Carotid Bruit Research Articles

Primary care for tinnitus: practice and opinion among GPs in England

Rationale, aim and objectiveEffective tinnitus management starts with appropriate general practitioner (GP) triage, which in England can be guided by the Department of Health's Good Practice Guide (GPG). Despite the prevalence of the condition, there has never been a systematic survey of its management in primary care in England. We aimed to evaluate how people with tinnitus are assessed and managed in general practice, noting variation in practice across GPs and health authorities, and evaluating how closely typical practice aligns to the GPG for tinnitus.MethodsA nine-item postal questionnaire was sent to 2000 GPs randomly selected to proportionally represent the number of primary care trusts and strategic health authorities in England.ResultsWe received 368 responses. Responses indicated a mix of frequent and infrequent practices, for example, 90% of GPs assessed the impact of tinnitus on quality of life, but fewer examined cranial nerves (38%) or assessed for a carotid bruit (26%) during a tinnitus consultation. In the management of tinnitus, 83% routinely removed earwax, and 87% provided information-based advice. In contrast, only 4% of responders would offer antidepressant drugs or psychological therapies. Thematic analysis revealed a desire for concise training on tinnitus management.ConclusionsGP assessment and management of tinnitus represents potential inequity of service for tinnitus patients. While the GPG aims to promote equity of care, it is only referred to by a minority of clinicians and so its utility for guiding service delivery is questionable. Although some GPs highlighted little demand for tinnitus management within their practice, many others expressed an unmet need for specific and concise GP training on tinnitus management. Further work should therefore evaluate current informational resources and propose effective modes of delivering educational updates.

Predictive values of risk factors in carotid duplex scanning before peripheral vascular surgery

The objective of this study was to determine the predictive values of multiple atherosclerotic risk factors in using routine carotid duplex scanning for patients with peripheral vascular disease, even in the absence of any sign of carotid disease. From 1998 through 2000, 108 patients admitted for peripheral vascular reconstruction to our institution were preoperatively screened for carotid artery stenosis. Patients were examined for neurologic status and cervical bruits. As atherosclerotic risk factors, hyperlipidemia, diabetes, smoking, sex and age, coronary artery disease (CAD), coronary artery bypass surgery (CABG), and previous vascular operation were recorded, preoperative ankle-brachial pressure indexes (ABI) were calculated. All patients underwent routine carotid color duplex examinations preoperatively. Eighty five patients (78.7%) had mild (<50%) or no carotid artery stenosis, and 23 patients (21.3%) had significant (≥50%) carotid artery stenosis. Age (≥60 years), coronary artery disease, and carotid bruit were individual factors, and the combination of age ≥55 and hyperlipidemia had a significant value in predicting presence of ≥50% stenosis of one or both carotid arteries by univariate analysis. By multivariate logistic regression analysis, however, only carotid bruit was associated with carotid artery stenosis of ≥50% (p<0.001). Screening for asymptomatic carotid artery stenosis is indicated in patients with only carotid artery bruit and might be indicated in elderly patients with peripheral vascular disease. Routine screening or carotid artery stenosis in all patients is not an effective strategy.

Drug-Resistant Major Depression Associated With Carotid Artery Stenosis

Back to table of contents Previous article Next article Communications and UpdatesFull AccessDrug-Resistant Major Depression Associated With Carotid Artery StenosisFlorence Gressier, M.D., Hedi Khlif, M.D., Christian Denier, M.D., Ph.D., Patrick Hardy, M.D., Ph.D., Denis Ducreux, M.D., Ph.D., and Emmanuelle Corruble, M.D., Ph.D.Florence GressierLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Hedi KhlifLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Christian DenierLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Ph.D., Patrick HardyLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Ph.D., Denis DucreuxLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Ph.D., and Emmanuelle CorrubleLe Kremlin Bicêtre, FranceSearch for more papers by this author, M.D., Ph.D.Published Online:1 Apr 2011https://doi.org/10.1176/appi.ajp.2010.10101497AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: We report a case of drug-resistant major depression due to left carotid artery stenosis, with rapid and full recovery following carotid endarterectomy.A 74-year-old man living by himself, without any personal or familial psychiatric history, was admitted to our psychiatry department for drug-resistant major depression despite successive treatments with sertraline, clomipramine, and moclobemide over 3 years; a previous psychiatric hospitalization; and current treatment with imipramine (appropriate dosages and durations). He presented significant sadness, anxiety, sense of failure, loss of interest, anhedonia, concentration difficulties, indecision, suicidal ideas, asthenia, decreased appetite, decreased weight, and social withdrawal. He scored 21 on the Hamilton Depression Rating Scale (HAM-D) and 30 on the Mini-Mental State Examination.The patient had cardiovascular risk factors: past smoking, hypercholesterolemia, and long-standing hypertension treated with atenolol. Findings on his physical examination and blood serum screening (including thyroid hormones, vitamin B12, and folates) were normal. No audible carotid bruit was present. A systematic cerebral contrast MRI evidenced neither leukoaraiosis nor recent lesion on diffusion-weighted imaging sequences but showed a small silent infarct in the left parietal region on FLAIR sequences at the junction between the left anterior and middle cerebral arteries. Carotid Doppler ultrasonography showed internal carotid artery stenosis bilaterally with significant luminal narrowing (left: 90%, right: 40%). A four-vessel cerebral angiogram confirmed the left subocclusive carotid artery stenosis.After withdrawing antidepressant and starting aspirin and atorvastatin, the patient underwent an emergency left carotid endarterectomy under local anesthesia.A dramatic improvement in depressive symptoms was observed within 4 days after the procedure, especially in anxiety and loss of interest. After 1 week, the patient's HAM-D score was 5. No depressive relapse had occurred 8 weeks later.A mood disorder due to a general medical condition (carotid artery stenosis) with major depressive-like episode was diagnosed.Even if age and an asymptomatic left parietal infarct could be considered predisposing factors for depression (1), three factors suggest that major depression was related to severe carotid artery stenosis in this case: no familial or personal psychiatric history, full recovery within 4 days of carotid endarterectomy (a time course atypical for recovery from idiopathic major depression), and absence of relapse 8 weeks after carotid endarterectomy. Moreover, carotid artery stenosis has been associated with depressive symptoms and suicide in two previous case reports, even in the absence of cerebral infarction (2, 3), and cerebral hypoperfusion was the suspected underlying mechanism. Indeed, our report is consistent with a previous case showing a positive effect of carotid endarterectomy on major depression (2).Consequently, in patients with cardiovascular risk factors, and even if carotid bruit is not present, drug-resistant major depression requires systematic carotid Doppler ultrasonography as early as possible to screen for carotid artery stenosis, since carotid endarterectomy can produce rapid and full recovery of carotid artery stenosis-related drug-resistant major depression.Le Kremlin Bicêtre, FranceDr. Gressier has received consulting fees and honoraria from Servier; Dr. Corruble has received consulting fees and honoraria from Lundbeck, Servier, Eisai, and Bristol-Myers Squibb; the remaining authors report no financial relationships with commercial interests.Accepted for publication in December 2010.

Carotid Bruits and Cerebrovascular Disease Risk: A Meta-Analysis

Conclusion: Carotid bruits may be a marker of increase risk of neurologic events. Summary: A classic teaching is that the presence of carotid bruits significantly increases the risk of myocardial infarction and cardiovascular death. This teaching is supported by a large recent meta-analysis (Pickett CA, et al, Lancet 2008;371:1587-94). The strength of the relationship between cerebrovascular events and carotid bruits is less clear. The Systolic Hypertension in the Elderly study found carotid bruits were a weak predictor of stroke with relative risk of 1.3 (Shorr RI, J Gen Intern Med 1998;13:86-90). The Evans County Study, however, found a stronger relationship, with a relative risk of 4.1 for a combined end point of stroke and transient ischemic attack (Heyman A, N Engl J Med 1980;302:838-41). Nevertheless, osculation for carotid bruits in asymptomatic patients is not recommended by the US Preventative Services Task Force and the Canadian Task Force (US Preventative Services Task Force, Ann Intern Med 2007;147:854-9; and Mackey A, et al, Canadian Task Force on the Periodic Health Examination. Canadian Guide to Clinical Preventative Health Care. Ottawa: Health Canada; 1994:692-704). The authors sought to investigate if carotid bruit was associated with an increased risk of transient ischemic attack, stroke, or stroke death. Their meta-analysis was based on a search of MEDLINE from 1996 to December 2009 and EMBASE from 1974 to December 2009 using the terms bruits and carotid. Articles were included only if they prospectively reported the incidence of stroke, transient ischemic attack, or stroke death in initially asymptomatic adults. They identified 28 prospective cohort articles for the meta-analysis. The articles monitored a total of 17,913 patients for 67,708 patient years. Studies directly comparing patients with or without bruits on the rate ratio of new transient ischemic attack found a ratio of 4.00 (95% CI, 1.8-9.0; P < .0005, n = 5 studies). For stroke, the ratio was 2.5 comparing patients with and without carotid bruits (95% CI, 1.8-3.5; P < .0005, n = 6 studies). With respect to stroke death and patients with or without carotid bruits the ratio was 2.7 (95% CI, 1.33-5.53; P = .002, n = 3 studies). Among the pool of studies that provided data on rates of transient ischemic attack rates, the ratios were 2.6/100 patient-years (95% CI, 2.0- 3.2; P < .0005, n = 24 studies) for those with bruits compared with 0.9/100 patient-years (95% CI, 0.2-1.6; P = .02, n = 5 studies) for those without carotid bruits. For those with bruits, stoke rates were 1.6/100 patient-years (95% CI, 1.3-1.9; P < .005, n = 26 studies). For those without bruits, stroke rates were 1.3/100 patient-years (95% CI, 0.8-1.7; P < .05, n = 6 studies). Death rates were 0.32 (95% CI, 0.2-0.44; P < .005, n = 13 studies) for those with bruits and 0.35 (95% CI, 0.00-0.81; P = .17, n = 3 studies) for those without bruits. Comment: The data suggest a higher neurologic risk associated with carotid bruits than is generally appreciated. The study, however, has several limitations. Most studies included in the meta-analysis did not report enough information to evaluate the effects of compounding variables. Also, we do not know the degree of stenosis associated with carotid bruits in this study, and all strokes and transient ischemic attack tracked were not necessarily ipsilateral to the bruit. At the very least, however, carotid bruits appear to identify patients at increased neurologic risk. In conjunction with the known increased risk of cardiac events associated with carotid bruits, it is certainly reasonable to conclude that a carotid bruit identifies patients who require aggressive modification of atherosclerotic risk factors. Listening to the neck may not be such a bad thing!

Assessment of carotid artery stenosis before coronary artery bypass surgery. Is it always necessary?

Extracranial internal carotid artery stenosis is a risk factor for perioperative stroke in patients undergoing coronary artery bypass surgery (CAB). Although selective and non-selective methods of preoperative carotid screening have been advocated, it remains unclear if this screening is clinically relevant. To test whether selective carotid screening is as effective as non-selective screening in detecting significant carotid disease. The case records of patients consecutively undergoing CAB were reviewed. Patients were stratified retrospectively into high- or low-risk groups according to risk factors for significant carotid stenosis and perioperative stroke: peripheral vascular disease (PVD), carotid bruit, diabetes mellitus, age >70 years and/or history of cerebrovascular disease. Prevalence of carotid stenosis detected by ultrasonography, surgical management and perioperative stroke rates were determined in each group. Overall, 205 consecutive patients underwent preoperative carotid screening. The prevalence of significant carotid stenosis was 5.8%. Univariate analysis confirmed that PVD (P=0.005), carotid bruit (P=0.003) and diabetes mellitus (P=0.05) were significant risk factors for stenosis. Carotid stenosis was a risk factor for stroke (P=0.03). Prevalence of carotid stenosis was higher in the high-risk group (9.1%) than the low-risk group (1.2%) (P<0.05). All concomitant or staged carotid endarterectomies/CAB (5/205) and all patients who had perioperative strokes (5/205) were in the high-risk group (P=0.01). In our cohort, selective screening of patients aged >70 years, with carotid bruit, a history of cerebrovascular disease, diabetes mellitus or PVD would have reduced the screening load by 40%, with trivial impact on surgical management or neurological outcomes.

066 Assessment of carotid artery stenosis before coronary artery bypass surgery

Extracranial internal carotid artery stenosis is a risk factor for perioperative stroke in patients undergoing coronary artery bypass (CAB) surgery. Although both selective and nonselective methods of preoperative carotid screening have been advocated, it remains unclear if this screening is clinically relevant. Files of patients consecutively undergoing CAB were reviewed. Patients were retrospectively stratified into high- or low-risk groups according to risk factors for significant carotid stenosis and perioperative stroke identified in the literature: presence of peripheral vascular disease, carotid bruit, diabetes mellitus, age over 70 years and/or previous history of cerebrovascular disease. Prevalence of carotid stenosis detected by ultrasonography, surgical management, and perioperative stroke rates were determined in each group. 205 consecutive patients underwent preoperative carotid screening. The prevalence of significant carotid stenosis detected by ultrasonography was 5.8%. Univariate analysis confirmed that peripheral vascular disease (p = 0.005), carotid bruit (p = 0.003) and diabetes mellitus (p = 0.05) were significant risk factors for stenosis. Carotid stenosis was a risk factor for stroke (p = 0.03). Prevalence of carotid stenosis was higher in high-risk group than in low-risk group (9.1% vs 1.2%; p<0.05). All concomitant or staged carotid endarterectomies/CAB (5/205) and all patients who suffered perioperative strokes (5/205) were in the high-risk group (p = 0.01). In our cohort, selective screening of patients with either an age over 70, a carotid bruit, a history of cerebrovascular disease, a diabete mellitus or a peripheral vascular disease would have reduced the screening load by 40% with trivial impact on surgical management or neurologic outcomes.

44-Year-Old Man With Shortness of Breath, Fatigue, and Paresthesia

44-year-old man presented to the Primary Care Internal Medicine clinic with a 1-month history of shortness of breath, fatigue, and paresthesia. He reported increasing shortness of breath while stocking shelves at work and recently stopped recreational jogging because of this symptom. He also described a new, painless numbness and tingling in his fingertips bilaterally. The patient denied any history of chest pain, syn- cope, palpitations, muscle weakness, incontinence, weight changes, or recent illness. He was taking no prescription or over-the-counter medications or food supplements. He had no other relevant medical or surgical history. He had never used tobacco or illicit drugs and consumed an average of 1 alcoholic beverage per month. He had no siblings. Family history was remarkable for coronary artery disease in his father and osteoarthritis in his mother. Physical examination revealed a blood pressure of 101/58 mm Hg, with a regular pulse of 86 beats/min. The patient was afebrile, alert, and well nourished. Head and neck evaluation demonstrated a supple neck without ten- derness to palpation or carotid bruits. Scleras were normal. Neck range of motion and strength were normal. Findings on thyroid and lymph node examinations were unremark- able. Cardiac examination revealed normal first and second heart sounds without murmurs, gallops, or rubs. Lung sounds were clear. The patient's skin was pale. Abdominal examination revealed no tenderness, masses, or hepatosple- nomegaly. Cranial nerve examination revealed no abnor - malities in cranial nerves II through XII. Sensation was intact throughout, except for reduced pinpoint discrimina- tion of the bilateral finger tips. The Phalen maneuver and Tinel sign were negative. The extremities, including the th- enar musculature, were of normal tone, bulk, and strength, with symmetric and normal reflexes throughout. The lower extremities had mild varicosities but were not edematous. Babinski testing was normal. Gait testing was normal ex- cept for mild unsteadiness during the tandem walk.

Living with the LLSA: Transient Ischemic Attack: Risk Stratification and Treatment

Living with the LLSA: Transient Ischemic Attack: Risk Stratification and Treatment

Classic Coronary Artery Disease in an Unlikely Patient

Classic Coronary Artery Disease in an Unlikely Patient

Clinical diagnosis of segmental arterial mediolysis: Differentiation from vasculitis and other mimics

Segmental arterial mediolysis (SAM) is a rare vasculopathy of unknown etiology characterized by disruption of the arterial medial layer, with resultant susceptibility to vessel dissection, hemorrhage, and ischemia. Since the first case of SAM described by Slavin and Gonzalez-Vitale in 1976 (1), approximately 50 cases have been reported in the literature (2). Although the abdominal visceral arteries are most frequently affected in SAM (3), any vessel may be involved, including the retroperitoneal (4), intracranial (2, 5, 6) and coronary arteries (7–9). The histopathologic changes begin with vacuolar degeneration of smooth muscle cells in the arterial media, followed by fibrin deposition at the medial-adventitial junction (7). This in turn predisposes to dissecting aneurysms (3, 10). The angiographic appearance of SAM is variable, ranging from arterial dilation to aneurysm formation (single or multiple) to stenoses or occlusion, frequently with dissection (3, 11). Correspondingly, symptoms arise both from stenoses and occlusions (e.g., postprandial pain from intestinal ischemia) and from dissections and aneurysms (e.g., sudden and catastrophic intraperitoneal bleeding). In contrast to true vasculitis, inflammatory cells in SAM are present inconsistently and, when present, are thought to be secondary rather than primary to the pathogenesis of the disease (1). The differential diagnosis of SAM includes atherosclerosis, fibromuscular dysplasia, infection (e.g., mycotic aneurysm and endocarditis), connective tissue diseases (e.g., Bechet’s disease and polyarteritis nodosa), neurofibromatosis, and inherited defects in vessel wall structural proteins (e.g., type IV Ehlers Danlos and Marfan’s syndrome) (Table 1). Herein, we describe two cases of SAM seen at our instituation over the past 20 years and review the salient clinical presentation and treatment of SAM. We report characteristics that may be helpful in distinguishing cases of SAM from other entities in the differential diagnosis. Table 1 Clinical and laboratory features distinguishing Segmental Arterial Mediolysis (SAM) from its mimics*. Case 1 The patient was a 25-year-old female who was admitted to the hospital with an eleven-month history of intermittent episodes of anorexia, abdominal pain, and diarrhea. Symptoms had persisted despite discontinuation of oral contraception and initiation of low-dose aspirin therapy. Her past medical history was unremarkable. Family history was unremarkable except for benign hypermobility syndrome in the patient’s mother. On physical examination, the patient was normotensive and had normal height and arm span. She had no carotid, subclavian, abdominal, or femoral bruits. Skin, chest, abdominal, and neurologic examinations were normal. Joint exam was remarkable only for hyperextensibility of the knees, reducible flexion contractures of the fingers, and hammertoe deformities of the feet. Complete blood count revealed anemia with hemoglobin of 11 g/dl. Serum creatinine, liver enzymes, amylase, and lipase were normal, and urine pregnancy test was negative. Antinuclear antibody assay (ANA) was positive to a low titer of (1:80). The erythrocyte sedimentation rate was 20 mm/hr. The remainder of the serologic, metabolic, immunologic, and hematologic evaluations were within normal limits, including negative hepatitis serologies, negative double-stranded DNA, anti-Smith, and anti-ribonucleoprotein (RNP) antibodies, and normal complement C3 and C4 levels. Computed tomography (CT) of the abdomen showed thickening of the colonic wall with mucosal enhancement and fat stranding surrounding the splenic flexure. Colonoscopy revealed ischemic colitis of the splenic flexure. Biopsies of the ischemic areas were not obtained due to risk of possible perforation. Biopsies of the non-ischemic areas were normal, as was magnetic resonance angiography (MRA) of the abdomen. Conventional mesenteric angiography revealed focal stenoses of the right and left hepatic arteries, occlusion of the left colic artery near the splenic flexure with collateral vessel formation, and hyperemia of multiple branches of the splenic artery (Figure 1). Figure 1 Angiographic and histologic features of segmental arterial mediolysis in Case 1. (a) Focal stenoses of the right and left hepatic arteries (arrows). (b) Hyperemic blush in the left colonic flexure, suggesting formation of small collateral vessels from ... Because of persistent ischemic colitis, the patient underwent a partial colectomy of the splenic flexure. Vascular pathology of the colonic arteries showed patchy, isolated destruction of the arterial media involving both the internal and external elastic laminae (Figure 1). In a few sections the media was absent, with direct juxtaposition of the intima and the adventitia. In areas of medial destruction, there was intimal proliferation with marked luminal narrowing. All of the lesions were of a similar age. There was no evidence of inflammation, and giant cells, neutrophils, and cholesterol deposits were absent. After two years of followup, the patient remains asymptomatic.

Rare Long Term Complication of “Push” Introducing Technique for PEG Tube Insertion

Purpose: PEG tube insertion can be accomplished by a “pull” (Ponsky) or “push” (Russell) techniques. The Ponsky technique has dominated clinical practice today, however, many tubes, especially for head & neck cancers are still inserted with the Russell technique. Hemorrhagic complications of PEG tube placement and removal are relatively low, estimated at 2.5% in large series. We present a case of a 58 year old man seen urgently in the ER for melena. He has liver cirrhosis from alcohol and Hepatitis C with portal hypertension and has a Levine shunt. He is on Warfarin for DVT and has chronic renal failure. He had esophageal cancer resected 15 years ago, and during that time had a temporary gastrostomy tube. Our patient was well until two days prior to admission when he started having melena stool. He denied any epigastric pain, nausea/vomiting, shortness of breath, or rectal bleeding. He was feeling dizzy and had presyncopal symptoms without loss of consciousness. On examination, he was alert and oriented with no cyanosis, jaundice, clubbing, carotid bruits, or lower limb edema. Blood pressure was 92/60 mmHg and pulse 112/minute and afebrile. Abdomen was soft, no organomegaly and no ascites. No melena or stool was seen on rectal examination. Labs show an INR 11, Hg 3.2 g/dL, platelets 170,000, and creatinine 2.15 mg/dL. The patient was admitted to the CCU and started on Octreotide and Pantoloc® infusions with concern that the bleeding was variceal. Octaplex® was given to reverse his INR, and DDAVP given for his platelet dysfunction, after which he had urgent gastroscopy. The esophagus was completely normal, a small fundal varix was seen in the stomach, and no active bleeding was identified. However, in the body of the stomach, a metallic spring attached to a suture going through the wall was seen with some adjacent ulceration, thought to be the cause of melena. Explanation for the findings in the stomach and what to do about them were unclear. Surgical opinion was not helpful initially, however, another senior surgeon later identified the metallic spring as a likely remnant from the introducer used for PEG placement with the Russell “push” technique. The patient underwent a second endoscopy to remove the spring and release the suture. This is the first case report we are aware of, with a gastric bleed caused by a retained introducer apparatus many years after the PEG was removed. The “Russell introducer” method involves direct puncture of an endoscopically insufflated stomach. Introducer and outer peel-away sheaths are inserted over which the gastrostomy tube is pushed. The case highlights a rare complication of this technique, and suggests care should be taken when PEG is removed.

Classic Coronary Artery Disease in an Unlikely Patient

Classic Coronary Artery Disease in an Unlikely Patient

Carotid Bruits and Cerebrovascular Disease Risk

Current guidelines recommend against routine auscultation of carotid arteries, believing that carotid bruits are poor predictors of either underlying carotid stenosis or stroke risk in asymptomatic patients. We investigated whether the presence of a carotid bruit is associated with increased risk for transient ischemic attack, stroke, or death by stroke (stroke death). We searched Medline (1966 to December 2009) and EMBASE (1974 to December 2009) with the terms "carotid" and "bruit." Bibliographies of all retrieved articles were also searched. Articles were included if they prospectively reported the incidence of transient ischemic attack, stroke, or stroke death in asymptomatic adults. Two authors independently reviewed and extracted data. We included 28 prospective cohort articles that followed a total of 17 913 patients for 67 708 patient-years. Among studies that directly compared patients with and without bruits, the rate ratio for transient ischemic attack was 4.00 (95% CI, 1.8 to 9.0, P<0.0005, n=5 studies), stroke was 2.5 (95% CI, 1.8 to 3.5, P<0.0005, n=6 studies), and stroke death was 2.7 (95% CI, 1.33 to 5.53, P=0.002, n=3 studies). Among the larger pool of studies that provided data on rates, transient ischemic attack rates were 2.6 per 100 patient-years (95% CI, 2.0 to 3.2, P<0.0005, n=24 studies) for those with bruits compared with 0.9 per 100 patient-years (95% CI, 0.2 to 1.6, P=0.02, n=5 studies) for those without carotid bruits. Stroke rates were 1.6 per 100 patient-years (95% CI, 1.3 to 1.9, P<0.0005, n=26 studies) for those with bruits compared with 1.3 per 100 patient-years (95% CI, 0.8 to 1.7, P<0.0005, n=6) without carotid bruits, and death rates were 0.32 (95% CI, 0.20 to 0.44, P<0.005, n=13 studies) for those with bruits compared with 0.35 (95% CI, 0.00 to 0.81, P=0.17, n=3 studies) for those without carotid bruits. The presence of a carotid bruit may increase the risk of cerebrovascular disease.

Vascular neck bruit in a teenager

A healthy 16-year-old female presented to our internal medicine clinic with a 6-month history of dizziness and two fainting attacks within the past month. She mentioned feeling a buzzing noise in the left side of her neck, for which she sought medical advice. Physical examination revealed left carotid bruit but was otherwise unremarkable. Lipid profile and hypercoagulable screen revealed normal values. Doppler ultrasound examination (Figure 1) and then MR angiography of the neck vessels (Figure 2) were performed. Figure 1 (a) Axial ultrasound image of the left common carotid artery. (b) Sagittal Doppler ultrasound image of the left common carotid artery. Figure 2 (a) Axial time-of-flight MR angiographic image of the neck vessels. (b) Three-dimensional projection of the vessels in the left side of the neck. How would you describe the findings? What are the diagnosis and associated risks? Is there a differential diagnosis and what would you do next? Doppler ultrasound of the carotid vessels showed normal vessel wall thickness with no atheromatous plaques, but there was a focal concentric narrowing of the lumen of the left common carotid artery (CCA). This was caused by a circumferential band of tissue (Figure 1a) projecting into the lumen and causing more than 70% stenosis; this was consistent with a congenital carotid web. The colour Doppler ultrasound demonstrated high-flow jet and aliasing in the area of highest velocity, with a significant increase in peak systolic velocity (to 410 cm s−1) and end-diastolic velocity (to 215 cm s−1) (Figure 1b). Time-of-flight (Figure 2a) and intravenous contrast-enhanced (Figure 2b) MR angiography of the neck vessels confirmed the ultrasound findings of a focal CCA web, located 4 cm below the bifurcation. The patient was referred for vascular surgery, where an endarterectomy and a saphenous vein patch angioplasty were performed. To the naked eye, the intraoperative appearance of the artery suggested focal dissection (Figure 3). This was supported by the patient's sporting history of several years as a practitioner of karate, with possible exposure to focal trauma. However, the histopathological examination of the endarterectomy specimen revealed that the web was covered with intima and composed of benign fibromyxoid tissue with no evidence of dissection, haemorrhage, inflammation or atherosclerosis. The pathology findings are consistent with a congenital anomaly (web) rather than with a post-traumatic event. Follow-up after 6 months revealed a capacious patch angioplasty with no evidence of renewed stenosis. Figure 3 Intraoperative picture of the left common carotid artery showing a concentric ridge-like lesion in an otherwise smooth internal vessel wall.

Extracranial Carotid Stenosis and Peripheral Arterial Disease in Thai Patients With Coronary Artery Disease

We assessed the prevalence of carotid stenosis (CS) and peripheral arterial disease (PAD) in patients with coronary artery disease (CAD) to determine the relationship between these conditions in a Thai population. All patients with coronary angiography during June 2008 and August 2009 were studied. Carotid duplex and ankle-brachial index (ABI) were performed. One hundred and seventy-seven patients were studied (95 men, mean age of 65). Carotid stenosis and PAD were diagnosed in 16 patients (9%) and 68 patients (38.4%), respectively. The presence of carotid bruit and older age were independent predictors of CS and PAD, respectively. There was no correlation between the presence of CS/PAD and the extent of coronary artery lesions. Although CS was uncommon in patients with CAD, the patients with cervical bruit should be screened for CS. Prevalence of PAD was high, confirming the presence of diffuse atherosclerosis in many patients with CAD.

Taking PET for a Walk — an Unusual Cause of Bilateral Leg Claudication

To the Editor: Large-vessel giant cell arteritis (LV-GCA) is a rare condition that is increasingly recognized with the advent of imaging techniques such as positron emission tomography (PET). However, the utility of PET in extracranial GCA is poorly defined and rarely reported, especially in lower-limb LV-GCA. We describe a case of GCA affecting the lower limbs in which PET, corroborated with computed tomography angiogram (CTA) and duplex ultrasound, was used to accurately assess and monitor the activity of this rare arteritis. A 59-year-old woman with minimal atherosclerotic risk factors presented with a 3-month history of progressive bilateral leg claudication. She initially noticed tightness in her right calf after walking 100 meters on level ground. The discomfort was proportional to exertion, and would promptly resolve with rest. There was similar, although less intense, discomfort in her left calf, and associated bilateral numbness in her middle 3 toes. Three months previously she had unlimited exercise tolerance on level ground. One month after the onset of claudication, her symptoms progressed to include bilateral thigh discomfort on exertion. There was no scalp tenderness, visual disturbance, jaw or tongue claudication, or polymyalgic or joint symptoms. She had lost 2.5 kilograms (4% total body weight) over 3 months. Her medical history was unremarkable. Her atherosclerotic risk factors included a brief 2.5 pack-year smoking history and a family history of lower-limb arterial disease (sister requiring femoropopliteal bypass at age 49 years) and old-age ischemic heart disease. On examination, the left popliteal artery and bilateral pedal pulses were absent. The right popliteal pulse was weakly palpable, and femoral pulses were present. There were no femoral, renal, or lower abdominal bruits. Temporal arteries were nontender, with normal pulses. There were no carotid, subclavian, or axillary artery bruits. Lower-limb neurological examination was normal. Initial blood tests showed a mildly elevated … Address correspondence to Dr. T. Tsai; e-mail: t.tsai{at}unsw.edu.au

A 46‐year‐old woman with chin pain and a fainting spell

History of the present illness The patient had a history of primary central nervous system (CNS) lymphoma that had recurred in the past but had been in remission for 2 years. She was admitted to the hospital in August 2008, following a syncopal episode. For several weeks prior to her syncope, she had experienced generalized malaise and the sensation of total body weakness. On the day of admission, she was nauseated and had one episode of non-bloody emesis. As the day progressed, she felt lightheaded and eventually lost consciousness while walking to the bathroom. In the emergency department, she was suspected of dehydration. However, an electrocardiogram revealed complete heart block (CHB). A temporary transjugular pacing wire was placed, intravenous fluids were started, and she was admitted to the Cardiac Unit. The patient stated that she had been completely well until 2 months before admission, when she began to experience easy fatigability. One month before admission, she developed a series of episodes of myalgias that involved her shoulders and neck. These symptoms responded to acetaminophen. She had also experienced periodic night sweats during this time. Two weeks before admission, the patient presented to her oncologist with the symptom of chin pain that radiated bilaterally toward the angle of her mandible. The pain was described as “sharp and shooting.” It sometimes appeared to be worsened by jaw movement. The patient indicated that chewing exacerbated the pain, starting with the first bite. Her oncologist had obtained a brain magnetic resonance imaging (MRI) study to exclude a lymphoma recurrence. The MRI study was interpreted as showing no new lesions. The pain did not respond to nonsteroidal antiinflammatory drugs and had been present for 2 weeks at the time of her syncope.

Prevalência de estenose carotídea em pacientes com indicação de cirurgia de revascularização miocárdica

FUNDAMENTO: Embora a aterosclerose carotídea seja a principal causa de acidente vascular cerebral, a prevalência de estenose clinicamente significativa (>50%) permanece desconhecida em nosso meio, principalmente em indivíduos com indicação de cirurgia eletiva de revascularização do miocárdio. OBJETIVO: Identificar a prevalência e o grau de estenose carotídea em indivíduos com indicação de cirurgia de revascularização miocárdica em um centro de referência em cardiologia no Brasil. MÉTODOS: Estudo transversal no qual 457 pacientes consecutivos e de ambos os gêneros foram avaliados, entre maio de 2007 e abril de 2008, através de ultrassonografia com Doppler em cores de artérias carótidas, no pré-operatório de cirurgia de revascularização miocárdica eletiva. Para a análise estatística foi usado o programa SPSS 10.1. Um valor-p<0,05 foi considerado significativo. Houve perda de 7 pacientes no decorrer do estudo. RESULTADOS: A média de idade (±desvio padrão) foi de 62,2 ± 9,4 anos sendo que 65,6% eram do gênero masculino. A prevalência de estenose carotídea significativa foi de 18,7%. Quanto à estratificação do grau de estenose carotídea: ausência de estenose ocorreu em 3,6%, estenose inferior a 50%, em 77,8%, estenose entre 50% e 69% em 11,6%, estenose entre 70% e 99% em 6,9% e oclusão da artéria em 0,2%. A sensibilidade e especificidade em relação ao sopro carotídeo foram, respectivamente, 34,5% e 88,8%. CONCLUSÃO: A prevalência de estenose carotídea significativa foi alta na amostra estudada, sugerindo tratar-se de população de alto risco para acidente vascular cerebral.

Oscillating Atherosclerotic Plaque in the Internal Carotid Artery

Duplex ultrasound is used not only to detect atherosclerotic disease but also to define characteristics of the disease. Carotid plaque is often described by its echogenicity and surface characteristics. The following case report depicts the findings of atherosclerotic plaque that appeared to oscillate. An asymptomatic 60 year-old male presented with a right carotid bruit. His medical history is significant for type II diabetes mellitus, hypertension, hyperlipidemia and hypothyroidism. The ultrasound revealed the right internal carotid artery (ICA) peak systolic velocity (PSV) was 125 cm/s with an end diastolic velocity (EDV) of 33 cm/s. Heterogeneous atherosclerotic plaque was present at the origin of the ICA. A portion of the plaque was observed on real-time imaging to be oscillating with the cardiac cycle. The segment was approximately 5 mm in length and swayed from the wall of the vessel into the center stream of flow as normal flow/pressure variations occurred with the cardiac cycle. The right ICA was categorized as having a 50–69% stenosis. Mild atherosclerotic plaque was found in the left ICA with a PSV of 71 cm/s and EDV of 27 cm/s. These findings were categorized as a less than 50% stenosis. Bilaterally, the external carotid arteries demonstrated mild plaque while the common carotid arteries were free of disease. A magnetic resonance angiogram confirmed the presence of a stenosis and the patient underwent a successful right carotid endarterectomy. At surgery the plaque was found to be partially disrupted and described as mobile, correlating with the plaque features observed on ultrasound. This report describes the importance of fully evaluating the plaque characteristics during ultrasound examination. Based on velocities and the percent stenosis, this patient would have likely gone into surveillance and not to surgery. Identification of this potentially hazardous unstable plaque leads to rapid treatment, thus avoiding serious complications.

Adventitial Fibromuscular Dysplasia of the Renal Artery

A 19-year-old healthy woman presented with new onset of severe migrainous headache. She did not take medications or use illicit drugs. There was no personal or family history of hypertension. Physical examination revealed a blood pressure of 220/130 mm Hg in both arms. There was no fourth heart sound. She had full and symmetric pulses in the upper and lower extremities with no radial/femoral delay. There were no carotid, subclavian, or abdominal bruits. Fundoscopic examination revealed normal retinal arteries without hypertensive retinopathy. Renal function and serum potassium were normal. Renal artery duplex ultrasonography revealed elevated peak systolic and end-diastolic velocities in the mid to distal portion of the right renal artery, consistent with severe right renal artery stenosis. The left renal artery was normal. The right kidney measured 8.8 cm with atrophy of the right cortical margin. The left kidney was 11.5 cm. There were normal renal resistive indexes …