large blood vessels. Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). Since Hans Selye first described the neuroendocrine cascade generated by experimentally induced stress half a century ago, phenomena such as the axonal release of neurotransmitters (including serotonin), accumulation of metabolites such as homocysteine, platelet-activating factor, and nitric oxide also have been implicated in the pathogenesis of depression. Moreover, vascular consequences of depression such as heart rate and pulse pressure variations may lead to endothelial dysfunction in critical microcirculation networks (cerebral, myocardial, and renal) and initiate physicochemical alterations in interstitial compartments adjacent to vital organs. The appropriate use of ambulatory monitoring of vascular parameters, such as heart rate and pulse pressure, and eventually, early identification of genetic and metabolic markers may prove helpful in the early detection of events preceding and predicting the clinical manifestations of depression.

Cardiovascular Diseases↗
PubMed2006

Effect of green tea on angiogenesis and severity of atherosclerosis in cholesterol-fed rabbit.

BACKGROUND AND AIMS: Since the development of the atherosclerotic plaque requires the growth of new microvessels in the plaque itself (vasa vasorum), we postulated that green tea may exert an anti-atherogenic effect. METHODS AND RESULTS: Thirteen male New Zealand white rabbits were studied for 17 weeks. All rabbits were fed an hypecholesterolemic diet. After 2 weeks of adaptation rabbits were randomly assigned into two groups. Animals in Group A were fed the hypercholesterolemic diet and received plain tap water ad libitum. Animals in Group B were fed with the same diet and furthermore received 2.5% (g/g) green tea for 17 weeks. CONCLUSION: According to our results the atherosclerotic lesions were more severe in Group B than in Group A specimens. Also, the number of VEGF positively stained foam cells and smooth muscle cells of Group B were significantly greater than in Group A. About 30% less plaque was found in Group A than in the control group (Group B). So, our study showed that the consumption of green tea leads to a reduction of atherosclerosis as well as a significant decrease of VEGF expression in the atherosclerotic plaque of rabbit aorta. The hypothesis that probably green tea may produce its anti-atherogenetic effect through an anti-angiogenetic mechanism needs more investigation.

Angiogenesis Inhibitors↗
PubMed1996

Microparticle deposition in periarterial microvasculature and intramural dissections after porous balloon delivery into atherosclerotic vessels: quantitation and localization by confocal scanning laser microscopy.

Local delivery of pharmacologic or genetic agents with a porous balloon catheter offers a potential therapeutic approach to reducing restenosis and atherosclerosis and minimizing undesirable systemic toxicity. However, the delivery efficiency and intramural retention of liquid agents is low. The local intramural delivery and prolonged retention of 5 microns microparticles (MP) has been described previously. The current study was designed to evaluate the distribution of locally delivered MPs and to determine the effects of MP size and infusion pressure on intramural delivery efficiency. A 1% suspension of fluorescent, latex MPs (1 or 4.5 microns in diameter) was infused at either 3 or 6 atm into atherosclerotic rabbit femoral arteries (n = 32) immediately after angioplasty. Four groups of arteries were evaluated: 1) 1 micron MPs infused at 3 atm; 2) 1 micron MPs at 6 atm; 3) 4.5 microns MPs at 3 atm; and 4) 4.5 microns MP at 6 atm. The location of MPs was evaluated by fluorescent and light microscopy and confocal laser scanning microscopy. The tissue was dissolved and the delivered MPs quantified. All groups manifested numerous MPs within the vasa vasorum and periadventitial microvasculature, with a substantially lesser number within the neointimal and medial layers. The intramural deposition of the MPs was associated with dissection within the intima or media caused by the antecedent angioplasty or local delivery, indicating that an intact vessel wall is an anatomic barrier to MP delivery. The median values of fractional intramural delivery, defined as the percentage of infused MPs retained within the arterial wall, were 0.059%, 0.071%, 0.047%, and 0.062% for the groups 1 through 4, respectively (p not significant [NS]). The values of intramural particle concentration, expressed as the total number of MPs per weight of arterial tissue, were 55, 65, 1.5, and 1.2 x 10(4) MPs/mg for groups 1 through 4, respectively (p < 0.001 for 1 micron vs 4.5 microns MPs). Although more 1 microM MPs were delivered than 4.5 microns MPs, the fractional intramural delivery was unaffected by particle size or infusion pressure. The local delivery of MPs at atherosclerotic sites after angioplasty is characterized by fractional intramural delivery values similar to values of nonparticulate agents, with few MPs deposited into intima or media in the absence of a dissection caused by the antecedent angioplasty or the delivery procedure itself.

Angioplasty, Balloon, Coronary↗
PubMed1977

Coronary arterial narrowing in Takayasu's aortitis.

A patient with Takayasu's aortitis and angina pectoris due to severe narrowing of the right and left coronary arterial ostia is described. Takayasu's arteritis produces a panaortitis, with thickening of the adventitia predominating, and an inflammatory cell infiltrate involving the adventitia, outer media and vasa vasorum. Narrowing of the coronary arteries in this disease is due to extension into these arteries of the processes of proliferation of the intima and contraction of the fibrotic media and adventitia that occur in the aorta. The distal coronary arteries usually do not manifest arteritis and are normal in caliber. Angina pectoris may be the first symptom of the disease if the coronary arteries are the initial site of severe arterial narrowing. The coronary arterial bypass graft operation is effective therapy for treating coronary arterial narrowing due to Takayasu's arteritis.

Adult↗
PubMed2003

Evidence of autoimmunity in chronic periaortitis: a prospective study.

BACKGROUND: Chronic periaortitis includes idiopathic retroperitoneal fibrosis, inflammatory aneurysms of the abdominal aorta, and perianeurysmal retroperitoneal fibrosis. It is considered to be due to advanced atherosclerosis, but is often associated with systemic autoimmune disorders. METHODS: We studied 16 consecutive patients who were diagnosed with chronic periaortitis by computed tomography. Each patient underwent a physical examination, routine laboratory tests, measurement of autoantibodies, thyroid echotomography, and chest radiography. Aortic wall or periaortic retroperitoneal samples from 9 patients who underwent surgery were available for histologic examination and immunohistochemical characterization of the inflammatory infiltrate. RESULTS: Twelve patients had constitutional symptoms, 14 had an elevated erythrocyte sedimentation rate, and 13 had an elevated C-reactive protein level. Antinuclear antibodies were positive in 10 patients. Three patients had autoimmune thyroiditis, and 1 had seropositive rheumatoid arthritis. Antineutrophil cytoplasmic antibodies were positive in 3 patients who presented with rapidly progressive renal failure. Pathologic examination of the aortic and periaortic specimens revealed moderate to severe inflammatory infiltration, mainly consisting of B cells and CD4(+) T cells. Vasculitis with fibrinoid necrosis involving the aortic vasa vasorum and the small and medium retroperitoneal vessels was found in seven of the nine histologic samples. CONCLUSION: These clinical and pathologic features support the hypothesis that, at least in some patients, chronic periaortitis is a systemic autoimmune disease, perhaps involving a vasculitic process of small and medium vessels.

Adult↗
PubMed1983

Chitosan: a new hemostatic.

Chitosan is a deacetylated derivative of arthropod chitin. We found that it formed a coagulum in contact with defibrinated blood, heparinized blood, and washed red cells. When knitted DeBakey grafts were treated with chitosan, they were impermeable to blood. Examination of these grafts at 24 hours revealed no rebleeding. Examination at one, two, three, and four months showed the grafts to be encased in smooth muscle with a living endothelial lining and an abundant vasa vasorum. Control grafts showed the usual fibrous healing.

Animals↗
PubMed1982

Buerger's disease (thromboangiitis obliterans): an analysis of the arteriograms of 119 cases.

One hundred and forty-four lower extremity arteriograms of 119 patients with Buerger's disease have been analysed. The 'corkscrew' appearance of collateral circulation was seen in 27.1% of 144 limbs affected by thromboangiitis obliterans, but in only 3.2% of 63 limbs affected by arteriosclerosis obliterans. We believe that the corkscrew vessel is highly characteristic of Buerger's disease and represents dilated vasa vasorum of the occluded main artery. The appearance of corkscrew vessels extending from the arterial occlusion sites to the periphery of the feet without opacification of the main pedal arteries indicated a poor prognosis.

Adult↗
PubMed2001

The adventitia of atherosclerotic coronary arteries frequently contains Chlamydia pneumoniae.

The presence of Chlamydia pneumoniae in the human arterial system has mainly been determined in atherosclerotic plaque, whereas the adventitia has remained relatively unexplored. We assessed the presence of C. pneumoniae in all three vessel wall layers of coronary (n=72) and brachial (n=48) arteries in relation to local atherosclerosis. Immunohistochemical staining of C. pneumoniae was observed in plaque and adventitia. Cells stained for C. pneumoniae were detected in the same areas as cells stained for macrophages in adjacent sections. C. pneumoniae staining in the adventitia was associated with the extent and severity of atherosclerosis. Coronary sections with C. pneumoniae staining in both adventitia and plaque more often contained advanced atherosclerosis than sections with staining only in the adventitia. Staining was observed more often in the coronary artery than in the brachial artery (24/72 vs. 5/48 and 51/72 vs. 8/48 for plaque and adventitia, respectively, P=0.004 and P<0.001). PCR confirmed the presence of C. pneumoniae DNA in the adventitia. In summary, the adventitia of atherosclerotic coronary arteries frequently contains C. pneumoniae that seems to be located within macrophages. These results might indicate a possible route for infected circulating macrophages to home into atherosclerotic lesions in the artery via vasa vasorum.

Aged↗