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Biomedical subjects

W H Pearce

Publications and source records attributed to W H Pearce.

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

Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis.

BACKGROUND: Histologic studies of carotid plaques have demonstrated an association between symptomatic disease and plaque rupture. The purpose of this study was to characterize the cellular changes associated with plaque rupture. METHODS: Carotid plaques were obtained from 61 patients undergoing carotid endarterectomy for established indications. Plaques were fixed in formalin, embedded in paraffin, and stained with hematoxylineosin and Movat pentachrome stain to demonstrate plaque structure. Each plaque was examined with light microscopy and classified as containing evidence of plaque rupture (n = 29) or no plaque rupture (n = 32). By using immunohistochemical staining, the fibrous cap was examined for the presence of smooth muscle cells (alpha-actin), macrophages (KP-1), T lymphocytes (UCHL-1), and cell activation (HLA-DR). Data were analyzed with chi-squared analysis. RESULTS: With plaque rupture, macrophages and T lymphocytes were significantly more common than in specimens without evidence of rupture. Similarly, macrophages and T lymphocytes expressing HLA-DR were more often found in sections containing plaque rupture. Furthermore, vascular smooth muscle cells were more common with intact fibrous caps and were diminished with cap thinning. CONCLUSIONS: Rupture of the fibrous cap in carotid artery lesions is associated with increased numbers of macrophages and T lymphocytes, which are in an activated state. The activated inflammatory cells may release cytokines or metalloproteinases, which may be responsible for loss of the fibrous cap. Thus inflammation appears to play a role in the pathogenesis of the neurologic symptoms associated with carotid artery stenosis.

Actins↗
PubMed1997

Helical computed tomography of the normal thoracic outlet.

PURPOSE: This study was performed to determine the detailed anatomy of the thoracic outlet in normal subjects using helical computed tomography (CT), with particular attention to vascular compression with arm movement. METHODS: Ten volunteers underwent detailed clinical evaluation and helical CT scanning of the upper thorax and neck with the arm in a neutral position and with the arm abducted 90 degrees or greater and externally rotated. Anterior scalene-clavicle distance (SC), costoclavicular distance (CC), and vessel diameters were measured with electronic calipers in each position. Comparisons were made with Student's t test. RESULTS: With abduction the SC decreased from 18.4 +/- 3.9 mm to 5.2 +/- 2.4 mm (p < 0.001), and the CC decreased from 12.6 +/- 2.7 mm to 6.3 +/- 3.3 mm (p = 0.005). At these same anatomic planes, the vein diameter decreased from 11.0 +/- 1.6 mm at the neutral position to 5.1 +/- 1.5 mm (p < 0.001) and from 16.1 +/- 3.0 mm to 7.4 +/- 2.6 mm with the arm abducted (p < 0.001). The artery diameter changed from 6.6 +/- 0.8 mm to 6.2 +/- 0.5 mm (p = 0.08) and from 7.2 +/- 0.8 mm to 6.0 +/- 0.5 mm (p = 0.001) with arm movement. CONCLUSIONS: Both the distances between the anterior scalene muscle and the clavicle and between the clavicle and the first rib are significantly reduced with abduction of the upper extremity. Venous compression is universal at both the SC and CC spaces in normal subjects with this maneuver. Arterial narrowing occurs less frequently and appears to be minor. Minor changes in these thoracic outlet dimensions (SC/CC) may produce venous compression without movement.

Adult↗
PubMed1997

Perioperative low molecular weight heparin for infrageniculate bypass.

PURPOSE: Recent studies suggest that subcutaneous low molecular weight heparin (LMWH) is a safe, effective alternative to intravenous heparin (IVH) for deep venous thrombosis. LMWH may also be a safe, effective alternative to IVH when necessary for lower extremity bypass procedures performed with polytetrafluoroethylene (PTFE) grafts. The purpose of this study was to compare subcutaneous LMWH with IVH for perioperative anticoagulation in patients who underwent infrageniculate bypass procedures with PTFE grafts. METHODS: Of 361 lower extremity bypass operations performed at a single center over a 32-month period, 76 were to the tibial or below-knee levels using PTFE grafts for limb salvage. Seven patients were excluded because of absolute indications for perioperative IVH (ventricular thrombus in 1 patient, prosthetic valve in 2, cardiac dysrhythmia in 2, and documented hypercoagulable syndrome in 2), leaving 68 patients (35 women; mean age, 69.8 years) with 69 bypass procedures for study. Grafts completed in the past 16 months were treated with LMWH (28 grafts; Oct. 1994 to Jan. 1996) and were compared with 41 consecutive control grafts from the previous 16-month interval (Apr. 1993 to Oct. 1994) who received IVH. There were similar percentages of composite bypasses (IVH, 50%; LMWH, 46%), patients with tissue loss or gangrene (IVH, 56%; LMWH, 61%), and patients with prior ipsilateral bypass (IVH, 57%; LMWH, 56%) in each group. Age, sex, and atherosclerotic risk factors were also similar between the two groups. RESULTS: Morbidity rates (IVH, 19%; LMWH, 11%) and mortality rates (IVH, 2.5%; LMWH, 4%) were not significantly different. There were no significant differences in the number of grafts that failed before discharge (IVH, 1; LMWH, 0) or percentage of hemorrhagic complications (IVH, 15%; LMWH, 7%). The mean number of postoperative hospital days (IVH, 9.5; LMWH, 7.2; p < 0.009) and coagulation monitoring studies (IVH, 22; LMWH, 8.4; p < 0.0001) were significantly decreased in patients who were anticoagulated with LMWH. The mean number of days before conversion to oral anticoagulation (IVH, 7.3; LMWH, 8.0) did not differ significantly. CONCLUSIONS: When perioperative anticoagulation is deemed necessary, LMWH provides a safe, effective alternative to IVH for infrageniculate PTFE bypass grafting procedures. LMWH may reduce the number of postoperative hospital days and coagulation studies by allowing discharge before therapeutic anticoagulation with warfarin.

Aged↗
PubMed1997

Reduction in aortic aneurysm size: early results after endovascular graft placement. EVT Investigators.

PURPOSE: Previous reports demonstrate initial technical success with transluminally placed endovascular grafts (TPEG) for the treatment of abdominal aortic aneurysms. However, long-term changes in the size of the aorta and aneurysmal segments are unknown. The purpose of this study was to determine aortic dimensions at several levels by computed tomographic (CT) scans 1 year after TPEG. METHODS: Thirty-four patients underwent TPEG with 1-year CT scans. Patients were divided into three groups: group I, no perigraft leak; group II, early perigraft leak that sealed during the first year; and group III, persistent perigraft leak. Aortic minor and major diameters, perimeter, and area were measured at four locations: the celiac aorta, proximal neck, maximal aneurysm size, and distal neck. RESULTS: There were 32 men and two women, with a mean age of 73 +/- 8 years. In group I there were 20 patients (58%), and groups II and III had seven patients (21%) each. The overall mean aneurysm minor diameter decreased from 4.79 +/- 0.68 cm at implantation to 4.39 +/- 0.86 cm at 1 year (p < 0.0001). The aneurysm sac decreased by 0.63 +/- 0.58 cm in group I, and by 0.34 +/- 0.24 cm in group II. In group III, however, the aneurysm sac increased by 0.19 +/- 0.21 cm. Aneurysm size change did not correlate with inferior mesenteric or lumbar artery patency. The dimensions of the celiac aorta and proximal neck did not change significantly. However, diameter of the distal neck enlarged by 0.12 +/- 0.27 cm (p < 0.01). CONCLUSIONS: TPEG exclusion is associated with reduction of aneurysm size 1 year after implantation. Expansion of the aneurysms occurred with persistent perigraft leak. The aortic size at the celiac artery and proximal neck did not change. Dilation of the distal neck was minor but requires further long-term follow-up to determine clinical significance.

Aortic Aneurysm, Abdominal↗
PubMed1997

Elevations of tissue-type plasminogen activator and differential expression of urokinase-type plasminogen activator in diseased aorta.

PURPOSE: Elevations of plasmin have been implicated in the pathogenesis of abdominal aortic aneurysms (AAA) because of its ability to digest extracellular matrix proteins. Plasminogen activators regulate the conversion of plasminogen to plasmin. Tissue-type plasminogen activator (tPA) is more important in modulation of fibrinolysis, and urokinase-type plasminogen activator (uPA) is predominant in tissue remodeling. The purpose of this study was to determine the levels of plasminogen activators in diseased aorta because they may be responsible for the increased plasmin levels previously described in AAA. METHODS: Levels of tPA and uPA in AAA, occlusive, and normal (organ donor) aorta were studied in tissue explant supernatants. Supernatant tPA and uPA levels were measured with an enzyme-linked immunosorbent assay. Northern analysis was used to quantitate uPA messenger RNA (mRNA) levels in aortic tissue. RESULTS: Levels of tPA in the supernatants were similar in occlusive (20 +/- 4 ng/ml) and AAA (23 +/- 8) aorta, but threefold higher than in normal aorta (7 +/- 5; p < 0.005 for normal vs occlusive and p < 0.001 for normal vs AAA). In contrast, uPA supernatant levels were differentially expressed, with the highest level existing in AAA (9.7 +/- 2.7 ng/ml), followed by occlusive (4.9 +/- 3.5), and the lowest levels in normal aorta (1.2 +/- 0.7; p < 0.05 for normal vs occlusive, p < 0.001 for normal vs AAA, and p < 0.005 for occlusive vs AAA). Inhibition of protein or RNA synthesis by addition of cyclohexamide or actinomycin D, respectively, revealed no significant difference between treated and control supernatants, suggesting that the increases were caused by protein release rather than active synthesis. Levels of uPA mRNA followed the same trend as the supernatant uPA levels (AAA 1.07 +/- 0.54, occlusive 0.54 +/- 0.08, and normal aorta 0.01 +/- 0.01). CONCLUSIONS: Levels of tPA were similar in aneurysmal and occlusive aorta, but exhibited a threefold increase over normal aorta, suggesting that the elevations of tPA are associated with the arteriosclerosis present in both aneurysmal and occlusive disease. Differences in uPA levels were significant between all three groups, with the highest levels in AAA and the lowest levels in normal specimens. Northern analysis of uPA mRNA followed the same trend, suggesting that the increase in uPA may be regulated at the level of transcription. As uPA plays an important role in tissue remodeling, our findings may also reflect the relative tissue repair activities in these three types of specimens and may explain the previously reported increased levels of plasmin seen in AAA.

Adult↗
PubMed1997

Differential patterns of atherosclerotic disease in patients with unilateral hemiparesis resulting from poliomyelitis: case reports demonstrating the possible effect of hemodynamics.

The relative importance of hereditary and mechanical factors in the pathogenesis of aneurysms remains as controversial today as it was two decades ago. The cases of two patients with unilateral paresis resulting from poliomyelitis who presented with abdominal aortic aneurysms are reported. In addition, each patient had iliofemoral aneurysms contralateral to, and iliofemoral occlusive disease ipsilateral to, their affected extremity. The two cases detailed within this report suggest that hemodynamic forces may alter the pattern of disease in arteries affected by arteriosclerosis.

Aged↗
PubMed1997

Transcatheter embolization of a ruptured superior gluteal artery aneurysm: case report and review of the literature.

PURPOSE: To report the successful coil embolization of a true gluteal artery aneurysm and review therapeutic options for this rare condition. METHODS AND RESULTS: A ruptured superior gluteal artery aneurysm in a symptomatic 80-year-old man was successfully thrombosed by embolization using a combination of Gianturco coils and helical platinum microcoils. Six-month computed tomography demonstrated persistent thrombosis of the aneurysm and resolution of the perivascular blood. CONCLUSIONS: This report offers support for the use of catheter-based techniques as an alternative to standard surgical repair of gluteal artery aneurysms.

Aged↗
PubMed1996

Current management of visceral artery aneurysms.

BACKGROUND: Visceral artery aneurysms are an uncommon but important form of abdominal vascular disease. This study reviews a contemporary experience with special emphasis on newer methods of diagnosis and treatment. METHODS: From 1980 to 1994, 37 patients were diagnosed with 46 visceral artery aneurysms. These consisted of 22 splenic, 10 hepatic, 4 superior mesenteric, 2 gastroduodenal, 3 celiac, 2 left gastric, 1 pancreatoduodenal, 1 jejunal-ileal, and 1 inferior mesenteric artery aneurysms. Follow-up was complete for 28 patients, average of 37.7 months. There were 17 asymptomatic and 29 symptomatic aneurysms, including 11 presenting with rupture. RESULTS: Seventeen patients were treated surgically, with no surgical deaths. Surgical complications included splenic abscess (two) and failure to thrombose (one). Transcatheter embolization was used in 12 patients. Complications included splenic infarction (one) and recurrence (two), successfully treated with repeat embolization. Nine patients were treated with observation. Eight experienced no complications during follow-up; one died of a ruptured splenic artery aneurysm before treatment was initiated. CONCLUSIONS: The widespread use of computed tomography has led to increased detection of asymptomatic visceral artery aneurysms. Although surgery remains necessary in many patients, transcatheter embolization is effective in the treatment of selected visceral artery aneurysms with few complications and low recurrence.

Adult↗
PubMed1996

Plasminogen activator levels are influenced by location and varicosity in greater saphenous vein.

PURPOSE: The plasminogen system, which includes tissue type plasminogen activator (tPA), urokinase type plasminogen activator (uPA), and their main inhibitor, plasminogen activator inhibitor type 1 (PAI-1), plays a major role in both fibrinolysis and tissue remodeling. This study compares the levels of tPA, uPA, and PAI-1 at the groin and ankle in normal and varicose greater saphenous vein (GSV). METHODS: GSV was collected from patients undergoing varicose vein (VV) removal and from normal vein (NV) from arterial bypass procedures. Portions of the GSV at the groin and the ankle were minced and placed in serum-free media for 48 hours. Assays of the supernatants were obtained for tPA, uPA, and PAI-1 protein by enzyme-linked immunosorbent assay. Cyclohexamide and actinomycin D were also added to the media of the VV tissue explant supernatants to inhibit protein and RNA synthesis, respectively. RESULTS: Levels of tPA were significantly higher at the groin (11 +/- 2) than the ankle (5 +/- 1) in the VV (p < 0.005), and this trend was also seen in the NV (groin 10 +/- 2 and ankle 7 +/- 3). Levels of uPA were significantly higher in the groin VV (14 +/- 4.3) than in NV (3.0 +/- 0.8, p < 0.05). This difference, although not statistically significant, applied to the ankle as well (VV 14.5 +/- 6.3 and NV 5.3 +/- 2.7). No significant difference was seen between NV and VV for PAI-1 (NV, groin 155 +/- 73 and ankle 113 +/- 53, VV, groin 161 +/- 20 and ankle 142 +/- 38) or tPA. Inhibitor studies revealed no significant difference among control, cyclohexamide, and actinomycin D supernatants for tPA, suggesting release of protein rather than active synthesis. In contrast, inhibitor supernatants were significantly lower for uPA and PAI-1 than control supernatants (p < 0.05), suggesting that uPA and PAI-1 were actively synthesized. CONCLUSIONS: In the tissue explant supernatant model uPA and PAI-1 are actively synthesized, but tPA is not. Levels of PAI-1 were comparable in all four groups. Levels of uPA in the varicose GSV were higher than in NV, suggesting a role for uPA in the pathologic makeup of VV. Levels of tPA were higher at the groin versus the ankle position, potentially explaining the previously described increased fibrinolytic activity seen at the groin.

Aged↗
PubMed1996

Atherosclerotic plaque rupture in symptomatic carotid artery stenosis.

PURPOSE: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid plaques and to determine which characteristics are more commonly associated with plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS: Patients with symptomatic carotid artery disease were found to have more frequent plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic plaques and in only 32% of plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic plaques and in 48% of asymptomatic plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic plaques (84% vs 44% of asymptomatic plaques; p = 0.006). In addition, intraplaque fibrin was more common in symptomatic plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and plaque type (fibrous, necrotic, or calcified). CONCLUSIONS: As in the coronary artery system, rupture of the atherosclerotic plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the atherosclerotic plaque.

Aged↗
PubMed1996

Elevated levels of plasminogen-activator inhibitor type 1 in atherosclerotic aorta.

PURPOSE: Plasminogen activator inhibitor type I (PAI-1) inhibits the plasminogen activators that convert plasminogen to plasmin. In addition to initiating fibrinolysis, plasmin activates tissue matrix metalloproteinases, which cause degradation of the extracellular matrix (ECM) in the arterial wall. Elevated levels of PAI-1 ultimately decrease plasmin formation and may lead to an accumulation of ECM and arteriosclerosis. METHODS: PAI-1 was studied by four methods in atherosclerotic (aneurysmal and occlusive) and normal (organ donor) aorta: (1) PAI-1 secretion by tissue explant supernatants, including time course and inhibition studies; (2) tissue PAI-1 by protein extraction; (3) PAI-1 mRNA was quantitated by Northern analysis using glyceraldehyde-3-phosphate dehydrogenase to normalize for RNA loading; and (4) in situ hybridization was used to localize the cells that produced PAI-1 mRNA. RESULTS: Supernatant PAI-1 levels at 48 hours were 776 +/- 352, ng/ml in 11 atherosclerotic aortas and 248 +/- 98 ng/ml in 8 normal aortas (p < 0.005). Tissue PAI-1 levels per 100 mg of tissue were 99 +/- 58 ng in 11 atherosclerotic aortas and 38 +/- 20 ng in 5 normal aortas (p < 0.05). PAI-1 mRNA levels by Northern analysis were 0.91 +/- 0.49 in seven atherosclerotic aortas and 0.44 +/- 0.27 in five normal aortas. Supernatant time-course experiments revealed that PAI-1 increased over time. Inhibitor studies revealed that PAI-1 decreased to approximately one third of control values when cycloheximide or actinomycin D were added to the media, indicating that active synthesis of PAI-1 had occurred. In-situ hybridization localized PAI-1 mRNA predominately to endothelial cells and a few scattered vascular smooth muscle and inflammatory cells. Subgroup analysis revealed no statistically significant differences between aneurysmal and occlusive PAI-1 levels in any of the experiments. CONCLUSION: PAI-1 secretion, as measured by tissue explant supernatants, and total tissue PAI-1 in the protein extracts were significantly increased in atherosclerotic aorta. This elevation was also observed in the mRNA, which suggests that the increase is controlled at the level of transcription. PAI-1 mRNA was localized to endothelial, vascular smooth muscle, and inflammatory cells. We conclude that elevated levels of PAI-1 exist in diseased aorta. These elevated levels may lead to an accumulation of ECM, thereby contributing to the arteriosclerosis found in aortic occlusive and aneurysmal disease.

Adult↗
PubMed1996

Carotid endarterectomy. Lessons from intraoperative monitoring--a decade of experience.

OBJECTIVE: The authors analyzed a single institution's 10-year experience with intraoperative monitoring during 709 primary carotid endarterectomies and investigated the impact of contralateral internal carotid artery stenosis on carotid artery stump pressure (SP). SUMMARY BACKGROUND DATA: Stump pressure reflects the combination of contralateral carotid artery anatomy, collateral intracranial vasculature, and systemic blood pressure. By controlling for blood pressure with a stump index (SI) (SI = [SP/mean arterial pressure] x 100), a correlation between pressure and contralateral carotid artery anatomy can be demonstrated. Although the use of SP has long been advocated as an indicator of adequate cerebral perfusion, its correlation with perioperative complications while using an intraluminal shunt has not been evaluated completely. METHODS: From a series of 886 primary carotid endarterectomy cases, SP and mean arterial pressure were measured prospectively in 709 procedures. Temporary intraluminal shunts were used in cases with demonstrated contralateral carotid occlusion, prior cerebrovascular accident (CVA), or SPs less than 35 mmHg. Ipsilateral and contralateral angiographic degree of carotid stenosis was recorded at the time of the operation. Neurologic status was recorded prospectively for all 709 procedures. Operative electroencephalogram (EEG) changes and SP then were compared with the neurologic status of the patient in the perioperative period. RESULTS: The mean SP for the group (n = 709) was 46.7 +/- 15.3 mmHg (mean +/- standard deviation [SD]) with a mean SI of 54.9 +/- 22.6. The distribution for the SI is a more gaussian curve than that for SP. There were 19 ipsilateral CVAs (2.7%). The mean SP in the nonstroke group was 47.1 +/- 15.2 mmHg (mean SI = 54.7 +/- 16.5) compared with 31.9 +/- 13.2 mmHg (mean SI = 38.8 +/- 18.2) in the stroke group (P < 0.0001). Stroke rate for SP < or = 35 mmHg was 7% (13/185) versus 1.1% (6/524) for SP > 35 (p < 0.0001). Stump index and SP are related to contralateral carotid artery stenosis. The pattern of SI or SP versus contralateral stenosis is biphasic, with an increase at 75%. If SI is < or = 40, the mean contralateral stenosis is 55.1%; if SI is > 40, the mean contralateral stenosis is 35.1% (p < 0.05). Continuous EEG monitoring was completed for the 549 most recent operations. Patients who had a perioperative stroke had EEG changes observed during the procedure in only 6 of 12 cases (50% sensitivity), with 76% specificity. Using SP < or = 35 mmHg, sensitivity was 68% and specificity was 75%.

Aged↗
PubMed1996

Endothelial cell function: biologic and physiologic functions in health and disease.

Endothelial cells (EC) form a monolayer with a strategic role in the control of many physiologic and biologic pathways. Although the endothelium initially was thought to be an inert and passive barrier of the vasculature, the diverse functions of EC have been better defined in the past decade. EC play an important role in the control of coagulation, vasomotor tone, growth of vascular smooth muscle cells, white cell trafficking, ischemic and reperfusion injuries, and the development of arteriosclerosis. Owing to their location in the arterial tree, EC also are considered a potential target for gene therapy. The introduction of foreign DNA into EC by in vitro transfection with viral vectors has produced encouraging results when using genes that encode for proteins such as insulin and urokinase. The seeding of EC onto vascular grafts appears to convey the thromboresistant properties of saphenous vein to an artificial surface. This review focuses on the important biologic and physiologic functions of EC in health and disease.

Animals↗