SEARCH · PubMed Health

Results for “VESSELS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources

PubMed1995

Retinal blood vessel width measured on color fundus photographs by image analysis.

The purpose of this paper was to develop a technique using computerized image analysis to measure the width of retinal arteries and veins on color fundus photographs. The width of the retinal vessel was determined from digitized fundus photographs by programs based on edge detection and boundary tracing. The average vessel width was determined at different distances or eccentricities from the center of the optic disc and using various lengths of vessel segment. Measurements of superior and inferior temporal vessel width for 20 eyes by 2 operators showed that about 75% of the measurements could be obtained without the use of plan points. The average percent coefficient of variation of the measurements was 2.17% for 3 measurements of each vessel. This technique provides a reproducible and objective method for obtaining the following parameters: the edges of the vessel, the length of the vessel segment to be measured, location of the measurement along the vessel and subsequent retinal vessel width. This technique is readily suitable for application to clinical studies particularly clinical trials.

Adult↗

PubMed1997

On the Nusselt number in heat transfer between multiple parallel blood vessels.

Arrays of two or more parallel blood vessels in a tissue matrix have been studied extensively in the context of bioheat transfer. The average vessel Nusselt number (based on the difference between the mixed-mean blood temperature and the average vessel surface temperature) is a crucial parameter in such studies. Various workers have noted tht in particular cases the average Nusselt number is identical to that for fully developed flow in a single vessel in an infinite medium. In other words, the Nusselt number is unaffected by the presence of other vessels. It is proven here that this surprising result holds true for arbitrary number, size, flow direction, and velocity profile in the blood vessels, and for very general boundary conditions on the outer tissue boundary. A useful corollary is that the average wall temperature in a particular vessel may be found by evaluating the temperature fields due to the other vessels and the tissue boundaries at a single point, the center of the vessels in question.

Blood Flow Velocity↗

PubMed2003

Vessel size measurements in angiograms: manual measurements.

Vessel size measurement is perhaps the most often performed quantitative analysis in diagnostic and interventional angiography. Although automated vessel sizing techniques are generally considered to have good accuracy and precision, we have observed that clinicians rarely use these techniques in standard clinical practice, choosing to indicate the edges of vessels and catheters to determine sizes and calibrate magnifications, i.e., manual measurements. Thus, we undertook an investigation of the accuracy and precision of vessel sizes calculated from manually indicated edges of vessels. Manual measurements were performed by three neuroradiologists and three physicists. Vessel sizes ranged from 0.1-3.0 mm in simulation studies and 0.3-6.4 mm in phantom studies. Simulation resolution functions had full-widths-at-half-maximum (FWHM) ranging from 0.0 to 0.5 mm. Phantom studies were performed with 4.5 in., 6 in., 9 in., and 12 in. image intensifier modes, magnification factor = 1, with and without zooming. The accuracy and reproducibility of the measurements ranged from 0.1 to 0.2 mm, depending on vessel size, resolution, and pixel size, and zoom. These results indicate that manual measurements may have accuracies comparable to automated techniques for vessels with sizes greater than 1 mm, but that automated techniques which take into account the resolution function should be used for vessels with sizes smaller than 1 mm.

Anatomy, Cross-Sectional↗

PubMed1992

Strain distribution in small blood vessels with zero-stress state taken into consideration.

The active and passive deformation of a blood vessel is related to the stress in it. Any analysis of stress and strain must begin with the zero-stress state. Recent reports on large blood vessels such as the aorta, pulmonary arteries, and vena cava have shown that, at zero-stress state, blood vessels are not tubes, but opens sectors. This report presents data on the zero-stress state of small blood vessels with lumen diameters down to approximately 50 microns. Zero-stress state of a vessel was obtained by cutting the vessel into rings and then the rings into sectors; each sector is characterized by an opening angle, alpha. In rat ileal and plantar arterioles, the opening angles are in the order of 100-250 degrees; those in the venules are in the order of 50-100 degrees. The effect of norepinephrine on the opening angle alpha is minor; it decreases alpha of the superior mesenteric artery, and increases alpha of the ileocecocolic and ileal arteries. EDTA has little effect on alpha of arteries greater than 100 microns in diameter, but decreases alpha of arteries less than 100 microns. The physiological meaning of the opening angle is demonstrated in terms of the residual strains in a vessel at the no-load state and homeostatic strains at normal blood pressure. The strains in real vessels are compared with those in hypothetical vessels having an opening angle of zero. It is shown that ignoring the opening angle will cause a large error in strain evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Mosaic tumor vessels: cellular basis and ultrastructure of focal regions lacking endothelial cell markers.

Endothelial cells of blood vessels in tumors may be thin, fragile, and defective in barrier function. We found previously that the endothelium of vessels in human colon carcinoma xenografts in mice is a mosaic structure. Approximately 85% of tumor vessels have uniform CD31 and/or CD105 immunoreactivity, but the remainder have focal regions that lack these common endothelial markers. The present study assessed the ultrastructure of the vessel lining and the integrity of the basement membrane in these regions. Using immunolabeling and confocal microscopy, we identified blood vessels that lacked CD31 and CD105 immunoreactivity and then analyzed the ultrastructure of these vessels by transmission electron microscopy. Eleven percent of vessels in orthotopic tumors and 24% of vessels in ectopic tumors had defects in CD31 and CD105 staining measuring on average 10.8 microm (range, 1-41.2 microm). Ultrastructural studies identified endothelial cells at 92% of CD31- and CD105-negative sites in orthotopic tumors and 70% of the sites in ectopic tumors. Thus, most regions of tumor vessels that lack CD31 and CD105 immunoreactivity represent attenuated endothelial cells with abnormal expression of endothelial cell markers, but some are gaps between endothelial cells. More than 80% of the defects lacked immunoreactivity for multiple basement membrane proteins.

Animals↗

PubMedDate not supplied

Postnatal growth of the heart and its blood vessels.

Although rapid growth of the heart during early postnatal development ceases with maturation of the organism, the potential for cardiomyocyte growth is not lost and may be observed even in senescent hearts. Rapid developmental heart growth is accompanied by a proportional growth of capillaries but not always of larger vessels, and thus coronary vascular resistance gradually increases. Growth of adult hearts can be enhanced by thyroid hormones, catecholamines and the renin-angiotensin system hormones, but these do not always stimulate growth of coronary vessels. Likewise, chronic exposure to hypoxia leads to growth, mainly of the right ventricle and its vessels but without vascular growth elsewhere in the heart. On the other hand, ischaemia is a potent stimulus for the release of various growth factors involved in the development of collateral circulation. Heart hypertrophy develops in response to training, pressure or volume overload. Training usually leads to growth of larger coronary vessels but little growth of capillaries, except in young animals. However, growth of the capillary bed, but not the resistance vasculature capacity, can be induced by either increased coronary blood flow, bradycardia (electrically or pharmacologically induced) or increased inotropism, all of which are involved in the training stimulus. Thus, what actually promotes growth of larger vessels as opposed to capillaries in training is unclear. Pressure overload hypertrophy is mediated by both the renin-angiotensin system and the response of cardiomyocytes to stretch; both lead to activation of early oncogenes (c-fos, c-jun, c-myc) and angiotensin II activates several protein kinases involved in cell growth. In this condition, growth of larger vessels is inadequate, although some capillary growth may occur. Volume overload leads to cardiomyocyte hypertrophy and hyperplasia and some increase in vascular supply. Deficits in capillary supply in pressure or volume overload hypertrophy can be reversed by chronic administration of ACE inhibitors, dipyridamole, the bradycardic drug alinidine or pacing-induced bradycardia respectively, but in neither case is training effective. Mechanical and humoral factors are involved in growth of cardiomyocytes and vessels. For cardiomyocytes, stretch is most important, activating oncogenes, protein kinases and possibly the inositol phosphate pathway, but not ion channels, with regulation by the balance of angiotensin II, TGF-beta 1 and IGF-1, but not FGFs. For vessels, growth is stimulated by stretch and shear stress, possibly with involvement of VEGF. Increased shear stress disrupts the glycocalyx on the luminal side of vessels and releases plasminogen activator and metalloproteinases which disrupt the basement membrane and enable endothelial cell migration and proliferation. It also causes rearrangement of the endothelial cytoskeleton and transmission of mechanical signals to the abluminal side disturbing extracellular matrix and causing distortion of capillary basement membrane. Stretch acting from the abluminal side has a similar effect resulting also in basement membrane disruption and endothelial cell proliferation.

Aging↗

PubMed1998

Vessel size and long-term outcome after coronary stent placement.

BACKGROUND: The role of coronary stenting in the treatment of patients with small vessels is not well defined. The purpose of this study was to investigate the influence of vessel size on long-term clinical and angiographic outcome after coronary stent placement. METHODS AND RESULTS: The study comprised 2602 patients with successful stent implantation for symptomatic coronary artery disease. Patients were subdivided into 3 equally sized groups (tertiles) according to vessel size, with respective ranges of <2.8, 2.8 to 3.2, and >3.2 mm. Event-free survival at 1 year was 69.5% in the group with smaller vessels, 77.5% in the second group, and 81% in the group with larger vessels (P<0.001). Late lumen loss was similar between the 3 groups (1.12+/-0.73, 1.12+/-0.79, and 1.09+/-0. 88 mm, respectively). Angiographic restenosis rate was significantly higher in the small-vessel group (38.6%, 28.4%, and 20.4% in groups 1, 2, and 3, respectively; P<0.001). The analysis identified subgroups with different risk for restenosis even among patients with small vessels. Within this group, the restenosis rate may be as low as 29.6% in patients without additional risk factors and as high as 53.5% in patients with diabetes and complex lesions. CONCLUSIONS: Patients with small vessels present a higher risk for an adverse outcome after coronary stent placement because of a higher incidence of restenosis. However, the unusually high risk for restenosis is confined to those patients with small vessels who have concomitant risk factors such as diabetes and complex lesions.

Aged↗

PubMed2000

Clinical-histopathological correlation of the abnormal retinal vessels in cerebral malaria.

BACKGROUND: Clinically abnormal retinal vessels unique to cerebral malaria have previously been shown to be associated with a poor outcome in African children. There have been no studies of the histopathological correlates of these vessels. DESIGN: This is a descriptive study of the clinical-histopathological correlates of the retinal vessels of 11 children who died with cerebral malaria. RESULTS: The retinal vessels in children with cerebral malaria contained many parasitized red blood cells; these cells tended to cluster at the periphery of vessels or, in the case of capillaries, to fill the vessel. Those with late-stage parasites had markedly reduced amounts of hemoglobin. The pattern of dehemoglobinization corresponds to the pattern of clinically abnormal vessels. CONCLUSIONS: The sequestration of late-stage parasitized red blood cells with reduced amounts of hemoglobin accounts for the unique white and pale orange retinal vessels seen in cerebral malaria. Clinical examination of these "marked" vessels offers a method to monitor a basic pathophysiological process of cerebral malaria in vivo. Arch Ophthalmol. 2000;118:924-928

Animals↗

PubMed2003

Online human conjunctival vessel diameter analysis. A clinical-methodical study.

BACKGROUND: The present study investigates the possible application of a commercially available on-line measuring device of retinal vessels for conjunctival vessel assessment. METHODS: Repeated measurements in one randomly chosen eye were performed in 11 healthy volunteers (mean age 42.9 +/- 10 years). Measurements of one conjunctival vessel were obtained first without a stimulus followed by measurements after the application of one drop of a topical vasoconstrictor. The examinations were performed by Retinal Vessel Analyzer (RVA, IMEDOS/Germany). This system determines automatically on-line the vessel diameter along a chosen vessel segment. RESULTS: Measurements in the native state without eye drop application showed an intraclass correlation coefficient of 0.97 and a mean variation coefficient of 1.8%. After application of the topical vasoconstrictor a short acting vasodilatation was observed with a magnitude of +10.9% +/- 14.9 (p < 0.001), followed by an increasing vasoconstriction (after 4 min -12.0% +/- 7.6; p = 0.004). One volunteer had no measurable conjunctival vessels in the baseline measurements and was therefore excluded from the study. DISCUSSION: The suggested technique allows the measurement of changes in conjunctival vessel diameter with high precision. The method represents a non invasive technique for the assessment of effects on conjunctival vessels caused by topical or systemic drugs.

Adult↗

PubMed2004

Proliferation of D2-40-expressing intestinal lymphatic vessels in the lamina propria in inflammatory bowel disease.

Lymphatic vessels in the colon are normally distributed beneath the muscularis mucosae with rare branches reaching through the muscularis mucosae to the most basal aspect of the colonic crypts. In chronic inflammatory bowel disease demonstrating acute inflammation and architectural disarray, lymph vessel proliferation is seen within the lamina propria and within the submucosa. We analyzed the number and distribution of lymphatic vessels within the lamina propria and submucosa in chronic active and treated ulcerative colitis with restoration of architecture by immunostaining with D2-40, a specific monoclonal antibody against lymphatic vessels. We found significantly increased numbers of lymph vessels in chronic active ulcerative colitis both within the lamina propria and the submucosa as compared to normal mucosa. Numbers of lymph vessels in lamina propria were highest in severe chronic active ulcerative colitis and less in moderate and minimal residual disease with minimal architectural disarray (p<0.05). Lymph vessels in the submucosa were increased significantly above normal values in both severe, moderate and minimal residual disease. We conclude that lymph vessel distribution in chronic active ulcerative colitis extends into the lamina propria. With restoration of architectural morphology, the integrity of the lamina propria in regards to the distribution of lymph vessels is restored.

Antibodies, Monoclonal↗

PubMed2006

[Vascular access for haemodyalisis. Comparative analysis of the mechanical behaviour of native vessels and prosthesis].

INTRODUCTION: The prosthesis nowadays used in the vascular access for haemodialysis have low patency rates, mainly due to the luminal obstruction, determined by the intimal hyperplasia. Several factors have been related to de development of intimal hyperplasia and graft failure. Among them are the differences in the biomechanical properties between the prosthesis and the native vessels. In the searching for vascular prosthesis that overcomes the limitations of the currently used, the cryopreserved vessels (cryografts) appear as an alternative of growing interest. However, it is unknown if the mechanical differences or mismatch between prosthesis and native vessels are lesser when using cryografts. OBJECTIVE: To characterize and compare the biomechanical behaviour of native vessels used in vascular access and cryografts. Additionally, segments of expanded polytetrafluoroethylene (ePTFE) were also evaluated, so as to evaluate the potential biomechanical advantages of the cryografts respect to synthetic prosthesis used in vascular access. METHODS: Segments from human humeral (n = 12), carotid (n = 12) and femoral (n = 12) arteries, and saphenous vein (n = 12), were obtained from 6 multiorgan donors. The humeral arteries were studied in fresh state. The other segments were divided into two groups, and 6 segments from each vessel were studied in fresh state, while the remaining 6 segments were evaluated after 30 days of criopreservation. For the mechanical evaluation the vascular segments and 6 segments of ePTFE were mounted in a circulation mock and submitted to haemodynamic conditions similar to those of the in vivo. Instantaneous pressure (Konigsberg) and diameter (Sonomicrometry) were measured and used to calculate the viscous and elastic indexes, the compliance, distensibility and characteristic impedance. For each mechanical parameter studied, the mismatch between the prosthesis and the native vessel was evaluated. RESULTS: The ePTFE was the prosthesis with the higher mechanical mismatch (p < 0.05). The venous and arterial cryografts showed the least mismatch with native veins and arteries, respectively. The prosthesis with the least mechanical mismatch was different, depending on the native vessel evaluated, and for a native vessel, on the parameter considered. CONCLUSION: The mechanical mismatch between the native vessel and the vascular prosthesis used in a vascular access could be reduced using cryografts.

Adult↗

PubMed1989

Parapapillary retinal vessel diameter in normal and glaucoma eyes. I. Morphometric data.

The retinal blood vessels serve for nutrition of the retinal ganglion cells and their axons. This study was undertaken to evaluate the vessel diameter in normal and glaucoma eyes. The calibers of the superior temporal and inferior temporal retinal artery and vein were measured at the optic disc border and at a distance of 2 mm from the optic disc center; 473 eyes of 281 patients suffering from chronic primary open-angle glaucoma and 275 eyes of 173 normal subjects were examined. Fifteen-degree, color stereo optic disc photographs were used. In the normal eyes the inferior temporal vessels were significantly larger than the superior temporal vessels. This corresponds with: (1) the configuration of the normal neuroretinal rim, which is significantly broader in the inferior disc region than in the superior disc area; (2) the visibility of the retinal nerve fibers, which are better detectable in the inferior temporal area than in the superior temporal one; and (3) the foveola location 0.53 +/- 0.34 mm inferior to the optic disc center. The retinal vessel diameter was independent of the patients' age and optic disc and parapapillary chorioretinal atrophy size. In the glaucoma group the vessel caliber was significantly smaller than in the normal eyes. The differences were more marked for the arteries and the inferior temporal vessels, respectively. The vessel diameters decreased significantly with increasing glaucoma stage independently of the patients' age. The parapapillary retinal vessel diameter may reflect the need of vascular supply in the corresponding superficial retinal area. It may be correlated with the local ganglion cell density and retinal nerve fiber layer thickness.

Adult↗

PubMed1988

[Early development of cerebral blood vessels: on the relationship between cerebral histogenesis and internal vascularization].

The purpose of this study is to evaluate the morphological relevance to cerebral histogenesis and internal vascularization during early fetal development of rats. Using light and electron microscopes, fetal brains and spinal cords from embryonic day 11 (E11) to E 16 were observed with special attention to new blood vessel formation in the parenchyma. At stages of the neural groove and neural tube blood vessels were confined in the perineural mesenchyma around the matrix cell layer whose cytoarchitecture was arranged in a pseudostratified pattern and did not include the blood vessels. At the prosencephalic stage (E 13), primordium of the striatum which localized in the ventrolateral portion of the cerebral neopallium made up the migrating zone in outer most of the matrix cell layer and blood vessels firstly appeared in this area. Similarly, the blood vessels were also recognized at the ventro-lateral portion of the mesencephalon where the migrating zone was initially formed on E 13. In the cervical spinal cord, the blood vessels were initially recognized on E 12, when the migrating zone was formed at the area of anterior horn. At the early telencephalic stage during E 14-E 15, blood vessels were evenly distributed in the lateral cerebral neopallium, while the cerebral neopallium in the midline where took place later evolution than lateral neopallium was still remaining in the state of matrix cell layer only, and was also lacking the blood vessels. In this area, first appearance of the vessels was E 15 or E 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

[Intratumoral proliferation of the blood vessels].

The growth of vessels in experimental neoplasm occurs within 2-7 days after implantation. Newly formed vessels penetrate into the tumor only from the tissues of the tumor-carrying host. Vessels are formed in the tumor by budding. Proliferation of tumor cells begins only after the contact between them and the developing vascular network has been established. Myofibroblasts play an important role in the development of vessels. The intensity of new vessel formation is more than twice as high as in the wound process. The number of capillaries in developed tumors varies with an average of 30,000 in 1 mm2. Blood supply even within the same tumor is variable both in the form and location of the vessels. With increasing tumor volume intercapillary distances, diameter and length of the capillaries increase while the vascular bed volume, the general and local blood flow decrease. Reparation of the vascular bed in tumors occurs both due to preexisting vessels and by additional formation of new vessels. The muscular layer and innervation are lacking in the newly formed vessels. In the process of growth, compensatory-adaptative reactions directed to improvement of hemodynamics constantly develop in tumor tissues.

Animals↗

PubMedDate not supplied

Abnormal vessel patterns in phototoxic rat retinopathy studied by vascular replicas.

Permeability abnormalities of vessels in rat phototoxic retinopathy have been described for sodium fluorescein and the fluoresceinated dextrans. Since fenestrated vessels within the pigment epithelium (RPE-vessels) had connections to retinal capillaries but not to choroidal vessels, it was presumed that the continuous retinal vessels became fenestrated when located in the abnormal environment of the pigment epithelial cell. It was necessary to rule out a choroidal origin of these unusual RPE-vessels, since they may be a model for other vasculopathies. Vascular cast replicas of whole retinal and choroidal vessel beds from rats with advanced phototoxic retinopathy were studied by scanning electron microscopy. No connection between the retinal and choroidal vasculature was found. Retinal vessels entering the pigment epithelium formed medusa-like coils in local areas. Marked capillary dropout and vessel tortuosity were characteristic. The choroidal capillary bed was normal. This model is appropriate for study of the plasticity of retinal capillaries as seen in diabetic retinopathy and senile macular degeneration.

Animals↗

PubMed1996

Immunohistochemical characterization of developing and mature primate retinal blood vessels.

PURPOSE: To characterize developing retinal blood vessels with vascular markers and to relate the histochemical profile of maturing vessels to morphologic stages in retinal vascular development. METHODS: Vessels were examined in frozen and paraffin-embedded retinas and in wholemounts of Macaca monkeys ranging in age from fetal day 75 (F75) to adulthood. Endothelial cells were visualized immunohistochemically using antisera to von Willebrand's factor and CD31 with lectins Ulex europaeus, Bandeiraea simplicifolia, peanut agglutinin, Ricinis communis, and wheat germ agglutinin, and by ATPase and ADPase enzymatic histochemistry. Antibodies to vascular basement membrane and matrix markers laminin, fibronectin, and collagen types I and VIII, and antisera recognizing cell cycle-specific nuclear proteins (cyclin, Ki-67, Mib-1) also were used. RESULTS: Newly formed and mature vessels were reactive with reagents specific for CD31, von Willebrand's factor, types I and VIII collagens, laminin, fibronectin, U. europaeus, R. communis, and peanut agglutinin. Wheat germ agglutinin labeled vessels only after pretreatment with neuraminidase. All vascular markers appeared simultaneously, but some were distributed differentially between capillaries and larger vessels, along the central-peripheral extent of a vascular plexus, and among different vascular laminae. Markers of vessels failed to label spindle-shaped presumed vascular precursor cells lying peripheral to the advancing vessels during development. Spindle cells exhibited cyclin, Ki-67, and Mib-1 immunoreactivity. CONCLUSIONS: Immature and mature vitread and sclerad vessels displayed histochemical profiles that were qualitatively similar but that had subtle quantitative differences. Results do not support identification of spindle-shaped cells as vascular precursors in the developing monkey retina and are discussed in relation to mechanisms of retinal vascularization.

Aging↗

PubMed1995

How vessels narrow.

Vascular narrowing, the clinical dilatation of narrowed vessels, and the restenosis of those vessels are central topics in modern cardiology. This review discusses the cellular basis both for the spontaneous narrowing of vessels and for the restenotic process that occurs after angioplasty. The central issue, as discussed in this review, is likely to be remodeling of the vessel wall rather than simple accretion of lipid mass in atherosclerosis or simple physical dilatation following angioplasty. While it is true that the atherosclerotic lesion grows by accretion of lipid mass, this by itself does not narrow vessels. As we will discuss, the vessel has a phenomenal ability to accommodate changes of this sort. Narrowing must occur, at least in part, because of a failure of this normal ability to accommodate. In a similar manner, one might expect the restonotic vessel to simply remodel itself down to its preangioplasty size. The issue for cell and molecular biologists is what "remodeling" means. Until recently, the assertion has been that remodeling occurred as the result of the formation of new intimal mass; that is, the atherosclerotic vessel was seen as returning to its original dimensions following angioplasty as a result of forming a new intimal mass that filled in the dilated space. Recent studies using cell kinetic methods as well as intravascular ultrasound, however, have cast doubt upon this hypothesis. It now appears that the loss of gain following angioplasty is likely to be due to the formation of new tissues which remodel the vessel wall without necessarily adding mass to it. This is the same sort of process that is well described in wound healing. The nature of this new tissue is of great interest. Studies in this laboratory and others have identified genes which may be unique to this tissue and explain the remodeling response.

Animals↗

PubMed1999

Disease pattern in cranial and large-vessel giant cell arteritis.

OBJECTIVE: To identify variables that distinguish large-vessel giant cell arteritis (GCA) with subclavian/axillary/brachial artery involvement from cranial GCA. METHODS: Seventy-four case patients with subclavian/axillary GCA diagnosed by angiography and 74 control patients with temporal artery biopsy-proven GCA without large vessel involvement matched for the date of first diagnosis were identified. Pertinent initial symptoms, time delay until diagnosis, and clinical symptoms, as well as clinical and laboratory findings at the time of diagnosis, were recorded by retrospective chart review. Expression of cytokine messenger RNA in temporal artery tissue from patients with large-vessel and cranial GCA was determined by semiquantitative polymerase chain reaction analysis. Distribution of disease-associated HLA-DRB1 alleles in patients with aortic arch syndrome and cranial GCA was assessed. RESULTS: The clinical presentation distinguished patients with large-vessel GCA from those with classic cranial GCA. Upper extremity vascular insufficiency dominated the clinical presentation of patients with large-vessel GCA, whereas symptoms related to impaired cranial blood flow were infrequent. Temporal artery biopsy findings were negative in 42% of patients with large-vessel GCA. Polymyalgia rheumatica occurred with similar frequency in both patient groups. Large-vessel GCA was associated with higher concentrations of interleukin-2 gene transcripts in arterial tissue and overrepresentation of the HLA-DRB1*0404 allele, indicating differences in pathogenetic mechanisms. CONCLUSION: GCA is not a single entity but includes several variants of disease. Large-vessel GCA produces a distinct spectrum of clinical manifestations and often occurs without involvement of the cranial arteries. Large-vessel GCA requires a different approach to the diagnosis and probably also to treatment.

Aged↗