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Biomedical subjects

R W Thompson

Publications and source records attributed to R W Thompson.

At least 55 records · Page 3Linked to original sources
PubMed1997

Surgical treatment of thoracic outlet compression syndromes. II. Supraclavicular exploration and vascular reconstruction.

Supraclavicular exploration has become a widely utilized, versatile, and effective approach in the treatment of thoracic outlet compression syndromes. It is applicable to neurogenic, arterial, and venous form of TOS. Although certain aspects of the surgical anatomy are quite familiar to most vascular surgeons, considerable attention must be given to the details of this procedure to avoid inadequate decompression, serious injury, or predictable causes of recurrent compression. Supraclavicular exploration and its variations provide an excellent approach to the entire spectrum of problems encountered in patients with TOS, and in many centers it has superceded the transaxillary approach previously popularized for these disorders. Because supraclavicular exploration for TOS involves a number of unique technical considerations and because it is typically applied to a difficult clinical problem outside the routine experience of most vascular surgeons, it should be undertaken only with appropriate training and interest in the comprehensive management of patients with TOS.

Blood Vessel Prosthesis↗
PubMed1997

Ischemic colitis.

This article contains a current review of ischemic colitis, including its etiology, pathophysiology, diagnostic modalities, and treatment options. A special emphasis is given to ischemic colitis following aortic reconstruction.

Aortic Aneurysm, Abdominal↗
PubMed1997

Spontaneous closure of selected iatrogenic pseudoaneurysms and arteriovenous fistulae.

PURPOSE: We report our approach to the management of postcatheterization femoral artery pseudoaneurysms and arteriovenous fistulae in an attempt to determine the frequency of spontaneous resolution of selected lesions. METHODS: We studied 196 pseudoaneurysms, 81 arteriovenous fistulae, and 9 combined lesions that were identified by duplex scan. Indications for immediate surgical repair included pseudoaneurysm greater than 3 cm, enlarging hematoma, pain, groin infection, nerve compression, limb ischemia, concomitant surgical procedure, and patient refusal or inability to comply with follow-up. All other lesions were observed. RESULTS: One hundred thirty-nine patients underwent prompt surgical repair, and 147 patients were initially managed without operation. There were no limb-threatening complications associated with nonoperative management in this subset of patients. Eighty-six percent of the lesions being observed resolved spontaneously within a mean of 23 days, whereas 14% required surgical closure for a variety of reasons (at a mean of 111 days after the initial diagnosis). There was no statistically significant difference in the rate of spontaneous pseudoaneurysm closure (89%) as opposed to fistulae (81%) (p < 0.17). By life-table analysis, 90% of selected pseudoaneurysms had resolved by 2 months. Patients selected for observation underwent an average of 2.6 duplex scans per patient versus 1.4 scans per patient for those treated with immediate surgery (p < 0.01). CONCLUSION: The natural history of stable pseudoaneurysms and arteriovenous fistulae is benign and frequently results in spontaneous resolution, which allows properly selected patients to be managed without operation.

Analysis of Variance↗
PubMed1997

Prostaglandin E2 synthesis and cyclooxygenase expression in abdominal aortic aneurysms.

PURPOSE: The purpose of this study was to evaluate the expression of prostaglandin E2 (PGE2) and the two cyclooxygenase isoforms (cox1 and cox2) in human abdominal aortic aneurysm (AAA) tissue. METHODS: Ten specimens each of normal aortas and aneurysmal aortas were collected and used for histologic analysis and whole organ culture. An enzyme-linked immunosorbent assay for PGE2 was performed on the media from the aortic explant whole organ culture. An immunohistochemical analysis for PGE2 was performed, as was in situ hybridization for cox1 and cox2 on tissue sections. RESULTS: PGE2 production of AAA specimens was found to be 67,287 +/- 27,303 pg/ml as compared with 1698 +/- 858 pg/ml for normal aortic specimens (p < 0.001). PGE2 was localized by immunohistochemical analysis to the inflammatory infiltrate in AAAs. Minimal expression was noted in normal aortas. Using in situ hybridization, little expression of cox1 was noted in either the normal or the AAA specimens. Cox2 was expressed by macrophage-like cells within the inflammatory infiltrate of the AAA specimens but was not significantly expressed in the normal aorta. CONCLUSION: The expression of PGE2 is associated with the pathogenesis of human AAAs. Its expression is localized to macrophage-like cells within the inflammatory infiltrate and is controlled by the cox2 isoform of cyclooxygenase. Cox2 is, therefore, a potential target for pharmacotherapy of AAAs.

Aorta, Abdominal↗
PubMed1997

Vascular smooth muscle cell apoptosis in abdominal aortic aneurysms.

Apoptosis is a naturally occurring mechanism of cell death that plays an important role in both normal and pathological remodeling of the vessel wall. Abdominal aortic aneurysms (AAA) represent a unique and dramatic example of vessel wall remodeling characterized by degeneration of the elastic media. Although much attention has been focused on the proteolytic mechanisms that underlie elastin and collagen degradation in AAA, recent studies suggest that depletion of medial smooth muscle cells (SMC) makes an important contribution to this disease by eliminating a cell population capable of directing connective tissue repair. As described in this review, these investigations have revealed that SMC depletion in human aneurysm tissues is accompanied by biochemical, morphological and molecular changes consistent with SMC apoptosis. The exact mechanisms responsible for SMC apoptosis in AAA remain to be elucidated, but current evidence indicates that elevated cellular production of p53 and p21 participates in the process. These findings provide an important new starting point for further investigations on the cellular and molecular mechanisms underlying SMC depletion in AAA and how this process might trigger the accelerated progression of aneurysm disease.

Aortic Aneurysm, Abdominal↗
PubMed1997

Decreased vascular smooth muscle cell density in medial degeneration of human abdominal aortic aneurysms.

Abdominal aortic aneurysms (AAAs) are characterized by structural deterioration of the aortic wall leading to progressive aortic dilatation and eventual rupture. The histopathological changes in AAAs are particularly evident within the elastic media, which is normally dominated by vascular smooth muscle cells (SMCs). To determine whether a decrease in vascular SMCs contributes to medial degeneration, we measured SMC density in 21 normal and pathological human abdominal aortic tissue specimens using immunohistochemistry for alpha-SMC actin and direct cell counts (medial SMCs per high-power field (HPF)). Medial SMC density was not significantly different between normal aorta (n = 5; 199.5 +/- 14.9 SMCs/HPF) and atherosclerotic occlusive disease (n = 6; 176.4 +/- 13.9 SMCs/HPF), but it was reduced by 74% in AAA (n = 10; 50.9 +/- 6.1 SMCs/HPF; P < 0.01 versus normal aorta). Light and electron microscopy revealed no evidence of overt cellular necrosis, but SMCs in AAAs exhibited ultrastructural changes consistent with apoptosis. Using in situ end-labeling (ISEL) of fragmented DNA to detect apoptotic cells, up to 30% of aortic wall cells were ISEL positive in AAAs. By double-labeling techniques, many of these cells were alpha-actin-positive SMCs distributed throughout the degenerative media. In contrast, ISEL-positive cells were observed only within the intimal plaque in atherosclerotic occlusive disease. The amount of p53 protein detected by immunoblotting was increased nearly fourfold in AAA compared with normal aorta and atherosclerotic occlusive disease (P < 0.01), and immunoreactive p53 was localized to lymphocytes and residual SMCs in the aneurysm wall. Using reverse transcription polymerase chain reaction assays a substantial amount of p53 mRNA expression was observed in AAAs. These results demonstrate that medial SMC density is significantly decreased in human AAA tissues associated with evidence of SMC apoptosis and increased production of p53, a potential mediator of cell cycle arrest and programmed cell death. Given the role that SMCs normally play in maintaining medial architecture and in arterial wall matrix remodeling, the induction of SMC apoptosis likely makes an important contribution to the evolution of aneurysm degeneration.

Aorta, Abdominal↗
PubMed1996

Role of matrix metalloproteinases in abdominal aortic aneurysms.

Considerable progress has been made toward characterizing the enzymes and proteolytic events that occur in established human abdominal aortic aneurysms (AAA). Through studies involving a number of different laboratories and various experimental approaches, enzymes of the matrix metalloproteinase (MMP) family have consistently emerged as important molecular participants in aneurysm disease. The finding that elastolytic MMPs, particularly MMP-9 and MMP-2, are expressed and produced in increased amounts in human aneurysm tissue, has led to the possibility that these enzymes might serve as rational targets for pharmacotherapy in this disease. Recent studies using MMP-inhibiting tetracycline derivatives in the elastase-induced rodent model of AAA indicate that metalloproteinase suppression is a feasible and successful approach in the experimental setting. The definitive proof-of-principle for the therapeutic efficacy of anti-MMP or other anti-proteinase strategies to limit the growth of small AAA, however, will remain unknown until specifically tested in clinical trials.

Aortic Aneurysm, Abdominal↗
PubMed1996

Indomethacin prevents elastase-induced abdominal aortic aneurysms in the rat.

Perfusion of the rat abdominal aorta with elastase induces abdominal aortic aneurysms (AAA), in which the development of aortic dilatation correlates with the influx of inflammatory cells, increased production of matrix metalloproteinases (MMPs), and destruction of medial elastin. We tested the hypothesis that indomethacin, an inhibitor of macrophage MMP expression, might attenuate aneurysmal degeneration in this model. Fourteen adult male Wistar rats underwent 2-hr aortic perfusion with elastase. Six animals received injections of saline and eight animals received 4 mg/kg/day indomethacin for 7 days. Pre-perfusion, post-perfusion, and final aortic diameters (AD) were determined, and histology and substrate gel zymography were performed. Five out of six control animals developed AAA, while no aneurysms were observed in the indomethacin-treated group (P < 0.01). Whereas AD increased 126 +/- 16% in control animals, the mean increase in the indomethacin-treated group was only 56 +/- 6% (P < 0.001). Although animals in both groups demonstrated an inflammatory response dominated by macrophages, the marked destruction of medial elastin in the control group was not present in the treatment group. In addition, substrate zymography demonstrated decreased levels of MMP-9 in animals treated with indomethacin. Indomethacin inhibits aneurysm growth in this model, and the data suggest that it does so by decreasing macrophage expression of at least one elastolytic metalloproteinase, MMP-9.

Animals↗
PubMed1996

A longitudinal evaluation of prevalent negative beliefs about residential placement for troubled adolescents.

To investigate the validity of five prevalent negative beliefs about residential placement, we followed adolescents from a residential program and a comparison group at 3-month intervals for 4 to 8 years. This residential program in the Midwest uses the Teaching-Family Model in which six to eight adolescents live in a family-style environment. The interviews included five scales reflecting youths' views about important aspects of their lives in placement: (1) Delivery of Helpful Treatment, (2) Satisfaction with Supervising Adults, (3) Isolation from Family, (4) Isolation from Friends, and (5) Sense of Personal Control. Hierarchical linear modeling allowed us to estimate group differences while controlling for developmental trends, demographic factors, and prior differences between groups. The two groups were equivalent on all scales before the study. During the following placement, however, the treatment group's ratings were significantly more positive than the comparison group on four of the five scales and approached significance on the fifth. These findings suggest that negative beliefs about life in residential placement for adolescents may not apply to all programs.

Adolescent↗
PubMed1996

Femoropopliteal bypass for claudication: vein vs. PTFE.

The vascular graft of choice for femoropopliteal bypass in patients with intolerable claudication is controversial. We retrospectively reviewed our experience with 239 patients suffering from claudication secondary to superficial femoral artery obstruction. Femoropopliteal reconstruction was performed with saphenous vein to the below-knee popliteal artery in 66 patients (BK-vein). Polytetrafluoroethylene (PTFE) was used in 128 patients as a bypass graft to the above-knee popliteal artery (AK-PTFE) and 45 patients had a PTFE graft to the below-knee popliteal artery (BK-PTFE). All patients were enrolled in a postoperative graft surveillance program with graft revision when appropriate. There was one perioperative death (0.4%). Primary patency at 5 years for AK-PTFE, BK-PTFE, and BK-vein was 58.0%, and 60.3%, respectively, and was not significantly different among the graft groups. Graft revision for failed/failing grafts resulted in 5-year secondary patency rates of 79.2% (AK-PTFE), 73.3% (BK-PTFE), and 74.4% (BK-vein). These secondary patency rates were not statistically different. Eventual conversion to a vein graft in patients initially treated with PTFE maximized patency in the femoropopliteal segment with 5-year patency rates of 84.6% and 93.0% for the AK-PTFE and BK-PTFE graft groups, respectively. Major leg amputation was necessary during the entire course of the study in eight (3.3%) patients. We conclude that long-term patency rates for femoropopliteal bypass in patients with intolerable claudication are similar for PTFE and autologous saphenous vein grafts.

Aged↗
PubMed1996

Revascularization of the solitary kidney: a challenging problem in a high risk population.

BACKGROUND: Patients with significant atherosclerotic stenosis involving the artery to a solitary functioning kidney present a clinical challenge. METHODS: From August 1987 through August 1995, 35 of these patients (average age, 68.4 +/- 6.9 years) were treated. Comorbid conditions included previous myocardial infarction in 23% of the patients, congestive heart failure (CHF) in 34%, chronic obstructive pulmonary disease in 20%, and diabetes in 20%. The average creatinine level of the patients was 2.5 +/- 1.5 mg/dl. Indications for revascularization were hypertension in 86%, hypertensive crisis with CHF in 17%, and renal insufficiency in 69%. Procedures performed included 19 extra-anatomic bypasses, 8 concomitant with infrarenal aortic reconstruction and 2 concomitant with thoracoabdominal aortic aneurysm repair; 1 visceral segment endarterectomy; 1 renal artery endarterectomy with reimplantation; I superior mesenteric to renal artery bypass; 1 aortorenal bypass; and 2 percutaneous angioplasties with staged nephrectomies. RESULTS: At discharge, 91% of patients had stable or improved renal function with an average creatinine level of 1.7 +/- 0.8 mg/dl. Hypertension was cured or improved in 85%. Perioperative mortality was 6%, and major morbidity was 43%, including the need for permanent (9%) and temporary (9%) dialysis, respiratory insufficiency (18%), two early reoperations, six cardiac complications, one case of gastrointestinal bleeding, and one stroke. In the follow-up period (mean duration, 39.2 months), survival has been 73%, and no additional patients have required dialysis. CONCLUSIONS: Although significant perioperative morbidity exists in this high risk population, the long-term preservation of renal function and improvement in hypertension make solitary renal revascularization worthwhile.

Aged↗
PubMed1996

Intraoperative salvage in patients undergoing elective abdominal aortic aneurysm repair: an analysis of cost and benefit.

PURPOSE: Although autologous blood procurement has become a standard of care in elective surgery, recent studies have questioned its cost-effectiveness. We therefore reviewed our 3-year experience with intraoperative cell salvage in patients who underwent elective abdominal aortic aneurysm repair. METHODS: A 3-year retrospective chart review of elective abdominal aortic aneurysm (infrarenal and suprarenal) repair was performed. Transthoracic repairs were excluded. RESULTS: Estimated blood lost was 1748 +/- 1236 ml, or 35% of baseline blood volume (5012 +/- 689 ml). Overall, 164 (89%) received red blood cell (RBC) transfusions (3.5 +/- 2.0 U/patient). The cost per patient for cell salvage was $315 +/- $97, representing 31% of all RBC costs and 24% of total blood component costs. Mean salvage volume infused was 578 +/- 600 ml; at a mean hematocrit level of 55.7% the RBC volume infused from salvage during surgery was 313 +/- 328 ml (representing 27% of total RBC volume lost during the hospital stay). This mean RBC volume salvaged represented the equivalent of 1.6 blood bank RBC units. The mean blood bank costs saved by using cell salvage was $248, or 79% of the $315 actually spent for salvage. We found no decrease in percentage of patients undergoing transfusion until salvage volumes that were infused exceeded 750 ml, or the equivalent of two blood bank units; all of these patients who benefitted had estimated blood lost > or = 1000 ml. CONCLUSIONS: We conclude that use of intraoperative cell salvage was most beneficial for patients who had estimated blood loss greater than or equal to 1000 ml and cell salvage volumes infused greater than or equal to 750 ml. Patients who are estimated to lose less than 1000 ml receive little benefit yet incur substantial costs from intraoperative cell salvage.

Aged↗
PubMed1996

Doxycycline inhibition of aneurysmal degeneration in an elastase-induced rat model of abdominal aortic aneurysm: preservation of aortic elastin associated with suppressed production of 92 kD gelatinase.

PURPOSE: Increased local production of matrix metalloproteinases (MMPs) is a potential mechanism underlying structural protein degradation in abdominal aortic aneurysms (AAA). With an elastase-induced rodent model of AAA, we determined whether pharmacologic treatment with an MMP-inhibiting tetracycline might limit the development of experimental AAA in vivo. METHODS: Forty-eight Wistar rats underwent a 2-hour perfusion of the abdominal aorta with 50 U porcine pancreatic elastase and were then treated with either subcutaneous doxycycline (25 mg/day; n=24) or saline solution vehicle (n=24). Aortic diameter was measured before and after elastase perfusion was performed and before the rats were killed at 0, 2, 7, or 14 days, and AAAs were defined as an increase in aortic diameter to at least twice that before perfusion. At death the aortic tissues were either perfusion-fixed for histologic evaluation or extracted for substrate zymographic evaluation. RESULTS: Aortic diameter was not different between groups at 0 or 2 days, but it was significantly less in animals treated with doxycycline at both 7 and 14 days (mean+/-SEM, p<0.01). After day 2 the incidence of AAA was reduced from 83% (10 of 12 rats treated with saline solution) to 8% (1 of 12 animals treated with doxycycline). By histologic assessment doxycycline prevented the structural deterioration of aortic elastin without decreasing the influx of inflammatory cells. Increased aortic wall production of 92 kD gelatinase observed in a saline solution-treated control group was markedly suppressed in animals treated with doxycycline. CONCLUSIONS: Treatment with an MMP-inhibiting tetracycline inhibits the development of experimental AAA in vivo. This inhibition may be due to selective blockade of elastolytic MMP expression in infiltrating inflammatory cells. Additional experiments, however, are necessitated to fully delineate this process.

Animals↗