Angioplasty and stenting for carotid lesions: an argument against.
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Biomedical subjects
Publications and source records attributed to J S Yao.
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PURPOSE: In carotid artery disease, correlation of carotid plaque morphology with the patient's presenting symptoms has drawn conflicting conclusions. The purpose of this series was to correlate carotid plaque characteristics with the presenting symptoms from a large cohort of patients who underwent operation for carotid artery disease. METHODS: From a series of 1252 consecutive patients who underwent carotid endarterectomy, presenting symptoms were divided into three groups: transiently symptomatic (transient ischemic attack [TIA] or amaurosis fugax), prior stroke, and asymptomatic. Plaque characteristics, including ulceration, intraplaque hemorrhage, and degree of stenosis, were recorded prospectively for 1008 procedures. All endarterectomy specimens were inspected during the procedure, and plaque characteristics were recorded immediately after operation. RESULTS: There was a higher incidence of plaque ulceration in the transiently symptomatic and prior stroke groups (391 of 508 [77%] and 91 of 115 [79%]) than in the asymptomatic cohort (231 of 385 [60%]; p < 0.0001, chi2 test). There was no significant difference in the incidence of plaque hemorrhage between the transiently symptomatic and prior stroke patients compared with the asymptomatic patients. There was no statistical difference for ulcerated plaque or plaque hemorrhage between the transiently symptomatic and prior stroke group. Intraplaque hemorrhage occurred more frequently in patients with high-grade stenosis (90% to 99%) than in those with less than 90% stenosis (202 of 299 [68%] versus 97 of 299 [32%]; p = 0.01, chi2 test). CONCLUSIONS: On gross examination of the carotid specimen in the operating room, plaque ulceration correlates with an initial presentation of amaurosis fugax, TIA, or prior stroke compared with patients operated on for asymptomatic disease. The presence of intraplaque hemorrhage is associated with more advanced stenosis of the internal carotid artery. These findings suggest that plaque morphology does play an important role in the presentation of carotid artery disease.
Arterial injury is infrequent in the thoracic outlet syndrome but must be identified to prevent these younger patients from being dramatically disabled. This requires thorough interview and clinical examination, and then pursuit with a workup including complete bilateral arteriography with positional views. Helical computed tomography (CT) provides precise localization of arterial trauma with correlation to specific compressive elements. Unique features in athletes include a greater role of soft tissue hypertrophy and overuse in pathogenesis of arterial injury, more frequent compression of the axillary artery and its branches, and possible hand ischemia from direct trauma. In addition, these prospective or established professionals require optimum arm function to sustain their careers. Because of the desire to continue provocative arm use, decompression is performed early, and arm "claudication" is surgically treated. Operations are customized to achieve adequate decompression without compromising function. Surgical management consists of targeted resection of compressing structures, which is most often a cervical rib; arterial reconstruction to eliminate stenosis and the source of emboli; and improvement of distal perfusion with selection from an arsenal that includes catheter embolectomy, thrombolysis, and bypass grafting. Familiarization with the many unique diagnostic aspects and therapeutic options in arterial thoracic outlet syndrome produces excellent results in all but the most advanced cases.
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.
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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.
PURPOSE: Venous malformations (VMs) may be discrete or extensive, and larger lesions may be difficult to remove with surgery. Incompletely removed lesions have a tendency to recur. We report our experience with ethanol ablation of VMs. METHODS: All 12 patients (seven women; mean age, 37 years) were evaluated with magnetic resonance imaging before treatment. A total of 19 prior surgical excisions had been performed for seven of the patients. Symptoms were present in all 12 patients and included bleeding, pain, swelling, and limitation of exercise. The VMs were present in the lower extremities of seven patients, in the upper extremities of three patients, and in the flank and buttocks in two patients. RESULTS: The 12 patients have undergone 30 injection procedures, with six patients requiring one, three patients requiring two, two patients requiring three, and one patient having undergone 12 treatments. General anesthesia was used in 11 patients. Blood loss was minimal for all procedures, and 28 of the 30 procedures were technically successful. Skin ulceration was seen in approximately half of the treated VMs, all of which healed with local wound care. Focal VMs were injected in six patients and resolved with a single treatment in five patients. Patients were free of symptoms at a mean follow-up of 10 months. Extensive VMs were injected for discrete, symptomatic areas in five patients. These lesions all regressed and were asymptomatic at a mean follow-up of 23 months in all but one patient. However, these lesions required multiple treatments as additional areas became problematic. CONCLUSIONS: Ethanol sclerosis is a well-tolerated, safe, and effective adjunct to the management of VMs. Advantages of ethanol injection include the ability to treat a very localized area without an incision. Conversely, extensive lesions may be palliated as symptoms occur.
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.
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.
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.
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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.
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.
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.
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.
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%.
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.
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