Long-term follow-up of fenestrated endovascular repair for juxtarenal aortic aneurysm.

BACKGROUND: Fenestrated endovascular aneurysm repair (FEVAR) is increasingly being used for juxtarenal aortic aneurysms. The aim of this study was to review long-term results and assess the importance of changing stent-graft design on outcomes. METHODS: This was a retrospective review of all patients who underwent FEVAR within a single unit over 12 years (February 2003 to December 2015). Kaplan-Meier analysis of survival, and freedom from target vessel loss, aneurysm expansion, graft-related endoleak and secondary intervention was performed. Comparison between outcomes of less complex grafts (fewer than 3 fenestrations) and more complex grafts (3 or 4 fenestrations) was undertaken. RESULTS: Some 173 patients underwent FEVAR; median age was 76 (i.q.r. 70-79) years and 90·2 per cent were men. Median aneurysm diameter was 63 (59-71) mm and median follow-up was 34 (16-50) months. The adjusted primary technical operative success rate was 95·4 per cent. The in-hospital mortality rate was 5·2 per cent; there was no known aneurysm-related death during follow-up. Median survival was 7·1 (95 per cent c.i. 5·2 to 8·1) years and overall survival was 60·1 per cent (104 of 173). There was a trend towards an increasing number of fenestrations in the graft design over time. In-hospital mortality appeared higher when more complex stent-grafts were used (8 versus 2 per cent for stent-grafts with 3-4 versus fewer than 3 fenestrations; P = 0·059). Graft-related endoleaks were more common following deployment of stent-grafts with three or four fenestrations (12 of 90 versus 6 of 83; P < 0·001). CONCLUSION: Fenestrated endovascular aneurysm repair for juxtarenal aneurysm is associated with few aneurysm-related deaths in the long term. Significant numbers of secondary interventions are required, but the majority of these can be performed using an endovascular approach.

Arrhythmogenic and metabolic remodelling of failing human heart.

Heart failure (HF) is a major cause of morbidity and mortality worldwide. The global burden of HF continues to rise, with prevalence rates estimated at 1-2% and incidence approaching 5-10 per 1000 persons annually. The complex pathophysiology of HF impacts virtually all aspects of normal cardiac function - from structure and mechanics to metabolism and electrophysiology - leading to impaired mechanical contraction and sudden cardiac death. Pharmacotherapy and device therapy are the primary methods of treating HF, but neither is able to stop or reverse disease progression. Thus, there is an acute need to translate basic research into improved HF therapy. Animal model investigations are a critical component of HF research. However, the translation from cellular and animal models to the bedside is hampered by significant differences between species and among physiological scales. Our studies over the last 8 years show that hypotheses generated in animal models need to be validated in human in vitro models. Importantly, however, human heart investigations can establish translational platforms for safety and efficacy studies before embarking on costly and risky clinical trials. This review summarizes recent developments in human HF investigations of electrophysiology remodelling, metabolic remodelling, and ß-adrenergic remodelling and discusses promising new technologies for HF research.

Anchoring barbs and balloon expandable stents: what is the risk of perforation and failed stent deployment?

PURPOSE: Balloon expandable stents may on occasion be deployed in close proximity to the anchoring barbs of endovascular grafts. The aim of this study was to determine the risk and effect of balloon perforation by anchoring barbs and to assess whether these risks are different if the balloon is protected by a covered stent mounted upon it. METHODS: A bench-top model was developed to mimic the penetration of anchoring barbs into the lumen of medium sized blood vessels. The model allowed variation of angle and depth of vessel penetration. Both bare balloons and those with covered stents mounted upon them were tested in the model to determine whether there was a risk of perforation and which factors increased or decreased this risk. RESULTS: All combinations of barb angle and depth caused balloon perforation but this was most marked when the barb was placed perpendicular to the long axis of the balloon. When the deployment of covered stents was attempted balloon perforation occurred in some cases but full stent deployment was achieved in all cases where the perforation was in the portion of the balloon covered by the stent. The only situation in which stent deployment failed was where the barb was intentionally placed in the uncovered portion of the balloon. This resulted in only partial deployment of the stent. CONCLUSIONS: Balloon rupture is a distinct possibility when deploying balloon-expandable stents in close proximity to anchoring barbs. Care should be taken in this circumstance to ensure that the barb is well away from the uncovered portion of the balloon.

Fascial closure following percutaneous endovascular aneurysm repair.

INTRODUCTION: There are potential benefits of percutaneous over open femoral access for endovascular aneurysm repair (EVAR). Subsequent arterial closure using percutaneous devices is costly, whilst open repair risks potential wound complications and delayed discharge. The technique of fascial closure has perceived advantages but its efficacy is unclear. The aim of this study was to assess the safety and durability of fascial closure after EVAR. METHODS: Patients undergoing EVAR using devices up to 24 French were considered. Exclusion criteria included morbid obesity, high bifurcation, previous surgery, inadvertent high puncture, arteries < 5 mm and surgeon preference. The primary outcome measure was immediate technical success. All patients were followed-up clinically and with duplex at one and twelve months to determine secondary complications. RESULTS: Over a one-year period fascial closure of 69 common femoral arteries was attempted in 38 patients undergoing EVAR. Nine primary failures were due to haemorrhage in eight arteries and thrombosis in one artery; all had immediate, uncomplicated open revision. Of the 60 (87%) successful procedures, all had duplex surveillance at one month. Four pseudoaneurysms were identified, all treated conservatively. At one year, 61 fascial closures (88%) were imaged, four patients had died and two were lost to follow-up. Three of the pseudoaneurysms had resolved, the fourth patient had died (unrelated). No other complication attributable to fascial closure was found at either one or twelve months. CONCLUSION: Fascial closure is a safe, durable and cost-effective method of arterial closure following EVAR. Success and complication rates are comparable to other techniques.

Surveillance after EVAR based on duplex ultrasound and abdominal radiography.

INTRODUCTION: Computed tomography angiography (CTA) is considered the gold standard imaging technique for surveillance following endovascular aneurysm repair (EVAR). Limitations of CTA include cost, risk of contrast nephropathy and radiation exposure. A modified surveillance protocol involving annual duplex ultrasound (DUS) and abdominal radiography (AXR) was introduced, with CTA performed only if abnormalities were identified or DUS was undiagnostic. METHODS: Prospective records were maintained on patients undergoing infra-renal EVAR at a UK, tertiary referral centre. All patients enrolled with at least one-year follow-up were reviewed. Primary outcomes identified were aneurysm rupture and aneurysm-related complications. Secondary outcomes included number of CTAs avoided and cost. RESULTS: Median follow-up was 36 months (range 12-57) for 194 patients. The total number of sets of surveillance imaging was 412 of which 70 (17%) required CTA. Abnormalities were found in 30 patients, 18 confirmed by CTA. Eleven patients required secondary intervention, three initially identified by AXR, three by DUS, three by both DUS and AXR, and two by CTA following undiagnostic DUS. No patient presented with rupture or aneurysm-related complications not identified by modified surveillance. Mean annual savings were €223. CONCLUSION: EVAR surveillance based on DUS and AXR is feasible and safe. The complimentary nature of AXR and DUS is demonstrated.

Wholly endovascular repair of thoracoabdominal aneurysm.

BACKGROUND: The aim was to evaluate a wholly endovascular approach to the repair of thoracoabdominal aortic aneurysm (TAAA). METHODS: Six patients (median age 71 years) underwent wholly endovascular repair of TAAA (maximum diameter 56-85 mm) employing individually customized endografts. Procedures were performed under general anaesthesia, with spinal drainage in five patients. Patients were followed by serial computed tomography, plain radiography and duplex imaging for a median of 17 (range 8-44) months. RESULTS: All grafts were deployed as intended, with preservation of all target vessels. There were no postoperative deaths, strokes or paraplegia. One patient suffered a silent myocardial infarction. In two patients a persistent paraostial endoleak was treated by further balloon dilatation of the stent within the endograft fenestration. Imaging before discharge confirmed aneurysm exclusion in all patients. Two patients required late secondary intervention to abolish endoleaks due to side-branch disconnection. One patient suffered late occlusion of the coeliac axis without clinical sequelae, and late occlusion of a solitary renal artery in another resulted in dependence on dialysis. There have been no late deaths and all aneurysms remain excluded. CONCLUSION: Wholly endovascular TAAA repair is relatively safe, but long-term follow-up is required to establish its durability.

Fenestrated endovascular repair for juxtarenal aortic aneurysm.

BACKGROUND: The outcome of fenestrated endovascular aneurysm repair (F-EVAR) was evaluated. METHODS: Between February 2003 and December 2006, 45 patients (median age 73 (range 53-85) years) underwent primary (41) or secondary (four) F-EVAR for an abdominal aortic aneurysm with infrarenal neck anatomy unsuitable for a standard stent-graft. Median aneurysm diameter was 68 (range 55-100) mm and median infrarenal aortic neck length was 6 (range 0-13) mm. Customized fenestrated Zenith stent-grafts were employed in all procedures, incorporating fenestrations to preserve flow into renal (80), superior mesenteric (35) and coeliac (two) arteries. Eighty-two target vessels were stented (61 bare metal, 21 covered). RESULTS: All aneurysms were isolated successfully, with preservation of the target vessels. One accessory renal artery was lost. One patient died after 5 days from myocardial infarction, and another at 3 months from multiorgan failure secondary to atheroembolism. At median follow-up of 24 (range 1-48) months, all aneurysms were stable or shrinking, with no late ruptures or graft-related endoleaks. Six patients required a secondary intervention. The primary vessel patency rate was 96.6 per cent. There were four late deaths, unrelated to the aneurysm. CONCLUSION: F-EVAR enabled successful treatment of juxtarenal aortic aneurysm with a low complication rate.

Measurement of pulsatile haemodynamic forces in a model of a bifurcated stent graft for abdominal aortic aneurysm repair.

The longitudinal haemodynamic force (LF) acting on a bifurcated stent graft for abdominal aortic aneurysm repair has been estimated previously using a simple one-dimensional analytical model based on the momentum equation which assumes steady flow of an inviscid fluid. Using an instrumented stent-graft model an experimental technique was developed to measure the LF under pulsatile flow conditions. The physical stent-graft model, with main trunk diameter of 30mm and limb diameters of 12 mm, was fabricated from aluminium. Strain gauges were bonded on to the main trunk to determine the longitudinal strain which is related to the LF. After calibration, the model was placed in a pulsatile flow system with 40 per cent aqueous glycerol solution as the circulating fluid. The LF was determined using a Wheatstone bridge signal-conditioning circuit. The signals were averaged over 590 cardiac cycles and saved to a personal computer for subsequent processing. The LF was strongly dependent on the pressure but less so on the flowrate. The measured forces were higher than those predicted by the simplified mathematical model by about 6-18 per cent during the cardiac cycle. The excess measured forces are due to the viscous drag and the effect of pulsatile flow. The peak measured LF in this model of 30 mm diameter may exceed the fixation force of some current clinical endovascular stent grafts.

ß-adrenergic stimulation augments transmural dispersion of repolarization via modulation of delayed rectifier currents IKs and IKr in the human ventricle.

Long QT syndrome (LQTS) is an inherited or drug induced condition associated with delayed repolarization and sudden cardiac death. The cardiac potassium channel, IKr, and the adrenergic-sensitive cardiac potassium current, IKs, are two primary contributors to cardiac repolarization. This study aimed to elucidate the role of ß-adrenergic (ß-AR) stimulation in mediating the contributions of IKr and IKs to repolarizing the human left ventricle (n = 18). Optical mapping was used to measure action potential durations (APDs) in the presence of the IKs blocker JNJ-303 and the IKr blocker E-4031. We found that JNJ-303 alone did not increase APD. However, under isoprenaline (ISO), both the application of JNJ-303 and additional E-4031 significantly increased APD. With JNJ-303, ISO decreased APD significantly more in the epicardium as compared to the endocardium, with subsequent application E-4031 increasing mid- and endocardial APD80 more significantly than in the epicardium. We found that ß-AR stimulation significantly augmented the effect of IKs blocker JNJ-303, in contrast to the reduced effect of IKr blocker E-4031. We also observed synergistic augmentation of transmural repolarization gradient by the combination of ISO and E-4031. Our results suggest ß-AR-mediated increase of transmural dispersion of repolarization, which could pose arrhythmogenic risk in LQTS patients.

Swirling flow pattern in a non-planar model of an interposition vein cuff anastomosis.

One of the main causes of long-term failure of ePTFE grafts is the development of anastomotic intimal hyperplasia which leads to graft thrombosis. Experimental studies with bypass grafts have shown an inverse relationship between mean wall shear stress and intimal hyperplasia. The geometry of the anastomosis has a strong influence on the flow pattern and wall shear stress distribution. The aim of this in vitro study was to investigate the influence of non-planarity in a model of a distal anastomosis with interposition vein cuff, an anastomosis configuration that is increasingly being used because of improved clinical results. Laser Doppler anemometer measurements were carried out in silicone rubber models of interposition vein cuff anastomoses with planar and non-planar inflow. The pulsatile flow waveforms were typical of those found in femoro-infrapopliteal bypass. Axial and radial velocities were measured in the proximal and distal outflow segments. As expected a symmetrical helical flow pattern (Dean flow) was evident in the planar model. The model with non-planar inflow, however, gave rise to swirling flow in both the distal and proximal artery outflow segments for during the systolic phase. In patients, the anastomosis is usually non-planar. Since the configuration depends in part upon the tunnelling of the graft, this may be altered to some extent. Non-planar anastomotic configurations induce a swirling flow pattern, which may normalise wall shear stress, thereby potentially reducing intimal hyperplasia.

p53 mutation and locoregional treatment failure in head and neck squamous cell carcinoma.

BACKGROUND: The p53 gene (also known as TP53) may be the most common genetic target involved in the malignant transformation of human cells. Direct sequence analysis has demonstrated that alteration of this gene occurs in approximately 45% of head and neck squamous cell carcinomas. The consequences of p53 mutations in these cancers with respect to tumor behavior and patient survival have not been rigorously determined. PURPOSE: We evaluated the implications of p53 mutations in relation to the control of locoregional disease and overall survival following radiation therapy. METHODS: Data from 110 consecutive patients with invasive disease who were treated with primary radiation therapy (given with curative intent) or with adjuvant radiation therapy (following complete surgical extirpation of gross disease) were included in the analysis. A 1.8-kilobase fragment of the p53 gene encompassing exons 5-9 was amplified from the DNA of stored (frozen) tumor specimens; the amplified DNA was cloned and sequenced by use of standard techniques. Overall survival and locoregional disease-free survival after the completion of radiation therapy were estimated by the Kaplan-Meier method; survival comparisons were made by use of the logrank test or proportional hazards regression models. Reported P values are two-sided. RESULTS: Fortyeight (44%) of the 110 tumors had cells bearing p53 mutations. The risk of locoregional recurrence following either primary or adjuvant radiation therapy was significantly greater (i.e., the time to recurrence was shorter) for patients whose tumors contained mutant p53 genes (univariate model hazard ratio [HR] for p53 mutation versus wild-type = 2.2; 95% confidence interval [CI] = 1.2-4.1; P = .02). The presence of regional lymph node metastases (presence versus absence, HR = 2.0; 95% CI = 1.0-4.2; P = .05) and treatment type (primary radiation therapy versus surgery plus adjuvant radiation therapy, HR = 2.3; 95% CI = 1.2-4.3; P = .01) were also associated with greater risks of locoregional failure. The presence of p53 mutations and lymph node metastases and treatment with primary, as opposed to adjuvant, radiation therapy remained significant risk factors in multivariate regression analysis. No relationship was demonstrated between p53 status and overall survival (mutant versus wild-type, HR = 1.1; 95% CI = 0.6-2.1; P = .66); however, a relationship was shown for tumor stage and overall survival (stages III and IV [more advanced] versus stages I and II [less advanced], HR = 3.3; 95% CI = 1.0-10.8; P = .05). Mutation of the p53 gene was not associated with patient age, sex, tumor stage, primary tumor site, regional lymph node status, degree of tumor cell differentiation, or treatment method. CONCLUSIONS: Mutation of the p53 gene is associated with an increased risk of locoregional failure in patients with invasive head and neck squamous cell carcinoma who are treated with radiation therapy.

Infrequent inactivation of the retinoblastoma gene despite frequent loss of chromosome 13q in head and neck squamous cell carcinoma.

Our recent allelic analysis of head and neck squamous cell carcinomas identified a high incidence of chromosomal loss on 13q. To further define an area of minimal loss, we tested 60 primary head and neck squamous cell carcinomas in 59 patients for loss of heterozygosity (LOH) by using 10 polymorphic microsatellite markers spanning the long arm of chromosome 13. We examined the same primary tumors for inactivation of the retinoblastoma (Rb) gene by immunohistochemical analysis of paraffin-embedded specimens. Thirty-one of 60 (52%) tumors demonstrated LOH in at least one 13q marker. Twenty-nine of 31 (94%) lost a portion of 13q that included D13s133, which lies just telomeric to the Rb gene at 13q14.3. However, immunohistochemical staining revealed absence of Rb protein in only 6 of these 31 tumors (19.4%) with LOH. All but one tumor without LOH on 13q displayed normal Rb protein staining. Although Rb may be inactivated by an unusual mechanism in some head and neck squamous cell carcinomas, our data suggest that another tumor suppressor gene locus at 13q14 is likely to be involved in head and neck tumor progression.

Technical advances in studying cardiac electrophysiology - Role of rabbit models.

Cardiovascular research has made a major contribution to an unprecedented 10 year increase in life expectancy during the last 50 years: most of this increase due to a decline in mortality from heart disease and stroke. The majority of the basic cardiovascular science discoveries, which have led to this impressive extension of human life, came from investigations conducted in various small and large animal models, ranging from mouse to pig. The small animal models are currently popular because they are amenable to genetic engineering and are relatively inexpensive. The large animal models are favored at the translational stage of the investigation, as they are anatomically and physiologically more proximal to humans, and can be implanted with various devices; however, they are expensive and less amenable to genetic manipulations. With the advent of CRISPR genetic engineering technology and the advances in implantable bioelectronics, the large animal models will continue to advance. The rabbit model is particularly poised to become one of the most popular among the animal models that recapitulate human heart diseases. Here we review an array of the rabbit models of atrial and ventricular arrhythmias, as well as a range of the imaging and device technologies enabling these investigations.

Impact of chromosome 14q loss on survival in primary head and neck squamous cell carcinoma.

We screened 73 primary head and neck squamous cell carcinoma (HNSCC) specimens for loss of heterozygosity (LOH) on chromosome 14q. Analysis of 20 polymorphic microsatellite markers identified 29 (40%) HNSCCs exhibiting LOH of 14q in at least one locus. Six tumors had probable monosomy of 14q, displaying allelic loss for all informative markers tested, and 23 demonstrated partial losses on 14q. Fine mapping with 1-10 additional markers revealed two poorly defined regions of loss (4-7 cM) at 14q13-21 and 14q31-32.1 in seven tumors. In 53 patients with previously untreated tumors treated with curative intent, LOH of 14q in these tumors correlated with poor survival. Compared to patients with tumors that retain heterozygosity of 14q, those with 14q LOH had a 3-fold increased risk of death in multivariate analysis (hazards ratio, 3.2; 95% confidence interval = 1.2-8.4). These data have confirmed a high frequency of chromosome 14q loss in HNSCC and suggest that LOH of any region on chromosome 14q is an indicator of poor outcome.

New generation dopaminergic agents. 6. Structure-activity relationship studies of a series of 4-(aminoethoxy)indole and 4-(aminoethoxy)indolone derivatives based on the newly discovered 3-hydroxyphenoxyethylamine D2 template.

A series of 4-(aminoethoxy)indoles 7 and a related series of 4-(aminoethoxy)indolones 8 were synthesized and evaluated for their affinity for both the high- and low-affinity agonist states (D2High and D2Low, respectively) of the dopamine (DA) D2 receptor. The 4-aminoethoxy derivatives (i.e., 7 and 8) were designed as bioisosteric analogues based on the phenol prototype 4. The indolones 8 were observed to have high affinity for the D2High receptor. Comparison of their previously reported chroman analogues with the more flexible 4-(aminoethoxy)indoles revealed the chroman analogues to be more potent, whereas little loss in D2High affinity was observed when comparing the 4-(aminoethoxy)indolones with their respective chroman analogues. Several regions of the phenoxyethylamine framework were modified and recognized as potential sites to modulate the level of intrinsic activity. A conformational analysis was performed and a putative bioactive conformation was proposed which fulfilled the D2 agonist pharmacophore criteria based on the McDermed model. Structure-activity relationships gained from these studies have aided in the synthesis of D2 partial agonists of varying intrinsic activity levels. These agents should be of therapeutic value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side effects associated with complete D2 agonism or antagonism.

New generation dopaminergic agents. 1. Discovery of a novel scaffold which embraces the D2 agonist pharmacophore. Structure-activity relationships of a series of 2-(aminomethyl)chromans.

A series of 2-(aminomethyl)chromans (2-AMCs) was synthesized and evaluated for their affinity and selectivity for both the high- and low-affinity agonist states (D2High and D2Low, respectively) of the dopamine (DA) D2 receptor. The 7-hydroxy-2-(aminomethyl)chroman moiety was observed to be the primary D2 agonist pharmacophore. The 2-methylchroman moiety was discovered to be an entirely novel scaffold which could be used to access the D2 agonist pharmacophore. Attaching various simple alkyl and arylalkyl side chains to the 7-hydroxy 2-AMC nucleus had significant effects on selectivity for the D2High receptor vs the 5HT1A and alpha 1 receptors. A novel DA partial agonist, (R)-(-)-2-(benzylamino)methyl)chroman-7-ol [R-(-)-35c], was identified as having the highest affinity and best selectivity for the D2High receptor vs the alpha 1 and 5HT1A receptors. Several regions of the 2-AMC nucleus were modified and recognized as potential sites to modulate the level of intrinsic activity. The global minimum conformer of the 7-hydroxy-2-AMC moiety was identified as fulfilling the McDermed model D2 agonist pharmacophoric criteria and was proposed as the D2 receptor-bound conformation. Structure-activity relationships gained from these studies have aided in the synthesis of D2 partial agonists of varying intrinsic activity levels. These agents should be of therapeutic value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side effects associated with complete D2 agonism or antagonism.

Gene mutations in saliva as molecular markers for head and neck squamous cell carcinomas.

BACKGROUND: Cancer is caused by the accumulation of mutations that activate proto-oncogenes and inactivate tumor suppressor genes. The result is a clonal expansion of genetically identical daughter cells that eventually become clinical malignancies. The specific mutations acquired by the progenitor cell are like a fingerprint carried by each cell of the tumor. These mutations can serve as very specific markers for the presence of tumor cells in a background of normal cells. METHODS: Mutations in the p53 gene recovered from head and neck squamous cell carcinomas were sequenced, and these altered DNA sequences were used retrospectively as tumor-specific genetic markers for cancer cells in the patient's saliva. Cloned p53 sequences amplified by the polymerase chain reaction from DNA extracted from banked preoperative saliva specimens were screened for the presence of tumor-specific mutations using radiolabeled oligonucleotide probes. RESULTS: We identified tumor-specific mutations in preoperative saliva samples of 5 of the 7 patients evaluated (71%). CONCLUSIONS: These results suggest a potential for clinical applications of this novel approach to cancer detection using gene mutations as molecular markers for carcinomas.

Outflow distribution at the distal anastomosis of infrainguinal bypass grafts.

Outflow distribution at the distal anastomosis of infrainguinal bypass grafts remains unquantified in vivo, but is likely to influence flow patterns and haemodynamics, thereby impacting upon graft patency. This study measured the ratio of distal to proximal outflow in 30 patients undergoing infrainguinal bypass for lower limb ischaemia, using a flow probe and a transit-time ultrasonic flow meter. The mean outflow distribution was approximately 75% distal to 25% proximal, with above knee anastomoses having a greater proportion of distal flow (84%) compared to below knee grafts (73%). These in vivo flow characteristics differ significantly from those used in theoretical models studying flow phenomena (50:50 and/or 100:0), and should be incorporated into future research.

The head and neck manifestations of mycosis fungoides.

Mycosis fungoides (MF) is a cutaneous T-cell lymphoma that may progress to involve lymph nodes, the spleen, and other visceral organs. We have retrospectively reviewed our 10-year experience with MF at the Johns Hopkins Hospital. Forty-five patients received treatment for MF between 1983 and 1992. Approximately 70% of the patients with MF presented with cutaneous or extracutaneous lesions of the head and neck. The head and neck manifestations, clinical assessment, and treatment of our patient population are presented. Mycosis fungoides is a potentially lethal disease that frequently involves the head and neck region and should be included in the differential diagnosis of cutaneous head and neck lesions.

Elective carotid artery resection for advanced squamous cell carcinoma of the neck.

The authors performed a retrospective review of their 10-year experience of carotid artery resection without revascularization for advanced squamous cell carcinoma of the neck. From 1982 to 1991, seven patients underwent elective carotid artery resection without reconstruction at the University of Colorado Health Sciences Center in Denver. A vascular clamp with gradual carotid occlusion was placed preoperatively on four patients and awake temporary balloon occlusion of the carotid was used on three patients. The primary lesions were three laryngeal carcinomas, two oral cavity carcinomas, and two hypopharyngeal carcinomas. All seven resected specimens showed invasion of the carotid fascia on pathological exam, while five specimens exhibited actual destruction of the arterial wall. Cerebrovascular accidents occurred in two patients (one immediate and one delayed), and the perioperative mortality was 29% (one cerebrovascular accident and one gastrointestinal bleed). The five remaining patients died of locoregional recurrence or metastatic disease within 1 year after their carotid artery resection. Resection of the common or internal carotid artery without reconstruction has a significant morbidity and mortality. This operation did not improve the long-term survival in our limited series of patients who presented with histologically proven invasion of the carotid artery.