PubMed Health⌕ Search

Biomedical subjects

J S Yao

Publications and source records attributed to J S Yao.

At least 19 recordsLinked to original sources
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

Feasibility of transgastric ultrasonography of the abdominal aorta.

PURPOSE: Transesophageal echocardiography provides detailed images of the thoracic aorta, but imaging of the abdominal aorta and its branches does not occur routinely when the transesophageal echocardiography transducer is advanced into the stomach. Transgastric aortic ultrasonography (TAUS) was investigated as an intraoperative procedure to determine whether transgastric imaging of the abdominal aortic, mesenteric, and renal arteries could be obtained and whether pathologic lesions of these arteries could be identified. METHODS: Twelve patients with diagnoses of aortic aneurysmal or occlusive disease, chronic mesenteric ischemia, or renal artery stenosis that required operative treatment were examined. Preoperative transabdominal duplex imaging was performed in all 12 patients. Transgastric B-mode and color-flow ultrasonography of the abdominal aorta and branches was performed as an intraoperative procedure with the patients under general anesthesia. After the abdomen was opened but before the vascular reconstruction was performed, the transesophageal transducer was advanced into the stomach and directed by the surgeon's hand to obtain an image of the underlying aorta and branches. TAUS images were compared with those obtained by standard transabdominal duplex imaging. RESULTS: TAUS provided high-resolution images of both aneurysmal and occlusive aortic disease. In all 12 cases the images of the aortic lumen, plaque, and thrombus obtained with TAUS had greater detail and better resolution than those obtained with transabdominal duplex imaging. The origins of the renal arteries were seen with TAUS in 23 of 24 cases, whereas transabdominal ultrasonography obtained images of the origins in only 6 of 24 cases (p < 0.01). In the five renal arteries and the one mesenteric artery with hemodynamically significant stenoses in which transabdominal ultrasonography identified the stenoses based on velocity criteria alone, TAUS visualized the occlusive plaque at the origin of the renal and mesenteric arteries. CONCLUSION: Intraoperative TAUS is feasible and may be useful for evaluating atherosclerotic disease of the abdominal aorta and renal arteries.

Adult↗
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

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

Interactions between PE2, E1, and 6K required for assembly of alphaviruses studied with chimeric viruses.

During the assembly of alphaviruses, a preassembled nucleocapsid buds through the cell plasma membrane to acquire an envelope containing two virally encoded glycoproteins, E2 and E1. Using two chimeric viruses, we have studied interactions between E1, E2, and a viral peptide called 6K, which are required for budding. A chimeric Sindbis virus (SIN) in which the 6K gene had been replaced with that from Ross River virus (RR) produced wild-type levels of nucleocapsids and abundant PE2/E1 heterodimers that were processed and transported to the cell surface. However, only about 10% as much chimeric virus as wild-type virus was assembled, demonstrating that there is a sequence-specific interaction between 6K and the glycoproteins required for efficient virus assembly. In addition, the conformation of E1 in the E2/E1 heterodimer on the cell surface was different for the chimeric virus from that for the wild type, suggesting that one function of 6K is to promote proper folding of E1 in the heterodimer. A second chimeric SIN, in which both the 6K and E1 genes, as well as the 3' nontranslated region, were replaced with the corresponding regions of RR also resulted in the production of large numbers of intracellular nucleocapsids and of PE2/E1 heterodimers that were cleaved and transported to the cell surface. Budding of this chimera was severely impaired, however, and the yield of the chimera was only approximately 10(-7) of the SIN yield in a parallel infection. The conformation of the SIN E2/RR E1 heterodimer on the cell surface was different from that of the SIN E2/SIN E1 heterodimer, and no interaction between viral glycoproteins and nucleocapsids at the cell plasma membrane could be detected in the electron microscope. We suggest that proper folding of the E2/E1 heterodimer must occur before the E2 tail is positioned properly in the cytoplasm for budding and before heterodimer trimerization can occur to drive virus budding.

Animals↗
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

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

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↗
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

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↗