Embolic spinal cord infarction as a presentation of abdominal aortic aneurysm.
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Biomedical subjects
Publications and source records attributed to A Handa.
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The purpose of this study was to describe a balloon-assisted double-lumen microcatheter technique to perform a controlled and tight coil packing of a vascular segment for vessel occlusion. This technique can be performed immediately after a test occlusion with the balloon kept in place and was, as illustrated in six cases, in our experience safe, straight forward to use and fast.
OBJECTIVES: Our unit policy is to duplex on admission all patients undergoing carotid endarterectomy to confirm patency. The aim of this study was to evaluate whether this had led to avoidance of unnecessary carotid surgery in a significant number of patients. METHODS: Over a 7-year period from January 1997 to December 2003, a total of 475 patients were scheduled for carotid endarterectomy. Of these, 439 patients subsequently underwent carotid endarterectomy. These data were obtained from prospectively collected vascular departmental records and we also hand searched notes of the 36 cancelled patients. RESULTS: There were a total of 36 cancellations for various reasons. Of these, 8 were clearly occluded on duplex. A further 16 were highly suspicious of occlusion on duplex and thus surgery was deferred and selective angiography was undertaken. Of these 9 were confirmed to be occluded on angiogram and a further 4 had severe stenoses or virtual occlusion, 3 patients had a distal internal carotid artery occlusion. Thus a total of 24 patients had an occlusion either diagnosed directly on duplex or because of suspicion on duplex. Unnecessary carotid surgery was avoided in 24 of 475 (5%) of patients. CONCLUSION: This study shows that a preoperative duplex on admission for surgery results in 1 of 20 patients avoiding unnecessary carotid surgery.
OBJECTIVE: We undertook this study to determine whether changes in blood coagulability associated with peripheral arterial occlusive disease are due to contact with the atherosclerotic arterial wall or passage through distal ischemic tissue. METHODS: Thirty patients with peripheral arterial occlusive disease undergoing angiography participated in the study. Ankle-brachial pressure index was recorded before intervention. Blood samples taken from the aorta, common femoral artery, and common femoral vein were analyzed at thromboelastography. Angiograms were scored for stenotic disease by a radiologist blinded to the other results. RESULTS: When femoral artery samples were compared with aortic samples there was a decrease in reaction time (R; P <.05), an increase in maximum amplitude (MA; P <.05), and an increase in coagulation index (CI; P <.002), indicating an increase in coagulability as blood flowed down the iliac segment. These changes also correlated (DeltaR, r = 0.442, P <.05; DeltaMA, r = 0.379, P <.05; DeltaCI, r = 0.429, P <.05) with the severity of disease in the ipsilateral iliac segment. Significant differences in R (P <.05), angle (P <.05), MA (P <.005), and CI (P <.001) between common femoral arterial and venous samples confirmed that venous samples were more coagulable in this group of patients. This difference in Thromboelastography parameters across the arteriovenous segment correlated inversely with the degree of ischemia (represented by ankle-brachial pressure index; DeltaCI, r = -0.427, P <.05; DeltaMA, r = -0.370, P <.05) in the puncture side limb. CONCLUSION: Passage of blood down an atherosclerotic artery leads to an increase in coagulability proportional to the degree of stenosis in that vessel. Passage of blood through ischemic tissue may also contribute to increased coagulability in peripheral arterial occlusive disease.
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OBJECTIVES: to review the results of index operations in vascular surgery and to evaluate the impact of a specialist vascular training programme on patient outcome. METHODS: we undertook a 5-year (January 1995-December 1999) review of the weekly-collected mortality and morbidity data. The total number, 30-day mortality and stroke rate of all index operations i.e. AAA repairs (ruptured and elective), carotid operations and infra-inguinal bypasses (above and below knee, elective and emergency) was recorded. The number of operations performed by trainees under supervision was recorded. RESULTS: in the 5-year period 991 index operation were done of which 738 (74%) were done by trainees. Operations done by trainees were supervised by a consultant in 82% of cases with no significant effect on death or stroke rates. Overall vascular trainees performed 75% of the index operations of which 82% were supervised. CONCLUSIONS: trainees under supervision performed three out of four index operations. The mortality and morbidity of index operations in our unit compared well with accepted best mortality and morbidity figures. Our unit provides good training opportunities for vascular trainees whilst maintaining satisfactory standards of patient care.
OBJECTIVE: To ascertain the causes of sudden death (SD) by autopsy examination. METHODS: All cases of sudden death were subjected to a postmortem examination. In addition previous postmortem reports of sudden death over a two years were also included. Postmortem findings were correlated to clinical state and the cause of death was ascertained. The information was analyzed to find out the cause of sudden death in our patients. RESULTS: Out of a total of 130 autopsies there were 13 cases of SD. All were males (age 23 to 50 years). Death was within one your of onset of symptoms in five (38.5%) cases and within 24 hours in eight (61.5%) cases. Death was due to coronary artery disease (CAD) in 10 (76.93%) cases, aortoarteritis, cardiomyopathy and cerebrovascular accident (CVA) in (7.69%) case each. Amongst CAD patients triple vessel disease (TVD) was seen in eight cases (which included one case of cardiomyopathy), two vessel disease (DVD) in two and single vessel disease (SVD) in one. No specific preponderance of right or left coronary artery was seen. One patient of 21 year who died following exertion showed anomalous origin of coronary arteries. His right and left coronary artery originated from aortic arch 1.5 cm above the aortic valve. Right coronary artery was ill developed and had atheromatous plaque. The case of cardiomyopathy also had TVD. In the case of aortoarteritis all vessels were affected (carotids, renal and coronary). In one case of CVA bleeding was from an arterio-venous malformation in right temporal lobe. Nine out of 11 cases of CAD had atheromatous plaque without coronary thrombosis. CONCLUSIONS: Coronary artery disease (Triple vessel disease) contributed to maximum number of cases of SD. Aortoarteritis, cardiomyopathy and cerebrovascular accident (CVA) was the cause of death in one case each. Postmortem identified the cause of death in all cases.
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We describe successful replacement of the iliac vein using a descending aortic homograft. The ilio femoral system was avulsed after recannulation of the femoral vein during a third cardiac reoperation.
Vascular endothelial growth factor (VEGF), which is known to be an angiogenetic factor, plays an important role in the inflammation of synovial tissue. To investigate the relationships between VEGF and clinical symptoms in rotator cuff disease, VEGF expression was examined using RT-PCR and immunohistochemical analysis in 50 patients with this disease (26 with full-thickness cuff tear, 12 with partial-thickness tear, and 12 with subacromial bursitis). VEGF mRNA expression was detected in 40 out of 50 patients by RT-PCR. VEGF mRNA expression was found more frequently in the patients with motion pain (39 out of 41) than in those without motion pain (1 out of 9) with statistical significance (Fisher's test, P < 0.001). Thirty-one out of 33 patients with synovial proliferation showed VEGF mRNA expression, whereas the expression of this transcript was found in 9 out of 17 patients without synovial proliferation. This association with synovial proliferation was also significant (Fisher's test, P = 0.0013). Thirty out of 41 patients with motion pain had synovial proliferation but 3 out of 9 patients without motion pain had synovial proliferation. In all these 30 patients with both motion pain and synovial proliferation, VEGF mRNA expression was detected. This association between motion pain and synovial proliferation was also significant (Fisher's test, P < 0.05). The mean vessel count and area in subacromial bursa expressing VEGF was significantly higher than in those without VEGF (Mann Whitney's U test, P < 0.01). These results suggested that VEGF expression is associated with vascularity, synovial proliferation and shoulder motion pain in the rotator cuff disease.
Although clinically significant, much remains unknown about the healing of the torn rotator cuff tendon, because of unavailability of appropriate animal model. The human supraspinatus tendon faces the subacromial bursa superiorly, and the joint capsule inferiorly, while the digital flexor tendon is surrounded by the synovium. We hypothesized that the supraspinatus tendon heals by the process which is different from that observed with digital flexor tendons, in which epitenon cells migrate into the torn portion circumferentially. The avian supracoracoid tendon was adopted for this experiment because of its similarity to the human supraspinatus tendon. We developed a full-thickness tendon laceration followed by primary suture. The objective of this study was to detect localization of the responsible cells for repair of the tendon. We examined the process using histology and in situ hybridization. Starting at week 1 the peritendon cells of the bursal side proliferated and migrated into the laceration site. At week 6, the tendon stumps were continuous with new connective tissue. High-level expression of procollagen mRNA in the proliferating peritendon cells on the bursal side demonstrates to contribute to the reparative process, which progressed to the joint side. This mode of repair is different from that of the digital flexor tendon.
The relationship between protein structure and aggregation, as well as heat-induced gelling properties, of seven dried egg white (DEW) products was investigated. Strong correlations were found between average molecular weight and hydrophobicity plus surface SH groups of DEW-soluble protein aggregate (SPA). This suggests that hydrophobic interactions and disulfide bond formation between protein molecules were involved in the aggregation. The average molecular weight of DEW products with alkaline pHs was relatively higher than those with neutral pHs and the same degree of protein unfolding, probably because of more disulfide bond formation between protein molecules. In addition, strong correlations were found between hydrophobicity, surface SH groups plus average molecular weight of DEW-SPA, and physical properties of the gels from DEW products. These data indicated that controlling the aggregation of DEW proteins in the dry state is crucial to controlling the gelling properties of DEW.
A 20-year-old golf player who developed recurrent dislocation of the extensor carpi ulnaris (ECU) tendon is reported. The patient was successfully treated by release of the extensor retinaculum and partial resection of the ulno-dorsal ridge of the ulnar head, because the methods caused no redislocation and required only a brief period of rehabilitation.
The authors report the case of a 54-year-old male with extraaxial primary malignant lymphoma associated with calcified chronic subdural hematoma. He slowly developed progressive headache accompanied by a bulge in the left forehead. Skull radiogram showed a large biconvex calcification in the left frontoparietal region, with concave change in the overlying bone. Computed tomograms and magnetic resonance images revealed a left frontoparietal chronic subdural hematoma surrounded by a calcified rim, with marginal enhancement in the frontal portion extending upward to the subcutaneous tissue through the underlying bone. The lesion was suspected to be an infectious calcified hematoma. The patient underwent a craniotomy for the removal of the hematoma. It was observed that the tumor was located mainly in the epidural and subdural space. The extent of the tumor corresponded with the enhanced area of the lesion in the preoperative neuroimages. The histological diagnosis was malignant lymphoma of B cell origin. General examination, which included bone marrow study and Ga scintigraphy, failed to prove systemic lymphoma. Extraaxial primary malignant lymphoma is extremely rare, and this is the first report of a lymphoma associated with calcified chronic subdural hematoma. The authors review the literature and discuss the clinical features and the pathogenesis of the lesion.
Recently heparan sulfate was proposed as the host cell receptor for the dependovirus, adeno-associated virus type 2 (AAV2). We show that although heparan sulfate on the cell surface may contribute to the binding of AAV2 to permissive cells, the amount of heparan sulfate on the cell surface as determined by flow cytometry using four different monoclonal antibodies does not correlate with AAV2 binding to cells or recombinant AAV2 transduction efficiency. Experiments with either mutant CHO cells or cells treated with chlorate to remove sulfate groups showed that sulfation was not absolutely required for infection or binding: in the absence of cell surface sulfation, recombinant AAV2 was still able to be transduced in previously permissive cells. Heparin is commonly used as a substitute in studies of the interaction between heparan sulfate and ligand, and we demonstrate that the binding affinity of AAV2/heparin is low, with a K(d) value of approximately 2.0 nM. A study of the direct interaction between AAV2 and artificial glycosaminoglycans showed that a high degree of sulfation on heparin was critical for the ability to bind AAV2 and compete rAAV2 transduction and that both O- and N-sulfate groups are required. Overall, our data suggest that, as has been shown for other viruses, the presence of a high-affinity AAV2 receptor mediates AAV2 infection in addition to the low-affinity heparan sulfate binding.
We analyzed the expression of cell surface antigens and granulocyte colony-stimulating factor (G-CSF) receptors using flow cytometry, the expression of G-CSF mRNA receptor, using reverse transcription (RT)-PCR, and tested the effect of G-CSF on leukemia colony formation. A total of 14 lymphocytic leukemia patients were examined, seven with acute lymphocytic leukemia (ALL), two with adult T-cell leukemia (ATL), two with B-chronic lymphocytic leukemia (CLL), two with chronic myelocytic leukemia in lymphoid blastic crisis (CML-LBC), and one with plasma cell leukemia (PCL). The presence of G-CSF receptors was demonstrated in 4/14 (29%) patients, two with ALL, one with CLL, and one with CML-LBC, and was associated with stimulation of leukemia clonogenic cell growth by G-CSF. In addition, all four positive leukemia cell types expressed typical B-cell antigens. Our results indicated that G-CSF receptors are expressed on some portion of B-lymphoid leukemia and that their receptors are functional as growth stimulators.