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[Comparison of the value of angioscopy, angiography and ultrasonography in detection of pathologic vascular processes].

AIMS: The ability of angioscopy, angiography and sonography to evaluate arteriosclerotic vascular lesions were compared to determine if angioscopy is a valuable addition in the diagnostic armamentarium. METHODS: An in-vitro study was selected to enable microscopic assessment of the arteries. Angiography was followed by sonography and endoscopy and finally the vessels were evaluated macro- and microscopically. RESULTS: The configuration of the vascular stenosis (plaque-shape, semicircular-eccentric, circular-concentric) was more reliably defined with angioscopy as compared to angiography and sonography. Intense calcification of plaque was detected sonographically with a high sensitivity (90%) using the acoustic shadowing and high amplitude criteria. Angioscopy was superior in differentiating between simple and complicated plaques and the assessment of ulcerations, while the visualization of the entire vascular tree with potential collaterals remained the domain of angiography. CONCLUSIONS: Angioscopy seems to be valuable addition in the evaluation of arterial vascular disease. It can be used in the quality control after interventional radiology and surgery.

Angiography↗

The expression of N-methyl-D-aspartate-receptor-mediated component during epileptiform synaptic activity in hippocampus.

1 The possible involvement of N-methyl-D-aspartate (NMDA)-receptors in epileptiform synaptic activity in the kainic acid (KA) lesioned hippocampus was investigated. In this chronic model of epilepsy there is a loss of both the early and the late components of synaptic inhibition as well as changes in the membrane properties of the surviving CA1 pyramidal cells. 2 The action of the specific NMDA-receptor antagonist D-2-amino-5-phosphonovalerate (D-APV) was tested on evoked bursts of action potentials recorded intracellularly from cells of lesioned hippocampi. The effects of D-APV on control synaptic responses from the contralateral, unlesioned hippocampi were also recorded. 3 In the presence of Mg2+ (1 mM), D-APV (20 microM) had a profound effect on the evoked epileptiform activity. Both the number of action potentials in the burst, as well as the area under the excitatory postsynaptic potential (e.p.s.p.) was considerably reduced. Furthermore this D-APV-sensitive component of the epileptiform burst had a very early onset, coincident with the first action potential in the burst. 4 D-APV (20 microM) was ineffective in blocking the e.p.s.p. evoked by Schaffer collateral afferents onto CA1 cells in slices of hippocampus contralateral to the KA lesion. 5 D-APV had no effect on the passive membrane properties of either population of cells. Hyperpolarizing potentials such as the inhibitory postsynaptic potentials (i.p.s.ps) or the afterhyperpolarization following a current-induced burst of action potentials were also unaffected. 6 It appears that an NMDA-receptor component is expressed during synaptically evoked epileptiform activity in this chronic model of epilepsy.

2-Amino-5-phosphonovalerate↗

Identification, prognosis, and management of patients with carotid artery near occlusion.

BACKGROUND AND PURPOSE: Two large trials indicated that endarterectomy was less beneficial for symptomatic patients with internal carotid artery (ICA) near occlusion than for patients who had severe stenosis without near occlusion. Near occlusions complicate ratio calculations of ICA stenosis and require attention to detail for identification. The goal is to provide diagnostic criteria, illustrate identifying features, estimate accuracy of identification, and assess prognosis for patients with near occlusion. METHODS: We re-reviewed 1216 patients with severe (> or =70%) stenosis on angiography in the North American Symptomatic Carotid Endarterectomy Trial and European Carotid Surgery Trial. One of 5 (n = 262) had 2 or more criteria for near occlusion: (1) delayed cranial arrival of ICA contrast compared with external carotid artery (ECA); (2) intracranial collaterals seen as cross-filling of contralateral vessels or ipsilateral contrast dilution; (3) obvious diameter reduction of ICA compared with opposite ICA; or (4) ICA diameter reduction compared with ipsilateral ECA. RESULTS: Interrater agreement, sensitivity, and specificity were excellent (0.88, 90.6%, and 93.8%, respectively). By intention to treat, 3-year risks of ipsilateral stroke for medically treated patients with near occlusion was 15.1% versus 10.9% for surgically treated (absolute risk reduction [ARR] = 4.2%; P value = .33). Patients who continued to receive treatment in the medical arm for the trial's duration had a 3-year risk of 18.3% (ARR = 7.4%; P value = .13). Medically treated patients with severe stenosis but without near occlusion had a 3-year risk of 26.0% versus surgically treated of 8.2% (ARR = 17.8%; P value < .001). CONCLUSION: It is crucial to identify near occlusions on vascular imaging. Although it still is reasonable to consider endarterectomy for these patients, the benefit is muted.

Carotid Stenosis↗

Effect of infarcted myocardium on diagnostic accuracy of exercise echocardiography for detecting noninfarct-related coronary artery lesions.

BACKGROUND: The utility of exercise echocardiography for evaluating remote ischemia due to noninfarct-related artery (n-IRA) lesions in patients with prior myocardial infarction has not been established. METHODS: Quantitative coronary angiography and treadmill exercise echocardiography were performed within 2 weeks in 115 patients with prior myocardial infarction (>6 weeks) and 224 patients without myocardial infarction. Coronary lumen diameter stenosis > or =50% (by angiography) and the lack of a hyperdynamic response on exercise echocardiography were considered significant. Myocardial infarction size was defined as the number of myocardial segments with severe hypokinesis, akinesis, or dyskinesis on echocardiography at rest. RESULTS: For detection of n-IRA lesions in patients with prior myocardial infarction, the sensitivity of exercise echocardiography was similar (78% vs 79%, P = not significant), however, the specificity was significantly lower (77% vs 91%, P <.01) than for detection of significant stenoses in patients without prior myocardial infarction. Angiographic percent-diameter stenosis, presence of collateral vessel, achieved exercise level, and presence of peri-infarct ischemia did not affect the specificity of exercise echocardiography. However, the specificity of exercise echocardiography was significantly lower (69% vs 84%, P <.05) in patients with echocardiographically large infarction (infarction size > or =2) than in patients with small infarction (infarction size <2). CONCLUSION: In patients with prior myocardial infarction, exercise echocardiography showed low specificity for detection of noninfarct-related artery lesions, especially in patients with echocardiographically large myocardial infarction. These characteristics of treadmill exercise echocardiography should be considered when this technique is applied for patients with healed myocardial infarction.

Aged↗

Cardioprotection associated with preconditioning in the anesthetized ferret.

The cardioprotective effect of ischemic preconditioning (PC) was investigated in the anesthetized ferret model of myocardial ischemia followed by reperfusion. PC of 2, 5, or 10-min duration, followed by 10-min reflow, was studied in animals subjected to 60-min sustained LAD coronary artery ischemia followed by 5-h reperfusion. Infarct size was determined by tetrazolium staining. Sham PC ferrets had a mean infarct of 72% of risk zone. A 2-min or 5-min cycle of PC significantly reduced tissue damage to 54% (p < 0.05) and 44% (p < 0.01), respectively. Infarct reduction associated with 10-min ischemic PC was not significant (57% of AAR). The cardioprotective effects of 5-min PC were lost when sustained ischemia was prolonged to 75 or 90-min. Myocardial salvage afforded by 5-min PC was also abolished by both a) inhibition of ATP-sensitive potassium channels using either glyburide or 5-HD and b) blockade of adenosine receptors with the A1 selective agent DPCPX. In the absence of PC, activation of ATP-sensitive potassium channels with the cardiac-selective agonist BMS-180448 significantly (p < 0.01) reduced infarct size from 66% to 37% of the risk zone. Cardioprotection, or its loss, was not the result of hemodynamic alterations occurring during PC, drug administration, or the coronary occlusion and reperfusion phases. Based upon its body size and lack of extensive myocardial collateral circulation the ferret offers a usefull alternative small species for study of ischemia and reperfusion salvage. It is concluded in the ferret that: a) the threshold for PC is less than in either the rat, rabbit, or dog; unlike the dog and pig, the beneficial effects of PC are b) reduced when the ischemic PC interval is extended to 10-min or c) lost if sustained coronary occlusion is maintained for a period of 75-min or longer; and last, a role in PC for both d) ATP-sensitive potassium channels and e) adenosine A1 receptors can be demonstrated.

Animals↗

[Noninvasive methods of the examination in surgery of obliterating atherosclerosis of lower extremity arteries].

The purpose of the study was to determine surgical policy in atherosclerotic lesions of aorta and lower extremities arteries on the basis on non-invasive diagnostic methods--duplex scanning (DS) and computer tomographic angiography (CTA). From 1998 to 1999 47 patients were examined on this program (DS + CTA). At the first stage of the study, 17 patients underwent translumbal aorto-arteriography at the same time with DS and CTA. Analysis of the angiograms revealed that sensitivity of angiography for detection of lesions in aorto-iliac segment was 94%, in femoro-popliteal segment--78%. Diagnostic mistakes were associated with partial thrombosis of aneurysm's lumen, as a result of which the aorta looked non-dilated in angiograms. Femoral arteries contrasted unsatisfactory in 4 patients because of low collateral blood velocity distal to occlusion of iliac arteries. Initial segments of deep and superficial femoral arteries closed each other in angiograms on anterior-posterior projection, and it also led to low potential of angiography in assessment of femoral arteries state. Complex of non-invasive diagnostic methods (DS + CTA) allowed to correct diagnosis in each case. The methods complemented one another: CTA permitted to make three-dimensional reconstruction of vascular tree and to study its on various projections; DS--to study the vascular wall's state and hemodynamical parameters of blood flow. At the second stage of the study, high sensitivity of DS and CTA allowed to reject traditional angiography in preoperative period. Intraoperative findings confirmed the provisional diagnosis completely.

Adult↗

Induction of hippocampal LTD requires nitric-oxide-stimulated PKG activity and Ca2+ release from cyclic ADP-ribose-sensitive stores.

Long-term depression (LTD) of synaptic transmission can be induced by several mechanisms, one thought to involve Ca2+-dependent activation of postsynaptic nitric oxide (NO) synthase and subsequent diffusion of NO to the presynaptic terminal. We used the stable NO donor S-nitroso-N-acetylpenicillamine (SNAP) to study the NO-dependent form of LTD at Schaffer collateral-CA1 synapses in vitro. SNAP (100 microM) enhanced the induction of LTD via a cascade that was blocked by the N-methyl-D-aspartate receptor antagonist D-2-amino-5-phosphonopentanoic acid (50 microM), NO guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (10 microM), and the PKG inhibitor KT5823 (1 microM). We further show that LTD induced by low-frequency stimulation in the absence of SNAP also is blocked by KT5823 or Rp-8-(4-chlorophenylthio)-guanosine 3',5'-cyclic monophosphorothioate (10 microM), cyclic guanosine 3',5' monophosphate-dependent protein kinase (PKG) inhibitors with different mechanisms of action. Furthermore SNAP-facilitated LTD was blocked when release from intracellular calcium stores was inhibited by ryanodine (10 microM). Finally, two cell-permeant antagonists of the cyclic ADP-ribose binding site on ryanodine receptors also were able to block the induction of LTD. These results support a cascade for induction of homosynaptic, NO-dependent LTD involving activation of guanylyl cyclase, production of guanosine 3',5' cyclic monophosphate and subsequent PKG activation. This process has an additional requirement for release of Ca2+ from ryanodine-sensitive stores, perhaps dependent on the second-messenger cyclic ADP ribose.

Adenosine Diphosphate Ribose↗

Chronic theophylline treatment in vivo increases high affinity adenosine A1 receptor binding and sensitivity to exogenous adenosine in the in vitro hippocampal slice.

The present investigation examined the effects of chronic treatment with the adenosine receptor antagonist theophylline in vivo, on in vitro hippocampal electrophysiology and adenosine A1 receptor binding in the same animals. Adult rats were injected once daily (i.p.) with theophylline for 1 week at 75 mg/kg, followed by an additional week at 100 mg/kg, or with saline for the same 2-week period. Two days following the last injection, hippocampal slices were prepared and population spikes recorded from the pyramidal cell layer of area CA1 were elicited by Schaffer collateral-commissural fiber stimulation. The degree of inhibition caused by superfused adenosine was compared between hippocampal slices from theophylline- and saline-treated rats. Tissue from the contralateral hippocampus was used in [3H]cyclohexyladenosine ([3H]CHA) receptor binding. Hippocampi from theophylline-treated animals showed a significantly greater number of [3H]CHA binding sites (apparent Bmax; 125% of control, P less than 0.05), without a significant change in binding affinity, and were more sensitive than controls to the inhibitory effects of adenosine on the population spike response. These results suggest that chronic adenosine receptor antagonism results in the up-regulation of adenosine A1 receptors which are functional and physiologically relevant in the in vitro hippocampus, and further supports the hypothesis that methylxanthine tolerance is mediated, at least in part, by an increase in adenosine receptor density.

Adenosine↗

Elbow instability.

An understanding of elbow instability is predicated on knowledge of the anatomy of the lateral collateral ligament complex and of the mechanism and kinematics of elbow subluxation and dislocation. The lateral collateral ligament complex is the key structure involved in recurrent elbow instability and it is virtually always disrupted in elbow dislocations that result from a fall. The ulnar part of the lateral collateral ligament complex (also known as lateral ulnar collateral ligament) is the critical portion of the ligament complex securing the ulna to the humerus and preventing posterolateral rotatory instability. The kinematics of elbow subluxation and dislocation are a three dimensional coupled motion referred to as posterolateral rotatory instability in which the forearm rotates off the humerus in valgus/external rotation during flexion from the extended position. Elbow instability is diagnosed on clinical examination by the lateral pivot-shift test, the posterolateral rotatory apprehension and drawer tests and on radiographic examination by performing stress x-rays. While the lateral pivot-shift test is difficult to perform, the posterolateral rotatory drawer test is much less difficult. The most sensitive test, however, is the posterolateral rotatory apprehension test. A positive apprehension test in a patient presenting with a history of recurrent painful clicking, snapping, clucking, or locking of the elbow should lead one directly to the suspected diagnosis of posterolateral rotatory instability. Treatment is surgical, by repair or reconstruction of the lateral collateral ligament complex, specifically the ulnar part. Deficiencies of the coronoid and/or radial head must be addressed.

Collateral Ligaments↗

Release of endogenous amino acids, including homocysteic acid and cysteine sulphinic acid, from rat hippocampal slices evoked by electrical stimulation of Schaffer collateral-commissural fibres.

This study examined the release of endogenous amino acids from acute hippocampal slices, upon stimulation of the Schaffer collateral-commissural fibres. One-minute samples of superfusate were collected via a cannula placed over the CA1 stratum radiatum, and were analysed by reversed-phase high performance liquid chromatography. Evoked potentials were recorded to ascertain stimulation efficacy. Four minutes of continuous 50 Hz stimulation produced a tetrodotoxin-sensitive release of aspartate and glycine in the second minute of stimulation, as well as a tetrodotoxin-sensitive release of cysteine sulphinic acid, during stimulation and of homocysteic acid, following stimulation. Such 50 Hz stimulation also produced a tetrodotoxin-insensitive decrease in methionine levels, but no significant changes in any of the other 15 amino acids measured. Four minutes of continuous 1 Hz stimulation produced no changes in the levels of any of the amino acids measured, but four 600-ms trains of 100 Hz stimulation, which, unlike the 1 Hz stimulation, produced long-term potentiation, resulted in significant increases in levels of cysteine sulphinic acid and homocysteic acid, but not of any of the other amino acids measured. These results suggest that aspartate, glycine, homocysteic acid, and cysteine sulphinic acid play a role in synaptic transmission in the Schaffer collateral-commissural fibres, and that cysteine sulphinic acid and homocysteic acid may be released specifically by high-frequency stimulation.

Amino Acids↗

Diffusion- and magnetisation transfer-weighted MRI in childhood moya-moya.

MRI in two children with moya-moya demonstrated low signal on T2-weighted images in the acute and subacute phases of ischaemia. Gradient-echo sequences, more sensitive to magnetic susceptibility, demonstrated these abnormalities better. Signal loss, due to temporary accumulation of iron, decreases progressively and disappears in the chronic stage of the disease. Diffusion-weighted MRI allows early detection of ischaemic lesions and can be used to monitor progressive spreading of the lesions. Magnetisation transfer maps provide sharp contrast, useful for demonstrating cortical atrophy.

Acute Disease↗

Magnetic resonance angiography of collateral vessel growth in a rabbit femoral artery ligation model.

Collateral vessel growth was visualized in a rabbit femoral artery ligation model by serial contrast-enhanced magnetic resonance angiography (MRA) at 1.5 T in comparison with X-ray angiography (XRA). XRA and MRA were performed directly after femoral artery ligation (day 0+) and after 7 and 21 days. XRA (in-plane resolution, 0.3x0.3 mm) was performed with arterial catheterization for fast injection of iodinated contrast agent just proximal to the aortic bifurcation. MRA (in-plane, 0.6x0.6 mm) was performed at 1.5 T with a five-element phased-array coil and slow injection of gadolinium-based MR contrast agent into an ear vein. Collateral vessel scores on two-dimensional XRA projections and on three-dimensional digitally subtracted rotational MRA maximum intensity projections were obtained by two observers and compared. Collateral vessel counts and minimal detectable vessel diameters for MRA and XRA were combined in a computational flow model to interpret differences in spatial detection limits between imaging modalities in terms of flow. Collateral vessel scores were significantly higher in the ligated limb at day 7 (P < 0.05) and more so at day 21 (P < 0.001), in comparison with day 0+ or in the non-ligated control limb on both XRA and MRA. Significantly more (smaller) vessels were visualized with XRA than with MRA, particularly on day 21 (P < 0.05). Inter-observer agreement was high for both XRA (kappa = 0.82) and MRA (kappa = 0.78). The flow model showed that collateral vessels with diameters > 0.3 mm scored by XRA as well as MRA represent nearly 100% of the total blood flow, whereas smaller (0.1-0.3 mm diameter) vessels that can only be detected with XRA contribute little to the blood flow. Serial contrast-enhanced MRA can non-invasively visualize sub-millimeter collateral vessels that represent nearly 100% of the restored blood flow, in a femoral artery ligation model.

Animals↗

Clinical, toxicological, and pharmacological studies of combination chemotherapy of adenocarcinoma with adriamycin and Baker's antifolate.

Ten patients with disseminated adenocarcinoma were treated with combination chemotherapy employing Adriamycin and Baker's Antifolate (BAF). There were seven patients with lung adenocarcinoma, two of whom achieved partial remission while the remaining five had their disease stabilized. Drug toxicity to the bone marrow, gastrointestinal mucosa, and skin was dose-limiting and was greater than the known toxicities of the individual drugs. Pharmacological studies of both drugs were performed on five patients to determine whether abnormal pharmacokinetics could explain this collateral toxicity. Adriamycin plasma concentrations and disappearance seemed to be unaffected by BAF. However, BAF levels were prolonged, apparently due to an Adriamycin effect on the plasma elimination of BAF, resulting in a prolonged exposure of sensitive tissues and organs to BAF. Consequently, when BAF and Adriamycin are used in combination, appropriate dose and schedule changes must be made to avoid any potentially serious side effects.

Adenocarcinoma↗

Effects of a spider toxin (JSTX) on hippocampal CA1 neurons in vitro.

The effect of a toxin (JSTX) obtained from Nephila clavata (Joro spider) on the CA1 pyramidal neurons of the hippocampus was studied using slice preparations. JSTX blocked the excitatory postsynaptic potentials (EPSPs) in the pyramidal neuron evoked by Schaffer collateral stimulation but was without effect on the antidromic action potentials or on the resting conductance. Depolarization induced by ionophoretic application of glutamate was readily suppressed by JSTX but aspartate-induced depolarization was much less sensitive to the toxin. Among preferential agonists activating 3 receptor subtypes for excitatory amino acids, quisqualate responses were most effectively suppressed by JSTX. Kainate responses were similarly suppressed but in some cells higher concentration of the toxin was needed to block the responses. N-methyl-D-aspartate (NMDA) responses were the least sensitive to JSTX but they were suppressed by +/- 2-amino-5-phosphonovaleric acid (APV). Long term potentiation (LTP) once it had taken place was not completely inhibited by APV. In the presence of JSTX, however, LTP was blocked and tetanic stimuli produced only a short-lived potentiation. In Mg2+ free solution, an orthodromic stimulation evoked repetitive spike responses which were superimposed on the depolarization following the initial spike. APV suppressed the depolarization and associated spikes leaving an orthodromic response which was sensitive to JSTX. The results suggest that JSTX blocks EPSPs in CA1 pyramidal neurons which are mediated by non-NMDA type receptors.

Action Potentials↗

Transcranial oximetry using fast near infrared spectroscopy can detect failure of collateral blood supply in humans.

We tested the hypothesis that transcranial oximetry by fast scanning near infrared spectroscopy can detect local desaturation of hemoglobin in arterial vessels of cerebral circulation with impaired blood supply. A total of 74 near infrared spectroscopy recordings were taken from the intact skull of humans. Perfusion of the hemisphere under the detector was assessed in one of four groups: (1) healthy volunteer; (2) patient, unaffected side; (3) patient, affected side with intact collateral blood supply; (4) patient, affected side, impaired collateral blood supply. Transcranial saturation was 0.90+/-0.01 (all values reported as mean+/-S.E.) in healthy volunteers (n=24), 0.92+/-0.008 in the unaffected hemisphere of patients (n=23), 0.92+/-0.001 in the affected side if collateral supply with blood was intact (n=16). There was no statistical significance between these groups. Saturation in affected hemispheres with impaired collateral blood supply (n=9) was 0.81+/-0.028, which was significantly different from all other groups (P<0.05, one way-ANOVA). We conclude, that transcranial pulse oximetry can detect local hypoxia if collateral blood supply fails.

Cerebrovascular Circulation↗

Release of the coracoacromial ligament can lead to glenohumeral laxity: a biomechanical study.

The purpose of this study was to determine change in glenohumeral joint translation after release of the coracoacromial ligament. Six fresh, frozen unpaired glenohumeral joints were tested in a neutral position and at 30 degrees internal and 30 degrees external rotation of the humerus at 0 degrees, 30 degrees, and 60 degrees of abduction on a custom glenohumeral joint translation testing apparatus. A joint compression load of 20 N was simulated; then a 15-N load was applied to the humerus in anterior, posterior, superior, and inferior directions, and translations on the glenoid were measured with an electromagnetic tracking device. The tests were then repeated after a 1.5-cm section of the coracoacromial ligament was released from the acromion. A multivariate analysis of variance was used for statistical analyses with a P value of.05 as the level of significance. At 0 degrees and 30 degrees of abduction, release of the coracoacromial ligament resulted in a significant increase in glenohumeral joint translations, in both the anterior and inferior directions. In addition, the differences in translation between before and after the release of the coracoacromial ligament decreased in all directions as glenohumeral abduction increased, and they were not significant at 60 degrees of abduction in any of the rotations. The results of this study suggest that the coracoacromial ligament has a role in static restraint of the glenohumeral joint. It provides a suspension function and may restrain anterior and inferior translations through an interaction with the coracohumeral ligament. Although this is a biomechanical study without simulation of the shoulder muscles, it indicates that the coracoacromial ligament contributes to glenohumeral stability. Caution should be exercised in the release of the coracoacromial ligament in those with rotator cuff pain associated with glenohumeral instability.

Aged↗

Subcortical strokes from intracranial aneurysm surgery: implications for intraoperative neuromonitoring.

Forty-five patients underwent surgery for anterior circulation aneurysms using intraoperative neurophysiologic monitoring at the Johns Hopkins Hospital during 1996. There were seven intraoperative strokes. Two were cortical strokes associated with irreversible somatosensory evoked potential (SEP) changes during temporary arterial occlusion. The remaining five were subcortical strokes, one of which was associated with transient SEP changes during temporary arterial occlusion, but the other four occurred despite normal SEPs throughout surgery. Somatosensory evoked potential monitoring is not sensitive for the detection of subcortical ischemia and infarction in the distribution of the deep perforating arterial branches during intracranial aneurysm surgery. Although attenuation of loss of cortical SEP responses may indicate cerebral ischemia from inadequate collateral circulation during temporary arterial occlusion, normal SEPs can not exclude subcortical ischemia sufficient to cause significant postoperative deficits, and may therefore provide a false sense of security during these surgeries.

Adult↗

Gastroepiploic veins: CT appearance in pancreatic disease.

The frequency with which gastroepiploic vein (GEV) enlargement was seen on CT and its relevance to disease of the portal venous system associated with pancreatic disease were studied. We performed a retrospective study of 50 patients with proved pancreatic disease and another 50 patients without such disease. The CT examinations were done in incremental dynamic fashion after a bolus injection of contrast medium. Scans were evaluated for collateral channel formation, including GEV enlargement, and for involvement of the portal venous system by pancreatic disease. Part of the GEV arcade was visible in 36 patients without pancreatic disease, and on average measured 3.2 mm in diameter (range, 1-5.5 mm). GEV enlargement was visible in 62% of the patients with disease; 16% demonstrated a vessel 6 mm or more in diameter. Thirty-four percent of the patients with disease had portal venous complications: 26% had isolated splenic vein involvement, 2% had isolated portal vein involvement, and 6% had a combination of splenic and portal vein involvement. Of the patients with splenic vein disease, 81% had collateral channel formation, 50% of them demonstrating isolated GEV enlargement. Patients with splenic vein disease due to acute pancreatic disease had a much higher instance of GEV enlargement (83.3%). Collateral vessels are commonly seen on CT scans of patients with splenic vein disease and most often occur via enlarged GEVs. Acute pancreatic disease is frequently associated with GEV enlargement, suggesting that the latter represents an early response to splenic vein disease. In contrast, multiple collateral pathways tend to develop in patients with chronic pancreatic disease.

Adult↗