Thrombus generation after adenovirus-mediated gene transfer into atherosclerotic arteries

Thrombosis represents a major issue during arterial local delivery. We evaluated the occurrence of thrombosis after adenovirus (Ad)-mediated gene transfer into normal and atherosclerotic arteries. A replication-deficient Ad vector expressing the beta-galactosidase reporter gene (Ad.RSV betagal; 4 x 10(9) PFU) was injected into normal and atherosclerotic arteries (n = 11 in both groups). The contralateral artery received either an Ad vector carrying no transgene (Ad.MLPnull) (n = 7 in both groups, 4 x 10(9) PFU) or vehicle buffer (n = 4 in normal group, n = 8 in atherosclerotic group). Animals were sacrificed 3 days following gene transfer for thrombus detection and assessment of beta-galactosidase activity. Thrombus was absent in normal arteries and in atherosclerotic arteries injected with vehicle buffer only. In contrast, nonocclusive thrombus was present in atherosclerotic arteries injected with either Ad.RSV betagal (5 of 11) or Ad.MLPnull (3 of 7). Beta-galactosidase activity was predominantly found in the endothelial layer of the transfected arteries. Gene transfer and expression occurred despite the presence of the thrombus (4 of 5), and its efficiency did not significantly differ regardless of the thrombus. We conclude that thrombus frequently occurred in atherosclerotic arteries after Ad-mediated gene transfer. Further studies are warranted to identify the mechanisms of thrombus generation after Ad-mediated gene transfer into atherosclerotic arteries.     

Platelet GPIIb/IIIa receptor inhibition by SC-49992 prevents thrombosis and rethrombosis in the canine carotid artery

OBJECTIVE: Platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptors represent the final common pathway for aggregation. GPIIb/IIIa inhibition with antibodies or RGD peptides prevents arterial thrombosis. The present study examined the ability of SC-49992 (SC), a GPIIb/IIIa receptor antagonist, to prevent thrombosis in a canine model of carotid artery thrombosis. METHODS: Both carotid arteries of anaesthetised dogs were instrumented with Doppler probes. A 300 microA current was applied to the intimal surface of the right carotid artery via an intraluminal electrode; time to occlusive thrombus formation was noted. SC (30 and 60 micrograms/.kg-1 x min-1, intravenously) or saline was infused for 240 min. The procedure for thrombus formation was repeated after 60 min of drug infusion for the left carotid artery. RESULTS: SC did not alter heart rate or blood pressure. Frequency of occlusive thrombus formation was reduced or prevented in a dose dependent manner (control = 100%, n = 12; SC 30 micrograms = 50%, n = 6; SC 60 micrograms = 0%, n = 6; p < 0.05). SC resulted in a reduction in thrombus weight (p < 0.05) v control. Ex vivo platelet aggregation to ADP and arachidonic acid was inhibited. Platelet reactivity remained inhibited 60 min after cessation of SC infusion. In a second group of animals, a carotid artery thrombus was formed and lysed with administration of anisoylated plasminogen streptokinase activator complex (0.05 U.kg-1). SC (60 micrograms.kg-1 x min-1, intravenously, n = 6) or saline (n = 6) was infused for 240 min. In dogs receiving saline there was an 83% rate of rethrombosis; none of the SC treated animals had reocclusion after recanalisation (p < 0.05). CONCLUSIONS: SC-49992 inhibits ex vivo platelet aggregation, prevents occlusive thrombus formation in a canine model of arterial thrombosis, and prevents rethrombosis after thrombolysis. The data are consistent with results obtained with murine monoclonal antibodies directed against the platelet GPIIb/IIIa receptor.     

An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange

This study was designed to measure circulating hepatocyte growth factor (HGF) in a rat model of arterial thrombosis. The carotid endothelial surface of rats was denuded with a balloon catheter and partially occluded. The amount of thrombus formation was expressed as the difference between the wet weights of paired treated and nontreated carotid arteries. Thrombus weight increased gradually up to 60 min after denudation. Plasma HGF did not increase before 30 min, but had significantly increased by 60 min compared with all previous measurements (p<0.05). Measurements of circulating HGF may be useful in the early diagnosis of arterial thrombosis.     

Reduced endothelial nitric oxide synthase expression and production in human atherosclerosis

BACKGROUND: NO regulates vascular tone and structure, platelets, and monocytes. NO is synthesized by endothelial NO synthase (eNOS). Endothelial dysfunction occurs in atherosclerosis. METHODS AND RESULTS: With a porphyrinic microsensor, NO release was measured in atherosclerotic human carotid arteries and normal mammary arteries obtained during surgery. eNOS protein expression was analyzed by immunohistochemistry. In normal arteries, the initial rate of NO release after stimulation with calcium ionophore A23187 (10 micromol/L) was 0.42+/-0.05 (micromol/L)/s (n=10). In contrast, the initial rate of NO release was markedly reduced in atherosclerotic segments, to 0.08+/-0.04 (micromol/L)/s (n=10, P<0.0001). NO peak concentration in normal arteries was 0.9+/-0.09 micromol/L (n=10) and in atherosclerotic segments, 0.1+/-0.03 micromol/L (n=10, P<0.0001). Reduced NO release in atherosclerotic segments was accompanied by marked reduction of immunoreactive eNOS in luminal endothelial cells, although specific endothelial cell markers (CD31) were present (n=13). Endothelial cells of vasa vasorum of atherosclerotic segments, however, remained positive for eNOS, as was the endothelium of normal arteries. CONCLUSIONS: In clinically relevant human atherosclerosis, eNOS protein expression and NO release are markedly reduced. This may be involved in the progression of atherosclerosis.     

TP-9201, a glycoprotein IIb/IIIa platelet receptor antagonist, prevents rethrombosis after successful arterial thrombolysis in the dog

BACKGROUND AND PURPOSE: We examined the ability of TP-9201, a platelet glycoprotein IIb/IIIa receptor antagonist, to prevent carotid artery rethrombosis in the anesthetized dog. METHODS: Occlusive thrombosis was induced by electrolytic injury of the left carotid artery. Thirty minutes later, 0.05 U/kg of anisoylated plasminogen streptokinase activator complex (APSAC) was infused locally to achieve clot lysis. Carotid artery recanalization was followed immediately by the infusion of either saline (10 mL/h, 240 minutes; n = 9), low-dose TP-9201 (120 micrograms/kg plus 3 micrograms.kg-1.min-1, 240 minutes; n = 7), or high-dose TP-9201 (185 micrograms/kg plus 5 micrograms.kg-1.min-1, 240 minutes; n = 7). Ex vivo platelet aggregation responses to ADP or arachidonic acid were determined. RESULTS: TP-9201 produced complete inhibition of platelet aggregation in citrated platelet-rich plasma but a partial and dose-dependent inhibition in heparinized platelet-rich plasma. A twofold and eightfold increase in the template bleeding time was associated with the infusion of low-dose and high-dose TP-9201, respectively. There were frequent cyclic flow reductions in both the saline and low-dose TP-9201-treated groups after thrombolysis. However, the high-dose TP-9201-treated group exhibited a sustained flow with minimal evidence of cyclic flow reductions. At the conclusion of the protocol, patent vessels were found more frequently in the high-dose TP-9201 (5/7; P = .0048) than in the low-dose TP-9201 treatment group (2/7; P = .17) when compared with the saline group (0/9). Infusion of high-dose TP-9201 was associated with a significant reduction in the thrombus mass as compared with the control vessels. CONCLUSIONS: Administration of TP-9201 in conjunction with successful thrombolysis inhibited ex vivo platelet aggregation and prevented rethrombosis of the canine carotid artery. This study demonstrates that TP-9201, an inhibitor of the platelet GPIIb/IIIa receptor, can inhibit platelet-vessel wall interaction and thus prevent rethrombosis.     

Does antithrombotic therapy influence residual thrombus after thrombolysis of platelet-rich thrombus? Effects of recombinant hirudin, heparin, or aspirin

BACKGROUND: Thrombolysis to normal flow in patients with acute myocardial infarction preserves left ventricular function and decreases mortality. Failure of early reperfusion, reocclusion, or residual thrombus may be due to concurrent activation of the platelet-coagulation system. Thus, we hypothesized that the best concomitant antithrombotic therapy (recombinant [r]-hirudin, heparin, or aspirin) will maximally accelerate thrombolysis by r-tissue-type plasminogen activator (rTPA) and reduce residual thrombus. METHODS AND RESULTS: Occlusive thrombi were formed in the carotid arteries of 29 pigs (by balloon dilatation followed by endarterectomy at the site of injury-induced vasospasm) and matured for 30 minutes before rTPA was started, with or without antithrombotic therapy. Thrombolysis was assessed with the use of angiography and measurement of residual thrombus. Pigs were allocated to one of five treatments: placebo, rTPA, rTPA plus r-hirudin, rTPA plus heparin, or rTPA plus intravenous aspirin. No placebo-treated pig reperfused. Two of six animals treated with rTPA alone reperfused compared with seven of seven animals treated with rTPA plus r-hirudin (reperfusion time, 33 +/- 10 minutes), six of seven animals treated with rTPA plus heparin (reperfusion time, 110 +/- 31 minutes), and two of six animals with rTPA plus aspirin. The activated partial thromboplastin time was prolonged in only the rTPA plus r-hirudin group (25 +/- 0.1 times baseline) and the rTPA plus heparin group (5.3 +/- 0.2 times baseline). Residual 111In-platelet and 125I-fibrin(ogen) depositions were lower in the heparin-treated group and lowest in the r-hirudin-treated group (heparin versus hirudin, respectively; incidence of residual macroscopic thrombus was six of six animals versus two of seven [P = .01]; 125I-fibrin(ogen), 170 +/- 76 versus 48 +/- 6 x 10(6) molecules/cm2 [P = .02]; 111In-platelets, 47 +/- 15 versus 13 +/- 2 x 10(6)/cm2, P = .10). No pigs developed spontaneous bleeding. CONCLUSIONS: Thrombin inhibition with heparin or r-hirudin significantly accelerated thrombolysis of occlusive platelet-rich thrombosis, but only the best antithrombotic therapy (r-hirudin) eliminated or nearly eliminated residual thrombus.     

Experimental creation of fusiform carotid artery aneurysms using vein grafts in rats

OBJECTIVE: We developed an in vivo model of growing fusiform aneurysms, using vein grafts to the rat carotid artery. This aneurysm model might demonstrate the pathological features of the development and growth of aneurysms to become giant aneurysms. METHODS: Placement of an interposed femoral vein graft to restore carotid artery flow was performed in Wistar rats. On Day 21, 75% of the grafts (mean diameter, 1.6 mm) were found to be dilated to resemble fusiform aneurysms (mean diameter, 5.82 mm), and 53% of these were giant. Quantitative analysis of the histological findings was performed using image-analyzing software. RESULTS: Histological findings were similar to those for human intracranial giant aneurysms. The average length of the initial grafts in the aneurysm group was 9.1+/-1.9 mm, and grafts were significantly longer and more tortuous than in the normal graft group (6.4+/-0.8 mm) (P = 0.01). Cross-sectional areas of the aneurysms (mean, 18.9 mm2) were significantly correlated with the following: 1) the area of intra-aneurysmal thrombosis (mean, 11.1 mm2) (P < 0.0001); 2) the number of intrathrombotic vascular channels (P = 0.005); and 3) the area of dissection, with hemorrhage, between the thrombus and the wall of the aneurysm (mean, 0.72 mm2) (P = 0.0013). Scanning electron microscopic examination showed evidence of endothelial damage associated with growth of the aneurysms. CONCLUSION: Recurrent hemorrhaging from intrathrombotic vascular channels caused dissection between the thrombus and the aneurysm wall, which led to growth of the experimental aneurysms to giant aneurysms. With this model, we demonstrated the growth mechanism of giant fusiform aneurysms.     

Percutaneous creation of acute type-B aortic dissection: an experimental model for endoluminal therapy

PURPOSE: To evaluate the feasibility of a percutaneously created type-B aortic dissection as an experimental model for percutaneous therapy. This model was used to evaluate the hemodynamic effects of single-balloon fenestration of the intimal flap. MATERIALS AND METHODS: Acute type-B dissections were created in descending aortae of 15 swine via a femoral (n = 6) or carotid (n = 9) approach. The initial subintimal tear was made with use of a Colapinto needle. The dissections were extended to a predefined position in the aorta. The proximal and distal tears were balloon dilated. The mural flap was balloon fenestrated in six animals, just above the celiac artery. Aortograms were obtained to establish the presence and extent of the dissection. Manometry was performed in both lumina to evaluate the hemodynamics of the dissected aorta and the effects of balloon fenestration in this model. Pathologic specimens were also examined. RESULTS: Creation of dissection was successful in 11 of 15 animals, with six developing true lumen narrowing (group A). The other five animals (group B) had flow in both lumina without evidence of true lumen narrowing. After the creation of a single-balloon fenestration in the group A swine, the arteriograms revealed no evidence of blood admixture between the true and false lumina, and there was no change in the intravascular pressures. Examination of the explanted aortae showed a more extensive circumferential dissection in group A animals as compared with group B. CONCLUSION: The percutaneously created acute type-B aortic dissection is a feasible model for experimentation. The hemodynamics of the aorta did not change after single-balloon fenestration in this model.     

Histologic and morphologic comparison of experimental aneurysms with human intracranial aneurysms

PURPOSE: Vein pouch aneurysms are the most commonly created experimental lesions in neuroendovascular research. We sought to determine whether an experimental aneurysm that is derived from a pancreatic elastase-digested arterial sac (EDASA) models the histology and morphology of human cerebral aneurysms more accurately than the vein pouch aneurysm does. METHODS: EDASAs were created in the common carotid arteries of four rabbits, and vein pouch aneurysms were created in the common carotid arteries of four pigs. Five recently ruptured human cerebral aneurysms were obtained at autopsy. Identical histologic preparations were made for all specimens, and a vascular pathologist performed blinded histologic analyses. Morphologic dimensions were measured with a micrometer at 40-fold magnification. RESULTS: In each human cerebral aneurysm, there was complete absence of internal elastic lamina and tunica media, and none showed evidence of mural inflammation or neointimal proliferation. Average wall thickness was 51 microm. All vein pouch aneurysms had a well-developed internal elastic lamina and tunica media, and all exhibited profound inflammation and neointimal proliferation. Average wall thickness was 290 microm. EDASAs were devoid of internal elastic lamina, their tunica medias were mildly atrophic, and the sac walls contained only mild inflammation and neointimal proliferation. Average wall thickness was 46 microm. CONCLUSIONS: EDASAs model the morphologic and histologic characteristics of human cerebral aneurysms more accurately than vein pouch aneurysms do.     

Meeting the challenge of diabetic blindness in the 90''s

We developed and characterized a model of global forebrain ischaemia in rats, permitting control of CBF at any desired ischaemic level with minimum surgery and without anticoagulation. Both common carotid arteries are occluded temporarily and systemic arterial pressure is lowered by pooling venous blood by lower body negative pressure with a cheap suction device. By measuring rCBF continuously (laser-Doppler-flowmetry) and regulating systemic arterial pressure, the model was used to automatically control cortical rCBF at predetermined ischaemic levels at 50, 30, 15, and 5% of normal rCBF (n = 5). When both common carotid arteries were occluded and systemic arterial pressure was lowered to 55 mmHg with hypobaric hypotension (n = 5), cortical CBF always fell to less than 5% of normal rCBF (n = 5). Prompt recirculation was achieved after reopening of the carotid arteries and return to normobaric body pressure. Hypobaric hypotension with bilateral common carotid occlusion requires only carotid surgery and measurement of systemic arterial pressure; it produces global forebrain ischaemia without anticoagulation as a true step function type insult. If rCBF is measured continuously, the model can be used to control ischaemic CBF to predetermined values.     

Role of carotid sonography as a first examination in the evaluation of patients with transient ischemic attacks and strokes: benefit in relation to age

PURPOSE: We studied the influence of age on the utility of carotid sonography in patients with transient ischemic attacks and strokes. METHODS: The results of Doppler ultrasound examinations of the carotid arteries in 613 consecutive patients with transient ischemic attacks (n = 450) or strokes (n = 163) were analyzed for different age groups. For each patient, the grade of stenosis was scored for the ipsilateral internal carotid artery. The results of the ultrasound examinations were correlated with angiographic findings and findings at endarterectomy. The extent of atherosclerosis for each age group was expressed as the ratio between the number of grade II-IV stenoses (> or = 50%) in the carotid arteries and the number of patients in that group ("atherosclerosis ratio"). RESULTS: Under the age of 40 years, high-grade atherosclerotic stenoses were not found. However, 3 relatively young patients had dissections of the internal carotid arteries. The atherosclerosis ratio exceeded 0.5 for age groups 65-69 years through 80+ years. Among the patients with high-grade stenoses, ischemic heart disease prevented endarterectomy in 63% of patients in age group 80+ years, 44% in age group 75-79 years, and 26% in age group 70-74 years. CONCLUSIONS: Carotid sonography did not detect any significant atherosclerotic changes in young patients but was useful for diagnosing other etiologies of ischemic cerebral disease, eg, carotid dissection. At the other end of the spectrum, the impact of carotid sonography on patient management appears to be limited in patients over the age of 70 years. Carotid sonography seems to be most useful for patients 40-69 years old.     

Morphology and function of preserved microvascular arterial grafts: an experimental study in rats

The aim of this study is to examine the morphology and function and small-caliber, arterial grafts after preservation in the University of Wisconsin solution (UW). Rat carotid arteries were stored in UW (n = 10) or in phosphate-buffered saline (PBS) (n = 10) for 1, 3, 7, and 14 days and were examined with light microscopy (LM) and scanning electron microscopy (SEM). Rat aortic preparations were stored in UW or PBS for 1 hour, 24 hours, 72 hours, 7 days, and 14 days and assessed for functional responses (stimulated contraction and endothelium-dependent relaxation). Segments (5 mm) of rat carotid arteries were stored in UW or PBS for 3 days, 7 days, and 14 days and orthotopically implanted as autografts and allografts. No immunosuppressive or anticoagulant agents were used. After 28 days of implantation, the grafts were assessed for patency and excised for LM and SEM. In UW, the endothelial layer remained intact up to 9 days of storage. In PBS, the endothelial layer showed deterioration after 1 day and was completely lost after 3 days. Functional responses were demonstrated to exist for as long as 7 days storage in UW. In PBS, no responses could be evoked after 24 hours storage. Autografts preserved in UW for 3 days (n = 6), 7 days (n = 6), and 14 days (n = 6) showed patency rates of 83.3%, 66.6%, and 66.6%, respectively, whereas patency rates of allografts were 66.6%, 33.3%, and 33.3%, respectively. Autografts stored in PBS for 3 days (n = 6), 7 days (n = 6), and 14 days (n = 6) showed patency rates of 33.3%, 33.3%, and 50%, respectively, whereas patency rates of allografts were 16.7%, 0%, and 33.3%, respectively. The UW preserved autografts showed normal morphology. All other groups showed vessel wall degeneration which in the allograft groups, were accompanied by lymphocellular infiltration. In conclusion, the endothelial layer and vessel wall of arteries are adequately preserved in UW. Functional responses are retained up to 14 days storage in UW, but, are lost after 24 hours storage in PBS. Autograft implantation studies accordingly show good performance of arterial segments preserved in UW, whereas allografts are subject to degradation as a result of rejection.     

Spontaneous dissection of cerebral arteries. I. Carotid arteries and their branches

Artery dissection means tearing apart of its layers by blood coming inside after endothelial damage. The authors describe the prevalence of that pathology of carotid, arteries (diagnosed rarely so far), pointing to early onset age and to its multifactorial aetiology and pathogenesis. They also outline the pathomechanism of the neurological symptoms and emphasize the variety of the clinical manifestations. The diagnostic possibilities of artery dissection are also presented.     

Magnetic resonance angiography demonstrates vascular healing of carotid and vertebral artery dissections

BACKGROUND AND PURPOSE: Dissection of the carotid and vertebral arteries is most accurately diagnosed with conventional angiography. MR techniques are sensitive for detecting the abnormalities associated with dissection but may lack specificity. We hypothesized that MR may be useful for serial monitoring of dissection and may therefore guide therapy. METHODS: All patients with angiographically proven carotid and/or vertebral artery dissection from July 1994 to June 1996 were followed for a median duration of 10.5 months. Of these 29 patients (44 vessels), 18 were concurrently evaluated with MR, and a target group of 9 patients (17 vessels) was prospectively followed with MR at 3-month intervals. RESULTS: In the 18 patients with both imaging studies at baseline, angiography revealed 30 dissected vessels while MR detected 27 (90%). In the target group of 9 patients, initial MR identified 15 of the 17 dissections diagnosed with angiography. Serial MR revealed complete healing in 5 vessels, improvement in 6 vessels, no change in 4 vessels, and worsening in 2 vessels. The radiographic features most likely to resolve were stenosis and mural hematoma, while occlusion and luminal irregularity tended to persist. Late ischemic events occurred in 2 patients, both with persistent MR evidence of dissection, one while subtherapeutic on warfarin therapy and the other occurring 1 week after warfarin was discontinued. CONCLUSIONS: MR is a reliable noninvasive method for following the vascular response to treatment and may guide the course of a clinical trial comparing medical therapies for carotid and vertebral artery dissection.     

A noninjury, diet-induced swine model of atherosclerosis for cardiovascular-interventional research

To investigate whether atherosclerotic vascular disease in the microswine model can be induced by atherogenic diet alone and does not require balloon injury or endothelial denudation as widely stated in the literature, 28 female Yucatan microswine were fed a high-fat, high-cholesterol diet, including 2% sodium cholate, for an average of 310 +/- 13 days. Four control swine were placed on a regular diet for an average of 287.2 +/- 7.8 days. Selective coronary arteriography and morphologic and histologic studies were performed at the end of this period. Coronary arteries were fixed in vivo by pressure perfusion of formalin. Angiograms and sequential histologic sections were reviewed by a double-blind team. The angiography did not show apparent disease in all vessels but generally revealed mild irregularity. Quantitatively, there was a 30.5 +/- 3.5% stenosis (mean +/- standard error, P < 0.05 vs. control) in left anterior descending (LAD), 40.7 +/- 4.5% of stenosis in right coronary artery (RCA) (P < 0.01 vs. control), and 24.8 +/- 3.7% of stenosis in left circumflex artery (LCX). The lesions were eccentric in 95% of LCA, 95.8% of RCA, and 75% of LCX, and the remainder were concentric lesions. Typical lesions were characterized by significant intimal proliferation, cholesterol clefts, necrotic cores, heavy extracellular fat deposition, and calcification. Control animals had only occasional, minimal intimal lipid deposition in coronary arteries. These findings suggest that the Yucatan microswine is an ideal coronary atherosclerosis animal model for vascular research. Lesions can be induced by atherogenic diet alone. Cholesterol uptake is increased by adding sodium cholate to the feed. Moreover, balloon injury of the intima or media is not required to induce significant atherosclerotic lesions in coronary arteries.     

Cervical reconstruction of the supra-aortic trunks: a 16-year experience

PURPOSE: The purpose of this study was to review 182 consecutive cervical reconstructions of supra-aortic trunks, which were performed over a 16-year period. METHODS: A total of 182 innominate, common carotid, or subclavian arteries were reconstructed with a cervical approach in 173 patients aged 23 days to 83 years. Indications included hemispheric (n = 79), vertebrobasilar (n = 56), upper extremity (24), and internal mammary/cardiac ischemia (n = 5), asymptomatic severe common carotid disease (n = 33), or other (n = 3). Primary atherosclerotic innominate (n = 6), common carotid (n = 84), and subclavian (n = 66) lesions underwent reconstruction. Thirty-one operations were performed for multiple trunk involvement, recurrent disease, arteritis, infection, dissection, coarctation, or aneurysm. There were 122 bypass grafting procedures (98 ipsilateral, 24 contralateral) and 60 arterial transpositions. RESULTS: One death (0.5%) and 7 nonfatal strokes (3.8%) occurred, none in patients who were asymptomatic. Perioperative morbidity included four asymptomatic occlusions (2%), 6 myocardial infarctions (3%), 10 pulmonary complications (5%), and 2 graft infections (1%). Follow-up periods ranged from 1 to 190 months (mean, 53 +/- 5 months). Nineteen patients (10%) were lost to follow-up. Fifty-seven late deaths occurred, most from cardiac causes. Seven reconstructions necessitated late revision. The cumulative primary patency rate at 5 and 10 years was 91% +/- 2% and 82% +/- 5%, respectively. The survival rate at 5 years was 72% +/- 4% and at 10 years was 41% +/- 6%. The stroke-free survival rate was 92% +/- 2% at 5 years and 84% +/- 2% at 10 years. CONCLUSION: Cervical reconstruction of symptomatic and asymptomatic supra-aortic trunk lesions carries acceptable death and stroke rates and provides a long-term patient benefit. This should be the preferred approach for asymptomatic lesions and for patients with significant comorbidity because it carries less morbidity than direct transmediastinal aortic-based reconstruction.     

Hepatic peribiliary cysts: multiple tiny cysts within the larger portal tract, hepatic hilum, or both

PURPOSE: To describe characteristic imaging features of hepatic peribiliary cysts. MATERIALS AND METHODS: Four patients with hepatic cysts in which the radiologic (n = 3) or histologic (n = 1) findings were consistent with peribiliary cysts of the liver (multiple small cysts seen exclusively in the larger portal tract, hepatic hilum, or both at gross examination and dilatations of extramural peribiliary gland at histologic examination) underwent computed tomography (CT) and ultrasound (US). In three patients, CT was performed after drip infusion of cholangiographic contrast material. RESULTS: Contrast material-enhanced CT clearly depicted many tiny cysts along the larger portal veins up to the third- or fourth-order branch (n = 3). US depicted multiple cysts in the echogenic portal tract definitely (n = 2) or equivocally (n = 2). On cholangiographic contrast-enhanced CT scans, cystic areas were located adjacent to or surrounding the bile ducts, and the possibility of biliary dilatation, communication, or both was disproved. CONCLUSION: Hepatic peribiliary cysts can be diagnosed with US and enhanced CT, especially with CT performed after administration of cholangiographic contrast material.     

Sublabial, transseptal, transsphenoidal approach to the pituitary region guided by the ACUSTAR I system

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.     

The dissected aorta: percutaneous treatment of ischemic complications--principles and results

PURPOSE: Describe the principles and results of percutaneous treatment of ischemic complications of aortic dissection. MATERIALS AND METHODS: Twenty-four patients with aortic dissection complicated by ischemic compromise of the liver or bowel (n = 15), kidney (n = 18), or lower extremity (n = 13) were evaluated by means of aortography, intravascular ultrasound, and manometry, and were treated percutaneously. Visceral arteries were classified as obstructed or nonobstructed. Obstruction was classified as static, in which the dissecting hematoma extended into and narrowed the lumen of a branch artery, or dynamic, in which the dissection flap prolapsed into the vessel origin or narrowed the true lumen (TL) above it. Treatment consisted of vascular stents alone (n = 4), or balloon fenestration (n = 20) without (n = 8) or with (n = 12) vascular stents. RESULTS: Obstruction was present in 77 arteries and was static in 12 arteries, dynamic in 45 arteries, static and dynamic in 17 arteries, and indeterminate in three arteries. Percutaneous treatment did not alter false lumen (FL) pressure, but reduced the peak systolic interluminal pressure gradient from 28 mm Hg to 2 mm Hg and restored flow in 71 of 77 arteries (92%). Six patients died within 30 days (25% operative mortality), none as a result of the procedure. Two additional patients died in follow-up from complications of an expanding FL. Technical complications in two patients due to altered hemodynamics after initial intervention were recognized and corrected percutaneously during the same procedure. CONCLUSIONS: Percutaneous fenestration and endovascular stent deployment are indicated to restore blood flow to arteries compromised by aortic dissection. The prognosis of patients is related to the ischemic injury sustained prior to the percutaneous interventional procedure and, in patients with acute type I dissection who have not undergone surgery, to the preoperative stability of the FL.     

Variations in breast cancer treatment by patient and provider characteristics

PURPOSE: To create a simple and reproducible model of chromic thrombosis for the evaluation of thrombolytic agents and devices. MATERIALS AND METHODS: A stenosis was created in the superficial femoral artery of domestic swine, and autologous blood clot was deposited above the stenosis. Follow-up last for up to 3 months. Degree of clot organization was determined at histologic examination. Two thrombolytic agents, urokinase and collagenase, were used to test this model. RESULTS: There was a 27% delayed recanalization rate with this model. At histologic examination, early thrombus organization was seen at the vessel periphery after 10 days. One-month-old thrombus was substantial but variable in amount. Three-month-old thrombus was completely organized. Neither urokinase nor collagenase proved effective against chronic clot in the doses and time course of this study. CONCLUSION: This simple method yields a chronic porcine clot in a reliable number of domestic swine in 1 month.