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Biomedical subjects

W H Pearce

Publications and source records attributed to W H Pearce.

At least 73 records · Page 4Linked to original sources
PubMed1995

Simultaneous abdominal aortic aneurysm repair and nephrectomy for neoplasm.

BACKGROUND: Abdominal aortic aneurysm and renal neoplasm are occasionally discovered concurrently. Simultaneous operative therapy may be an effective alternate management strategy to a staged procedure. PATIENTS AND METHODS: The medical records of 10 consecutive patients undergoing abdominal aortic aneurysm repair and nephrectomy for renal neoplasm were reviewed. Data collected included mode of presentation, preoperative evaluation, renal pathology, and in-hospital morbidity and mortality. Long-term follow-up was obtained through office records and telephone contact. RESULTS: In 7 patients, the renal mass was identified during evaluation of abdominal aortic aneurysm. The aneurysm was identified during evaluation of hematuria in 2 patients. One patient was discovered to have both conditions simultaneously. All patients underwent successful aneurysm repair and nephrectomy. Pathology revealed 6 renal cell carcinomas, 2 complex cysts, 1 hemangiopericytoma, and 1 oncocytoma. Four patients have died in the follow-up period: 1 of metastatic cancer and 3 of unrelated causes. There have been no cases of graft infection. CONCLUSION: Simultaneous abdominal aortic aneurysm repair and nephrectomy for neoplasm is an appropriate management strategy for selected patients.

Adenoma, Oxyphilic↗
PubMed1995

Late survival risk factors for abdominal aortic aneurysm repair: experience from fourteen Department of Veterans Affairs hospitals.

BACKGROUND: This study evaluates late survival risk factors for patients who underwent elective abdominal aortic aneurysm surgical procedures performed at 14 Department of Veterans Affairs hospitals across the United States between 1985 and 1987. METHODS: Preoperative risk factors for a representative sample of 280 male veterans were obtained from an extensive Department of Veterans Affairs Office of Quality Management study and subsequent chart review. The National Death Index was used to determine survival through December 1991. RESULTS: Mortality at 30 days was 2.9%. Kaplan-Meier survival probabilities were 89% (+/- 2%) at 1 year and 64% (+/- 3%) at 5 years. Multivariate hazards models indicated significantly poorer survival for patients with age greater than 69 years, chronic obstructive pulmonary disease, cerebrovascular disease, and left ventricular hypertrophy. A history of coronary artery disease including previous myocardial infarction or bypass operation did not predict late survival for this cohort. CONCLUSIONS: Given the substantial burden of comorbidity of veterans who use Department of Veterans Affairs facilities, the overall survival experience of this all male cohort compares well with previously published series and with overall U.S. male life expectancy. The fact that a history of coronary artery disease did not predict survival for this cohort may be related to selection bias; however, a more likely explanation is the presence of unsuspected coronary disease among patients without a documented history of angina or myocardial infarction.

Age Factors↗
PubMed1995

Mesenteric artery bypass: objective patency determination.

PURPOSE: Many authors have reported extended relief of intestinal ischemia by use of a variety of reconstructive techniques, but all have relied on symptomatic follow-up. None have objectively measured patency rates. The purpose of this study was to determine the primary patency rates of bypass grafts placed for acute and chronic splanchnic atherosclerotic occlusive disease with use of objective follow-up with mesenteric duplex ultrasound scanning or arteriography. METHODS: Twenty-five consecutive patients (mean age 61, female/male ratio of 2.7:1) who underwent placement of 38 splanchnic bypass grafts (29 saphenous vein grafts, 9 polytetrafluoroethylene) (22 retrograde, 16 antegrade) for ischemic symptoms (9 acute ischemia: 16 chronic ischemia) between 1984 and 1994 were monitored with either duplex scanning (30 grafts) or arteriography. Life-table and log rank analysis were used to determine and compare graft patency. RESULTS: Three patients (12%, 2 acute ischemia and 1 chronic ischemia) died after operation. Six patients (30%) had significant morbidity (4 acute ischemia and 2 chronic ischemia). During follow-up from 1 to 136 months (mean 35 months), no patient died of bowel infarction or required revision for recurrent symptoms. Objective testing revealed three graft occlusions. Symptomatic follow-up had a sensitivity of only 33% for graft occlusion when compared with objective measurement. The life-table primary patency rate was 89% at 72 months. Life-table survival for the same patients was 75% at 36 months. Patency rates for antegrade (93% at 36 months) versus retrograde (95% at 36 months) bypass and saphenous vein grafts (95% at 36 months) versus polytetrafluoroethylene (89% at 36 months) were not significantly different (p = 0.47 and 0.43, respectively). Late patency rates of grafts placed for acute ischemia (92% at 36 months) versus chronic ischemia (89% at 36 months) were not significantly different (p = 0.77). CONCLUSION: Splanchnic bypass for mesenteric ischemia, with a primary patency rate of 89% at 72 months, is an extremely durable form of revascularization. Long-term patency of grafts placed for acute ischemia does not differ significantly from that of bypasses for chronic occlusion. Duplex scanning allows standardized objective periodic follow-up of splanchnic reconstruction. Objective assessment is critical to accurately measure visceral revascularization patency rates.

Acute Disease↗
PubMed1995

Surgical management of atheroembolization.

PURPOSE: Atheroembolization may cause limb loss or organ failure. Surgical outcome data are limited. We report the largest series of atheroembolization focusing on patterns of disease, surgical treatment and outcome. METHODS: One hundred patients (70 men), mean age 62 +/- 11 years, operated on for lower extremity, visceral, or nonthoracic outlet upper extremity atheroemboli were identified prospectively and monitored over a 12-year period. The atheroembolic source was localized by use of a combination of computed tomography scanning (n = 55), arteriography (n = 93), duplex scanning (n = 25), transesophageal echocardiography (n = 6), and magnetic resonance imaging (n = 4). Occlusive aortoiliac disease (47 patients) and small aortic aneurysms (20 patients; mean aneurysm size 3.5 +/- 0.8 cm) were the most common source of atheroemboli. Imaging studies revealed 12 patients with extensive suprarenal aortic thrombus. Correction of the embolic source was achieved with aortic bypass (n = 52), aortoiliac endarterectomy and patch (n = 11), femoral or popliteal endarterectomy and patch (n = 11), infrainguinal bypass (n = 3), extraanatomic reconstruction (n = 6), graft revision (n = 3), upper extremity bypass (n = 11), or upper extremity endarterectomy and patch (n = 3). RESULTS: All four deaths within 30 days and all seven deaths within the first 6 months after operation were among the 12 patients with suprarenal aortic thrombus. The cumulative survival probabilities for all patients at 1, 3, and 5 years were 89%, 83%, and 73%, respectively. After operation, nine patients required major leg amputations and 10 required toe amputations. Renal atheroemboli led to hemodialysis in 10 patients. Recurrent embolic events occurred in five of 97 patients monitored for a mean of 32 months. All five recurrences occurred in the first 8 months after operation. Three patients with recurrent emboli had suprarenal aortic disease, one of whom had undergone axillofemorofemoral bypass. Four of 15 patients receiving postoperative warfarin anticoagulation had development of recurrent embolism. Only one patient not receiving postoperative warfarin had a recurrent event (p < 0.05 by Fisher exact test). CONCLUSION: The atheroembolic source is the aorta or iliac arteries in two thirds of patients who underwent operation. Computed tomography scanning of the aorta is a useful diagnostic technique. The source of the emboli can be eliminated surgically with low mortality or limb loss rates except when the suprarenal aorta is involved.

Adult↗
PubMed1995

In situ localization and quantification of seventy-two-kilodalton type IV collagenase in aneurysmal, occlusive, and normal aorta.

PURPOSE: Seventy-two-kilodalton type IV collagenase (MMP-2), a potent collagenase and elastase, is present in inflammatory disease states and may be important in the pathogenesis of aortic aneurysms. Alteration in expression of MMP-2 or its inhibitor, the tissue inhibitor of metalloproteinases type two (TIMP-2), could increase extracellular matrix degradation and lead to aneurysm formation. The purpose of this study is (1) to measure relative tissue levels of MMP-2 and TIMP-2 mRNA in aneurysmal, occlusive, and normal human infrarenal aorta; (2) to test for expression by cultured aneurysmal and normal vascular smooth muscle cells (VSMCs); and (3) to identify, in situ, the cells responsible for mRNA production within aneurysmal, occlusive, and normal aortic wall. METHODS: Total RNA extracted from aneurysmal (n = 8), occlusive (n = 9), and normal (n = 7) tissue was subjected to Northern analysis. Signals for MMP-2 and TIMP-2 were normalized to alpha-tubulin. Mean values +/- SE were compared by use of analysis of variance. Aneurysmal and normal VSMCs were cultured, passaged, and grown to confluence before RNA extraction and Northern analysis. In situ hybridization with digoxigenin RNA probes localized cells responsible for MMP-2 and TIMP-2 mRNA production in histologic sections of aneurysmal (n = 7), occlusive (n = 4), and normal (n = 3) aorta. RESULTS: Tissue MMP-2 mRNA levels were significantly greater in aneurysmal aorta (1.032 +/- 0.164, n = 5) than in either occlusive (0.553 +/- 0.027, n = 4, p < 0.02) or normal aorta (0.230 +/- 0.038, n = 3, p < 0.002). Differences in TIMP-2 mRNA levels were not significant (aneurysmal aorta 0.207 +/- 0.042, n = 3; occlusive aorta 0.413 +/- 0.164, n = 3; normal aorta 0.260 +/- 0.079, n = 4; p = 0.34), although numbers were small. Cultured aneurysmal and normal VSMCs constitutively expressed both MMP-2 and TIMP-2. In situ studies colocalized tissue MMP-2 and TIMP-2 expression to VSMCs and macrophages surrounding inflammation in aneurysmal adventita, but to atherosclerotic plaque in occlusive aorta. CONCLUSIONS: MMP-2 and TIMP-2 are expressed in aneurysmal, occlusive, and normal aorta. MMP-2 expression is significantly greater in aneurysmal than in either occlusive or normal aorta. Cultured aneurysmal VSMCs constitutively express both MMP-2 and TIMP-2. Differential patterns of expression seen in situ and elevated tissue MMP-2 mRNA levels in aneurysmal versus occlusive aorta suggest that MMP-2 may be responsible for localized plaque remodeling in occlusive disease and for diffuse adventitial collagen and elastin destruction in aneurysms.

Aged↗
PubMed1995

Arterial injuries in the thoracic outlet syndrome.

PURPOSE: This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches. METHODS: Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers. RESULTS: Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months). CONCLUSION: Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome.

Adolescent↗
PubMed1995

Plasminogen activator and plasminogen activator inhibitor expression by normal and aneurysmal human aortic smooth muscle cells in culture.

OBJECTIVES: Matrix metalloproteinases may play a major role in aortic wall degeneration causing abdominal aortic aneurysm (AAA). Available plasmin, required for MMP zymogen activation, is regulated by plasminogen activators (uPA, tPA) and plasminogen activator inhibitors (PAI-1, PAI-2). To appraise the impact of these regulatory proteins on aortic wall degeneration, expression at the level of translation and transcription was determined in human aortic smooth muscle cell (SMC) cultures. METHODS: Explants were derived from aneurysmal aortic tissue (n = 6) and from three male organ donors. Cells were also stimulated with 0.1-1.0 ng/ml IL-1 beta. RESULTS: uPA antigen and tPA antigen in the conditioned medium (CM) of normal SMCs were not detectable but AAA SMCs produced uPA (values are given as median (interquartile range)), [1.97 ng/ml/10(6) cells (1.50-8.21)] and tPA [7.02 ng/ml/10(6) cells (6.20-14.90)]. uPA antigen was absent from normal SMC cell extract (CE) but present in small amounts in AAA SMC CE [0.80 ng/mg protein (0.40-1.24)]. tPA was detectable in the CE of normal SMCs [3.2 ng/mg protein (1.90-3.40)] but at a lower concentration than in AAA SMCs [13.14 ng/mg protein (7.20-27.00)] (p < 0.05). IL-1 beta suppressed production of uPA and tPA in both types of SMCs. The difference in baseline PAI-1 release from normal SMCs and AAA SMCs was not statistically significant. Selective upregulation of PAI-1 was observed for AAA SMC after IL-1 beta stimulation. Northern analysis of AAA SMCs grown in serum containing medium exhibited clear bands for uPA. CONCLUSIONS: Human AAA SMCs are a source of elevated plasminogen activators. In the absence of a reciprocal rise of PAI an imbalance is created favouring proteolysis.

Aged↗
PubMed1995

In situ localization and quantification of mRNA for 92-kD type IV collagenase and its inhibitor in aneurysmal, occlusive, and normal aorta.

Ninety-two-kilodalton type IV collagenase (MMP-9) is present in aortic aneurysms and may be important to the pathogenesis of this disease. Alteration in expression of MMP-9 or its inhibitor, the tissue inhibitor of metalloproteinase type 1 (TIMP-1), could increase degradation of extracellular matrix and lead to aneurysm formation. The purpose of this study was (1) to measure tissue levels of MMP-9 and TIMP-1 mRNA in aneurysmal (AAA), atherosclerotic occlusive (AOD), and normal (NL) human infrarenal aorta; (2) to test for their expression by cultured AAA and NL vascular smooth muscle cells (VSMCs); and (3) to locate in situ the cells responsible for mRNA production within AAA, AOD, and NL aortic wall. Total RNA extracted from AAA (n = 8), AOD (n = 8), and NL (n = 7) tissue was subjected to Northern analysis. Signals for MMP-9 and TIMP-1 were normalized to alpha-tubulin. Mean values +/- SEM were compared by ANOVA. NL and AAA VSMCs were cultured, passaged, and grown to confluence before RNA extraction and Northern analysis. In situ hybridization with digoxigenin-labeled RNA probes localized cells responsible for MMP-9 and TIMP-1 mRNA expression within sections of AAA (n = 5), AOD (n = 2), and NL (n = 2) aorta. MMP-9 mRNA levels were significantly greater in AAA (0.855 +/- 0.180) than NL (0.046 +/- 0.23) (P < .02), but differences between AOD (0.406 +/- 0.196) and AAA or AOD and NL were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Aneurysm↗
PubMed1994

The popliteal artery as inflow for distal bypass grafting.

OBJECTIVE: To examine the patency and limb salvage characteristics of the popliteal-distal artery saphenous-vein bypass in patients with minimal superficial femoral artery disease. DESIGN: A retrospective review. SETTING: A tertiary care university hospital in the Chicago, Ill, metropolitan area. PATIENTS: Fifty-two popliteal-distal artery saphenous-vein bypasses for occlusive disease were performed in 51 patients between 1980 and 1993. The mean age at operation was 62 years (range, 37 to 85 years); 34 patients (67%) were male, 45 (88%) were smokers, 44 (86%) had diabetes, and 34 (67%) had coronary disease. The primary indications for operation were gangrene (21 patients [41%]), ulcer (15 patients [29%]), and rest pain (16 patients [31%]). INTERVENTION: Bypass of diseased arterial segments was performed using popliteal-distal artery saphenous-vein bypass grafts. The proximal anastomoses were either to the above-knee popliteal artery (50%) or to the below-knee artery (50%), with outflow to tibial (79%) or pedal vessels (21%). MAIN OUTCOME MEASURES: Overall patient survival, limb salvage, and primary and secondary graft patency. RESULTS: Follow-up of graft patency ranged from 1 day to 11 years (mean follow-up, 2.7 years). The perioperative mortality was 2% and life-table survival was 94% at 1 year, 68% at 5 years, and 50% at 10 years. Primary patency was 90% at 1 month, 82% at 1 year, and 75% at 5 years. There were 14 primary graft failures, only two of which could be traced to progression of proximal disease; five failures occurred less than 30 days after operation. Six of these 14 patients contributed to secondary patency that was 96% at 1 month, 90% at 1 year, and 79% at 5 years. Limb salvage was 96% at 1 month, 90% at 1 year, and 87% at 5 years (seven major amputations were required). No significant differences in patency, limb salvage, or survival were observed on comparison of the level of the proximal or distal anastomosis, type of vein graft, or presence of comorbidities. CONCLUSIONS: We conclude that popliteal-distal artery bypass provides excellent patency and limb salvage for patients with severe ischemia. The use of a popliteal artery inflow source is preferable in patients with a paucity of venous segments since progression of proximal disease rarely leads to graft failure.

Adult↗
PubMed1994

Human atherosclerotic abdominal aortic aneurysms produce interleukin (IL)-6 and interferon-gamma but not IL-2 and IL-4: the possible role for IL-6 and interferon-gamma in vascular inflammation.

Immunological mechanisms play an important role in the pathogenesis of atherosclerosis and atherosclerotic abdominal aortic aneurysms (AAA). Inflammatory leukocytes invade the vessel wall and produce cytokines which perpetuate the immune events underlying these diseases. Interleukin (IL)-1 beta, IL-8, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1, among others, may play a role in the generation by AAA. The aim of this study was to investigate the possible pathogenetic role of other proinflammatory cytokines, namely IL-2, IL-4, IL-6, and interferon (IFN)-gamma. Enzyme-linked immunosorbent assay of human explant culture supernatants revealed a significant increase in IFN-gamma production by AAA compared to occlusive (atherosclerotic) or normal (NL) aortic explants. IL-6 production was also increased in AAA compared to NL aortic explant supernatants. Neither AAA nor NL aortic tissues produced IL-2 or IL-4 in the same culture system. These results suggest that IL-6, a cytokine involved in T and B lymphocyte activation during inflammation, and IFN-gamma, which stimulates T and B lymphocytes, macrophages, endothelial cells and fibroblasts, may play a role in the pathogenesis of various vascular inflammatory diseases such as AAA.

Aorta, Abdominal↗
PubMed1994

Gender differences in interventional management of peripheral vascular disease: evidence from a blood flow laboratory population.

Recent studies of gender differences in the treatment of coronary artery disease have concluded that female patients often receive less aggressive care than male patients. This study compares rates of lower extremity surgical and endovascular procedures by gender for peripheral vascular disease patients seen in the blood flow laboratory at our institution in 1987. Revascularization rates were compared for 192 female and 218 male patients with abnormal blood flow examinations and no prior lower extremity procedures. Female patients were older (3.3 years; p < 0.02), had a lower prevalence of ankle/brachial indices greater than 0.5 (64.2% of males vs. 51.8% of females; p < 0.01), a higher prevalence of hypertension (p < 0.03), and a lower prevalence of smoking (p < 0.02). No significant baseline differences were found for the prevalence of limb salvage indications or other comorbid conditions. A total of 41 women (21.4%) and 64 men (29.4%) underwent subsequent lower extremity surgical or endovascular procedures in 1987 (p = 0.08). Men had a significantly higher procedure rate among the 311 patients without limb salvage indications (p = 0.03). When statistically significant covariates such as limb salvage, age, ankle/brachial index, comorbidity, and smoking are controlled for in logistic regression analysis, men were found to have more than twice the chance of being selected for procedures (p = 0.009). Although limited to practice patterns at one institution, these results suggest that other centers should examine criteria for interventional therapy in mild-to-moderate peripheral vascular disease.

Aged↗
PubMed1994

The ankle-brachial index as a predictor of survival in patients with peripheral vascular disease.

OBJECTIVE: To determine whether the ankle-brachial index (ABI) predicts survival rates among patients with peripheral vascular disease. DESIGN: A retrospective survival analysis of patients with abnormal ABIs who visited the authors' blood-flow laboratory during 1987. The National Death Index was used to ascertain survival status for all patients up to January 1, 1992. Kaplan-Meier and Cox proportional hazards analyses were used to determine the relationship between increasing lower-extremity ischemia, measured by ABI, and survival time. Clinical characteristics controlled for included age, smoking history, gender, and comorbidities, as well as the presence of lower-extremity rest pain, ulcer, or gangrene. SETTING: A university hospital blood-flow laboratory. PATIENTS/PARTICIPANTS: Four hundred twenty-two patients who had no prior history of lower-extremity vascular procedures and who had ABIs < 0.92 in 1987. RESULTS: Cumulative survival probabilities at 52 months' (4.3 years') follow-up were 69% for patients who had ABIs = 0.5-0.91, 62% for patients who had ABIs = 0.31-0.49, and 47% for patients who had ABIs < or = 0.3. In multivariate Cox proportional hazard analysis, the relative hazard of death was 1.8 (95% confidence interval = 1.2-2.9, p < 0.01) for the patients who had ABIs < or = 0.3 compared with the patients who had ABIs 0.5-0.91. Other independent predictors of poorer survival included age > 65 years (p < 0.001); a diagnosis of cancer, renal failure, or chronic lung disease (p < 0.001); and congestive heart failure (p < 0.04). CONCLUSION: The ABI is a powerful tool for predicting survival in patients with peripheral vascular disease. Patients with ABIs < or = 0.3 have significantly poorer survival than do patients with ABIs 0.31-0.91. Further study is needed to determine whether aggressive coronary risk-factor modification, a work-up for undiagnosed coronary or cerebrovascular atherosclerotic disease, or aggressive therapy for known atherosclerosis can improve survival of patients with ABIs < or = 0.3.

Aged↗
PubMed1994

Utility of transesophageal echocardiography in the diagnosis of disease of the thoracic aorta.

PURPOSE: Transesophageal echocardiography (TEE) offers a rapid, minimally invasive method for diagnosing thoracic aortic disease. High-resolution images are possible because of the close proximity of the esophagus and vascular structures within the chest. Lung and chest wall components have little influence on the image quality and a virtually unobstructed view of the heart, thoracic aorta, and pulmonary vasculature is seen. The role of TEE in diagnosing diseases of the thoracic aorta is rapidly developing. The purpose of this study is to define the role of TEE in the diagnosis of thoracic aortic disease. METHODS: Between July 1, 1989 and December 31, 1992, 1005 TEEs were performed at our center. Of these, 199 (125 men, 74 women) were entered into our aortic disease registry. Indications for the studies included 37 referrals to rule out aortic dissection, 18 to assess aortic aneurysm, 55 to assess for an intraaortic source of embolus, 9 to rule out intraaortic thrombus, and 13 with familial hyperlipidemia being followed to mark response to low-density lipoprotein apheresis. In 67 cases, subclinical aortic plaquing was found incidentally. No complications from the TEE procedure were encountered. RESULTS: In cases of suspected aortic dissection, TEE was equal to computed tomography (CT) scanning in identifying the type (DeBakey) and extent of thoracic aortic dissection. In addition, TEE provided information regarding functional status of the aortic valve, identified interluminal communications, and assessed blood flow and thrombus burden in the false lumen. TEE correctly identified true aneurysms, intraluminal thrombus, and plaques as possible sources of emboli. One false-positive CT scan result for aortic dissection was seen and was ruled out both by TEE and angiography. CONCLUSION: Biplane TEE can be considered the method of choice in diagnosing disease of the thoracic aorta. Information from TEE can be obtained at the patient's bedside or in the operating suite, to assess surgical results before procedure termination and afterward for follow-up. Adjunctive magnetic resonance imaging, CT scanning, or aortography may be needed to assess extension of the disease process into the abdomen or pelvis or to plan surgical intervention.

Adult↗
PubMed1994

Femorofemoral bypass for aortofemoral graft limb occlusion: a ten-year experience.

PURPOSE: Aortofemoral bypass (AFB) is a durable reconstruction; however, graft limb occlusion occurs in 10% to 20% of patients and results in limb ischemia. Treatment of AFB limb occlusion has been debated, but many recommended femorofemoral bypass (FFB). FFB grafts have had excellent patency rates. The durability of FFB specifically for AFB limb occlusion has not been reported. This study retrospectively examined a 10-year experience with FFB for AFB limb occlusion to determine FFB performance. METHODS: Between 1982 and 1992, FFB was performed on occluded AFB limbs in 22 patients (14 men and 8 women). Reoperation was performed for disabling claudication in five cases, but the remaining 17 patients (77%) had critical limb ischemia. FFB originated from the contralateral patent AFB limb in all cases. Distal anastomosis was to the common femoral artery (n = 8) or the profunda femoris (n = 14). FFB graft patency was confirmed by direct Doppler arterial examination over a mean follow-up of 47 months. RESULTS: The cumulative life-table primary patency rate of FFB was 54% at 5 years. Reoperative procedures performed in nine cases resulted in a secondary patency rate of 84% at 5 years. The limb salvage rate was also 84% at 5 years, reflecting the impact of successful reoperation. Major amputations (two below-knee, one above-knee) were necessary in only three cases. There were no perioperative deaths after FFB, and the cumulative 5-year survival rate was 77%. CONCLUSION: Aortic graft limb occlusion occurs less frequently than failure of infrainguinal grafts making the success of specific reoperative strategies difficult to document reliably. This study suggests that FFB is a safe and durable alternative for AFB limb failure. An aggressive policy of reoperation has resulted in successful extension of FFB graft function and an excellent rate of limb salvage.

Aged↗
PubMed1994

Interleukin-1 beta induces differential gene expression in aortic smooth muscle cells.

PURPOSE: Abdominal aortic aneurysms are characterized by an accelerated turnover of extracellular matrix proteins and by an inflammatory infiltrate that releases the cytokines interleukin-1 beta and tumor necrosis factor-alpha. We examined the gene expression of human aneurysmal aortic smooth muscle cells and normal aortic smooth muscle cells after treatment with interleukin-1 beta and tumor necrosis factor-alpha by measuring the changes in smooth muscle cell collagen, elastin, collagenase, and tissue inhibitor of metalloproteinase messenger ribonucleic acid levels in response to these cytokines. METHODS: Biopsy of aneurysmal aorta (n = 6) and donor normal aorta (n = 3) was obtained at operation. Medial smooth muscle cells were cultured, passaged (P2 to P4), and incubated with 0, 10, 100, or 1000 pg/ml interleukin-1 beta, tumor necrosis factor-alpha, or platelet-derived growth factor for 24 hours. Total ribonucleic acid was harvested. Percentage changes in messenger ribonucleic acid from control levels for type I and type III procollagen, elastin, collagenase, 72 kDa type IV collagenase, tissue inhibitor of metalloproteinase-1, and tissue inhibitor of metalloproteinase-2 were measured by Northern hybridization. Analyses were performed with analysis of variance (p < 0.05). All comparisons between aneurysmal aortic smooth muscle cells and normal aortic smooth muscle cells represent comparisons between one aneurysmal aorta and one normal aorta. RESULTS: Added interleukin-1 beta resulted in significant, dose-dependent increases in the collagenase messenger ribonucleic acid level at all concentrations tested in both aneurysmal aorta and normal aorta. The increase in the collagenase messenger ribonucleic acid level ranged from a minimum increase of 123% for 10 pg/ml interleukin-1 beta in aneurysmal aortic smooth muscle cells to a maximum of 450% for 1000 pg/ml interleukin-1 beta in normal aortic smooth muscle cells. Interleukin-1 beta caused a significant decrease in the steady-state messenger ribonucleic acid levels for type 1 procollagen in both aneurysmal and normal aorta. The greatest reduction in type 1 procollagen messenger ribonucleic acid levels occurred at 100 pg/ml interleukin-1 beta in both aneurysmal aortic smooth muscle cells (-39%) and normal aortic smooth muscle cells (-48%). The only observed qualitative difference between aneurysmal aortic smooth muscle cells and normal aortic smooth muscle cells was the change in tissue inhibitor of metalloproteinase-1 messenger ribonucleic acid levels in response to added interleukin-1 beta. In aneurysmal aortic smooth muscle cells interleukin-1 beta at 1000 pg/ml significantly increased messenger ribonucleic acid levels by 82%, whereas levels of tissue inhibitor of metalloproteinase-1 messenger ribonucleic acid in normal aortic smooth muscle cells did not change in response to added interleukin-1 beta. Interleukin-1 beta did not alter messenger ribonucleic acid levels for type III procollagen, elastin, type IV collagenase, or tissue inhibitor of metalloproteinase-2 in aneurysmal aorta or normal aorta. When tumor necrosis factor-alpha or platelet-derived growth factor were added, this did not significantly change aneurysmal aortic smooth muscle cells messenger ribonucleic acid levels for collagenase, type IV collagenase, tissue inhibitor of metalloproteinase-1, tissue inhibitor of metalloproteinase-2, and type I and type III procollagen. CONCLUSIONS: These findings suggest that interleukin-1 beta, through its effect on smooth muscle cell collagenase and collagen gene expression, mediates the increased matrix turnover observed in aneurysms. Macrophages may induce changes in aortic smooth muscle cell gene expression in a paracrine manner that could lead to aneurysm formation.

Aged↗
PubMed1994

Intercellular adhesion molecule-1 (ICAM-1) expression and soluble ICAM-1 (sICAM-1) production by cytokine-activated human aortic endothelial cells: a possible role for ICAM-1 and sICAM-1 in atherosclerotic aortic aneurysms.

The interactions of inflammatory cells, cytokines, and cell adhesion molecules (CAM) may be important in the pathogenesis of vascular diseases such as abdominal aortic aneurysms (AAA), in which inflammation plays a role. The aim of this study was to investigate the pathogenic role of ICAM-1, a molecule involved in leucocyte-endothelial interactions, in vascular inflammation. ELISA of human explant culture supernatants revealed a four-fold increase in sICAM-1 production by AAA (n = 9) versus normal (n = 8) aortic explants. Human aortic endothelial cell (hAEC) culture was used for further studies as an in vitro model for aortic inflammatory conditions. Tumour necrosis factor-alpha (TNF-alpha) or IL-1 beta treatment of hAEC resulted in an up to 1.8-fold significant increase in sICAM-1 production compared with resting cells. In addition, the expression of ICAM-1 on cytokine-stimulated versus resting hAEC was measured by radioimmunoassay. TNF-alpha significantly induced ICAM-1 expression on these cells. These results suggest that different forms of ICAM-1, present on or released by the activated aortic endothelium, may be involved in leucocyte adhesion to and migration into the vessel wall.

Aorta, Abdominal↗
PubMed1994

Interleukin-8 and tumor necrosis factor-alpha are involved in human aortic endothelial cell migration. The possible role of these cytokines in human aortic aneurysmal blood vessel growth.

Angiogenesis, the growth and proliferation of blood vessels, may be important in the pathogenesis of atherosclerosis and thus in human atherosclerotic abdominal aortic aneurysms (AAAs). Endothelial migration or chemotaxis is a vital component of the angiogenic response. Here, human aortic endothelial cells (hAECs) were used to investigate the effect of AAA tissue supernatants on hAEC chemotaxis. AAA tissue conditioned media were found to be chemotactic for hAECs. We have previously shown that the angiogenic cytokines interleukin (IL)-8, and tumor necrosis factor (TNF)-alpha are present in AAAs and normal aortic explant conditioned media. Currently, we have found that basic fibroblast growth factor (bFGF) and platelet-derived growth factor can also be detected in these supernatants. In order to identify whether some of these soluble mediators contributed to the chemotactic activity of these supernatants, conditioned media were preincubated with either neutralizing anti-IL-8, anti-TNF-alpha, anti-bFGF antibodies or control serum. Anti-IL-8 and anti-TNF-alpha significantly inhibited AAA tissue supernatant-induced hAEC chemotaxis (p < 0.05), while anti-bFGF did not (p not significant). These results indicate that IL-8 and TNF-alpha may be important in chemotactic activity for hAECs in vitro and possibly in AAA neovascularization. The abrogation of angiogenesis using neutralizing antibodies may be a future goal in the therapy of certain disease states such as AAA where angiogenesis plays an important role.

Antibodies, Monoclonal↗