Common carotid intima-media thickness does not add to Framingham risk score in individuals with diabetes mellitus: the USE-IMT initiative.

AIMS/HYPOTHESIS: The aim of this work was to investigate whether measurement of the mean common carotid intima-media thickness (CIMT) improves cardiovascular risk prediction in individuals with diabetes. METHODS: We performed a subanalysis among 4,220 individuals with diabetes in a large ongoing individual participant data meta-analysis involving 56,194 subjects from 17 population-based cohorts worldwide. We first refitted the risk factors of the Framingham heart risk score on the individuals without previous cardiovascular disease (baseline model) and then expanded this model with the mean common CIMT (CIMT model). The absolute 10 year risk for developing a myocardial infarction or stroke was estimated from both models. In individuals with diabetes we compared discrimination and calibration of the two models. Reclassification of individuals with diabetes was based on allocation to another cardiovascular risk category when mean common CIMT was added. RESULTS: During a median follow-up of 8.7 years, 684 first-time cardiovascular events occurred among the population with diabetes. The C statistic was 0.67 for the Framingham model and 0.68 for the CIMT model. The absolute 10 year risk for developing a myocardial infarction or stroke was 16% in both models. There was no net reclassification improvement with the addition of mean common CIMT (1.7%; 95% CI -1.8, 3.8). There were no differences in the results between men and women. CONCLUSIONS/INTERPRETATION: There is no improvement in risk prediction in individuals with diabetes when measurement of the mean common CIMT is added to the Framingham risk score. Therefore, this measurement is not recommended for improving individual cardiovascular risk stratification in individuals with diabetes.

Mannheim carotid intima-media thickness and plaque consensus (2004-2006-2011). An update on behalf of the advisory board of the 3rd, 4th and 5th watching the risk symposia, at the 13th, 15th and 20th European Stroke Conferences, Mannheim, Germany, 2004, Brussels, Belgium, 2006, and Hamburg, Germany, 2011.

Intima-media thickness (IMT) provides a surrogate end point of cardiovascular outcomes in clinical trials evaluating the efficacy of cardiovascular risk factor modification. Carotid artery plaque further adds to the cardiovascular risk assessment. It is defined as a focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the surrounding IMT value or demonstrates a thickness >1.5 mm as measured from the media-adventitia interface to the intima-lumen interface. The scientific basis for use of IMT in clinical trials and practice includes ultrasound physics, technical and disease-related principles as well as best practice on the performance, interpretation and documentation of study results. Comparison of IMT results obtained from epidemiological and interventional studies around the world relies on harmonization on approaches to carotid image acquisition and analysis. This updated consensus document delineates further criteria to distinguish early atherosclerotic plaque formation from thickening of IMT. Standardized methods will foster homogenous data collection and analysis, improve the power of randomized clinical trials incorporating IMT and plaque measurements and facilitate the merging of large databases for meta-analyses. IMT results are applied to individual patients as an integrated assessment of cardiovascular risk factors. However, this document recommends against serial monitoring in individual patients.

Serum GFAP is a diagnostic marker for glioblastoma multiforme.

A serum marker for malignant cerebral astrocytomas could improve both differential diagnosis and clinical management of brain tumour patients. To evaluate whether the serum concentration of glial fibrillary acidic protein (GFAP) may indicate glioblastoma multiforme (GBM) in patients with single supratentorial space-occupying lesions, we prospectively examined 50 consecutive patients with histologically proven GBM, World Health Organization (WHO) grade IV, 14 patients with anaplastic astrocytoma (WHO grade III), 4 patients with anaplastic oligodendroglioma, 13 patients with diffuse astrocytoma (WHO grade II), 17 patients with a single cerebral metastasis and 50 healthy controls. Serum was taken from the patients before tumour resection or stereotactic biopsy. Serum GFAP levels were determined using a commercially available ELISA test and were detectable in 40 out of the 50 GBM patients (median: 0.18 microg/l; range: 0-5.6 microg/l). The levels were significantly elevated compared with those of the non-GBM tumour patients and healthy controls (median: 0 mug/l; range: 0-0.024 microg/l; P < 0.0001, respectively). Non-GBM tumour patients and all healthy subjects showed zero serum GFAP levels. There was a significant correlation between tumour volume (Spearman Rho, CC = 0.47; 95% confidence interval, 0.2-0.67; P < 0.001), tumour necrosis volume (CC = 0.49; 95% confidence interval, 0.2-0.72; P = 0.004), the amount of necrotic GFAP positive cells (CC = 0.61; 95% confidence interval, 0.29-0.81; P = 0.007) and serum GFAP level among the GBM patients. A serum GFAP level of >0.05 microg/l was 76% sensitive and 100% specific for the diagnosis of GBM in patients with a single supratentorial mass lesion in this series. Therefore, it can be concluded that serum GFAP constitutes a diagnostic biomarker for GBM. Future studies should investigate whether serum GFAP could also be used to monitor therapeutic effects and whether it may have a prognostic value.

Anthropometric approximation of body weight in unresponsive stroke patients.

BACKGROUND AND PURPOSE: Thrombolysis of acute ischaemic stroke is based strictly on body weight to ensure efficacy and to prevent bleeding complications. Many candidate stroke patients are unable to communicate their body weight, and there is often neither the means nor the time to weigh the patient. Instead, weight is estimated visually by the attending physician, but this is known to be inaccurate. METHODS: Based on a large general population sample of nearly 7000 subjects, we constructed approximation formulae for estimating body weight from simple anthropometric measurements (body height, and waist and hip circumference). These formulae were validated in a sample of 178 consecutive inpatients admitted to our stroke unit, and their accuracy was compared with the best visual estimation of two experienced physicians. RESULTS: The simplest formula gave the most accurate approximation (mean absolute difference 3.1 (2.6) kg), which was considerably better than the best visual estimation (physician 1: 6.5 (5.2) kg; physician 2: 7.4 (5.7) kg). It reduced the proportion of weight approximations mismatched by >10% from 31.5% and 40.4% (physicians 1 and 2, respectively) to 6.2% (anthropometric approximation). Only the patient's own estimation was more accurate (mean absolute difference 2.7 (2.4) kg). CONCLUSIONS: By using an approximation formula based on simple anthropometric measurements (body height, and waist and hip circumference), it is possible to obtain a quick and accurate approximation of body weight. In situations where the exact weight of unresponsive patients cannot be ascertained quickly, we recommend using this approximation method rather than visual estimation.

Diffusion-weighted MR imaging lesions after filter-protected stenting of high-grade symptomatic carotid artery stenoses.

BACKGROUND AND PURPOSE: The clinical efficacy of filter devices in internal carotid artery (ICA) stent placement has been a matter of controversy. The aim of this retrospective study was to assess the number and extent of cerebral emboli, as represented by new lesions on diffusion-weighted MR imaging (DWI), in patients treated with filter-protected carotid stent placement. METHODS: Standard DWI (B0 = 1000) was performed within 48 hours before and 48 hours after filter-protected carotid stent placement in 50 patients with symptomatic, high grade (>70%), atherosclerotic ICA stenosis. Number, extent, and vascular territory of new DWI lesions after stent placement were assessed by consensus of 2 experienced neuroradiologists. Multifactorial statistical analysis was performed to determine risk factors associated with DWI lesions. RESULTS: New punctate DWI lesions with a median diameter of 2 mm were detected in 14 of 50 cases in the territory of the stented ICA and in 7 of 50 cases in other vascular territories. Median lesion load was 1 lesion (range, 1-15) per positive case in the stented ICA and 1 lesion (range, 1-7) in other vascular territories. All DWI lesions were clinically asymptomatic. Because of 1 hyperperfusion syndrome with temporary brain swelling, the 30-day stroke and death rate was 2%. Age >or =70 years was the only significant predictor for new DWI lesions, whereas sex, degree and site of stenosis, vascular risk factors, and stent and filter type showed no significant correlation. CONCLUSIONS: New DWI lesions after filter-protected carotid stent placement are substantially more frequent in the ipsilateral ICA territory compared with other vascular territories. Therefore, intraluminal filters cannot completely protect the brain from procedure-related embolization. However, individual lesion load and the risk of clinically relevant ischemia is low.

[Long term follow-up after intracranial vertebro-basilar artery stenting]. / Langzeitergebnisse nach Behandlung intrakranieller vertebrobasilärer Stenosen mit Stents.

PURPOSE: Recurrent ischemic symptoms attributable to intracranial high-grade vertebrobasilar artery stenoses are associated with a high risk of ischemic stroke, particularly if these occur in spite of aggressive medical treatment. Long term efficacy data for endovascular stent angioplasty of symptomatic intracranial stenoses are lacking. The purpose of this prospective study is to determine the rates of deaths, of ischemic events and of restenosis during long-term follow-up. MATERIALS AND METHODS: Between June 2001 and February 2004 twelve patients (11 male, 1 female; median 63 yrs; range, 46 - 75 yrs) with recurrent ischemic symptoms attributed to > or = 70 % intracranial vertebro-basilar artery stenoses, who had failed aggressive medical treatment, were included. Median follow-up was 24 months (range: 6 to 36 months). Intracranial stenoses were measured using 3D rotation angiography data sets and treated with balloon expandable stents. All patients were scheduled for follow-up including clinical (Barthel Index) and transcranial Doppler examinations and intraarterial angiography at 6 months after intervention. Clinical outcome was defined as the rate of stroke in any vascular territory or death during follow-up. Vascular outcome was determined by the rate of in-stent restenosis 50 % on follow-up as examined by intraarterial angiography at 6 months or by transcranial color-coded duplex sonography. RESULTS: Stent placement was technically successful in all patients. No patient had further cerebral ischemic symptoms; two patients died (1 myocardial infarct, 1 sudden death) during follow-up of median 24 months. The degree of stenoses was reduced from median 81 % (range 69 - 94 %) to 19 % (range 10 - 36 %) immediately after stent placement and to 32 % (range 22 - 48 %) after 6 months. No restenosis > or = 50 % occurred during follow-up. CONCLUSION: Based on this limited series, we believe that in patients, with recurrent symptoms despite aggressive medical treatment, endovascular stent placement in intracranial high-grade vertebrobasilar artery stenoses can be an effective and safe treatment option.

Chlamydia pneumoniae infection and early asymptomatic carotid atherosclerosis.

BACKGROUND: Chronic Chlamydia pneumoniae infection has been implicated in the pathogenesis of atherosclerosis but whether it plays a role at an early stage in the disease is uncertain. An early estimate of atherosclerosis can be obtained by ultrasonic imaging of the carotid artery to determine intima-media thickness (IMT) and the thickness of any atheroma plaques. METHODS AND RESULTS: In 983 normal population individuals aged 30 to 70 years, we measured common carotid artery (CCA) and carotid bulb IMT, and also carotid plaque thickness and the degree of internal carotid artery (ICA) stenosis. C. pneumoniae IgA titers of >/=16 and IgG titers of >/=64 were taken as positive. There was no association between C. pneumoniae IgA or IgG seropositivity with right, left, or mean CCA or bulb IMT, or with the presence of carotid plaques. There was a significant association between IgA seropositivity and >50% mean carotid stenosis with an odds ratio of 5.24 (95% CI 1.24 to 22.21, P=0.0245) after controlling for age and sex; after controlling for other cardiovascular risk factors, this was not significant 3.96 (95% CI 0. 84 to 18.78, P=0.082). No association was found between IgA or IgG seropositivity and markers of fibrinogen, log C-reactive protein, or leukocyte count. CONCLUSIONS: We found no evidence that serological evidence of C. pneumoniae infection is associated with early atherosclerosis. It is possible that IgA seropositivity is associated with more advanced disease but this hypothesis needs to be examined in a population with a higher prevalence of advanced atherosclerosis. We found no evidence that C. pneumoniae results in a chronic systemic inflammatory state.

Phosphodiesterase 4D gene, ischemic stroke, and asymptomatic carotid atherosclerosis.

BACKGROUND AND PURPOSE: Phosphodiesterase 4D (PDE4D) was identified recently as the first novel stroke gene to predispose to ischemic stroke independently of conventional risk factors. An association was only found with large vessel and cardioembolic stroke, suggesting a mechanism of accelerated atherosclerosis. We sought to replicate this association in ischemic stroke as a whole, and individual stroke subtypes, in a non-Icelandic European population. To assess a role in early atherosclerosis, we also sought associations with underlying asymptomatic atherosclerosis itself, assessed by carotid ultrasound in a community population. METHODS: A total of 737 consecutive white patients with stroke and 933 white community controls free of symptomatic cerebrovascular disease were examined using a case control methodology. For association with atherosclerosis, intima-media thickness (IMT) in a community population (n=1000) was assessed using carotid ultrasound. Nineteen single nucleotide polymorphisms (SNPs) and 1 minisatellite in the PDE4D gene were determined, with haplotyping undertaken using Phase 2.0. RESULTS: No association with ischemic stroke overall was identified. Six of the 19 SNPs were associated with cardioembolic stroke and 2 different SNPs with large vessel disease. There was no association with carotid artery IMT or carotid plaque in the asymptomatic community subjects. CONCLUSIONS: The PDE4D gene is not a major risk factor for ischemic stroke, or early atherosclerosis, within the 2 European population samples studied. On analysis of individual stroke subtypes, there is a possible association with cardioembolic stroke, but the lack of association with carotid IMT and plaque would suggest that this is via a mechanism other than accelerated atherosclerosis.

Pravastatin improves cerebral vasomotor reactivity in patients with subcortical small-vessel disease.

BACKGROUND AND PURPOSE: Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment. METHODS: In 16 patients (mean age 68+/-10 years) with subcortical small-vessel disease, cerebral vasomotor reactivity was tested using TCD insonating the middle cerebral artery. Cerebral blood flow velocity (CBFV) increase after bolus injection of 1 g acetazolamide was determined before and after 2-month treatment with pravastatin sodium 20 mg daily. RESULTS: Relative CBFV increase was significantly greater after pravastatin treatment (41.9+/-23.7% versus 55.7+/-18.3%, P=0.004). Comparison of CBFV at rest before and after treatment with pravastatin did not show significant differences. There was a strong negative correlation between the pravastatin-induced enhancement of vasomotor reactivity and the pretreatment CBFV increase (beta=-0.64, P=0.019). No associations were found between the effect of pravastatin on vasomotor reactivity and pretreatment levels or changes of LDL cholesterol. CONCLUSIONS: This pilot study provides the first evidence for a significant improvement of cerebral vasomotor reactivity by statin therapy in patients with cerebral small-vessel disease. The results may help to elucidate the preventive effect of statins and provide insights into the pathophysiology of cerebral small-vessel disease.

Expression of tissue factor in high-grade carotid artery stenosis: association with plaque destabilization.

BACKGROUND AND PURPOSE: The procoagulant protein tissue factor (TF) has been implicated in thromboembolic complications associated with advanced atherosclerosis. In this study, we investigated whether TF expression in high-grade stenoses of the internal carotid artery (ICA) is associated with clinical features of plaque destabilization and addressed the relationship between TF expression and plaque inflammation. METHODS: In 36 consecutive patients undergoing surgery for high-grade ICA stenosis, clinical evidence of plaque instability was provided by the recent occurrence of ischemic symptoms attributable to the stenosis and the detection of cerebral microembolism by means of transcranial Doppler ultrasound monitoring of the ipsilateral middle cerebral artery. Endarterectomy specimens were stained immunocytochemically for TF expression as well as macrophage (CD68) and T cell (CD3) infiltration. RESULTS: Morphologically, TF immunoreactivity was codistributed with plaque inflammation and predominantly localized to CD68+ macrophages. Accordingly, statistical analysis revealed a significant association of TF expression with plaque infiltration by macrophages (P<0.0001) and T cells (P=0.013). Plaques extensively stained for TF (median of TF+ total section area >40% in semiquantitative assessment) were more frequent in symptomatic (12/27) than in asymptomatic patients (1/9). Conversely, plaques exhibiting little TF expression (median of TF+ section area <20%) were more frequent in asymptomatic (3/9) than in symptomatic (1/27) patients (P=0.016). Likewise, we found a highly significant association of TF expression with the occurrence of cerebral microembolism (P=0.008). CONCLUSIONS: Induction of TF at sites of plaque inflammation may play an important role in the destabilization of high-grade ICA stenosis.

Endovascular treatment of symptomatic carotid stenosis using stent placement: long-term follow-up of patients with a balanced surgical risk/benefit ratio.

BACKGROUND AND PURPOSE: Carotid endarterectomy (CEA) is not necessarily beneficial in all patients with symptomatic high-grade (>/=70%) internal carotid artery (ICA) stenosis. Independent risk factors modulate both the individual stroke risk under medical treatment and the combined stroke and death risk after CEA. Endovascular stenting of symptomatic ICA stenosis may be an alternative to CEA in patients with a balanced surgical risk/benefit ratio. METHODS: We included 43 patients (71% men; median age, 67 years) with a recently symptomatic ICA stenosis with >/=70% luminal narrowing in whom the individual sum of medical and surgical risk factors suggested a balanced surgical risk/benefit ratio (risk-modeling appraisal derived from the European Carotid Surgery Trial). After stenting of the stenosed ICA with distal balloon protection, the mean+/-SD follow-up, including clinical and ultrasonographic examinations, was 20+/-11.8 months, with a median number of examinations of 5 per patient. RESULTS: Recanalization of ICA stenoses was technically successful in 40 of 43 procedures (93%). Within the 30-day postinterventional period 1 death occurred (2.5%), and the combined stroke and death rate within follow-up was 5%. Except for 1 asymptomatic ICA occlusion, no restenosis >/=70% occurred during follow-up. CONCLUSIONS: ICA stenting in symptomatic patients with a balanced surgical risk/benefit ratio is technically feasible, with a low periprocedural risk of stroke or death. Furthermore, the risk of future stroke and rate of significant restenosis during long-term follow-up appears to be low, suggesting that ICA stenting may be useful in carotid revascularization and stroke prevention.

Cerebral microembolism in patients with Sneddon's syndrome.

BACKGROUND: The pathogenesis of Sneddon's syndrome is unclear. This study addresses the question whether cerebral thromboembolism may be involved in the pathogenesis of the neurologic complications of the disorder. The study consisted of 13 patients with Sneddon's syndrome defined by both generalized livedo reticularis and a history of one or more cerebrovascular ischemic events; none had clinical or Doppler ultrasonographic evidence of atherosclerosis. METHODS: Transcranial Doppler microembolic monitoring of the middle cerebral artery; blood screening for antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies). RESULTS: Five patients (38%) showed clinically silent microembolism at transcranial Doppler monitoring, with individual microembolic event rates of the middle cerebral artery between 2 per hour and 33 per hour. In this group, the time since the last ischemic symptom was significantly shorter than in the eight patients without microemboli. Antiphospholipid antibodies were detected in three patients (23%), all of whom belonged to the microemboli-positive group. CONCLUSIONS: These data suggest that the detectability of both clinically silent cerebral microembolism and antiphospholipid antibodies may provide paraclinical evidence of active disease in patients with Sneddon's syndrome. The results support the notion that an immune-mediated prothrombotic state facilitating the formation of arterial thrombi with subsequent cerebral embolization, and/or triggering in situ thrombosis of cerebral vessels, plays a pathogenetic role in the neurologic manifestations of this disorder.

Intracerebral hemorrhage after experimental embolic infarction. Anticoagulation.

Embolic stroke was induced in rabbits using autologous blood clot. One hour after stroke, animals received heparin anticoagulation (AC) for five hours (acute AC) or five days (chronic AC). Animals received excessive AC (partial thromboplastin time greater than 3.0 times control), adequate AC (partial thromboplastin time, 1.2 to 2.5 times control), or saline. After the animals were killed, the brains were examined for macroscopic evidence of intracerebral hemorrhage. There was no significant increase over control in the incidence or severity of hemorrhage in any of the four treatment groups. The data suggest that heparin AC does not promote intracerebral hemorrhage after experimental embolic stroke.

Cheyne-Stokes respiration in ischemic stroke.

We monitored breathing pattern and arterial oxygen saturation in 32 conscious patients with acute ischemic stroke. Seventeen (53%) had Cheyne-Stokes respiration with concomitant drops in oxygen saturation, unrelated to infarct location. The ventilatory disturbance promptly reversed after intravenous theophylline ethylenediamine or oxygen inhalation. The therapy is a simple way of improving arterial oxygenation in a large subgroup of patients with acute ischemic stroke.

Cerebral microembolism in symptomatic and asymptomatic high-grade internal carotid artery stenosis.

Using transcranial Doppler (TCD) ultrasonography in patients with high-grade (> or = 70%) internal carotid artery (ICA) stenosis, we examined the relation between the rate of TCD-detected silent microembolism of the ipsilateral middle cerebral artery and a history of recent (< 121 days) ischemic symptoms attributable to the diseased ICA. In the so-defined neurologically symptomatic group (n = 33 patients), silent microembolic events occurred in 27 subjects (overall mean rate, 14/h +/- 29). Among 56 neurologically asymptomatic patients matched for the degree of ICA stenosis, only nine showed such events (overall mean rate, 0.35/h +/- 1.4). Across all 89 patients studied, an individual microembolic event rate > or = 2/h had a positive predictive value of 0.88 for a history of recent symptoms. Our data suggest that TCD monitoring can provide reliable paraclinical evidence of "unstable ICA disease."

Deficiency of both protein C and protein S in a family with ischemic strokes in young adults.

Protein C and protein S deficiencies increase the risk of venous thrombosis and pulmonary embolism, but their role in arterial thrombosis or embolism is controversial. We describe cerebral ischemia in two young women in a family with inherited deficiencies of both proteins C and S and provide evidence that a combined deficiency of proteins C and S may be a high risk factor for ischemic stroke in young adults.

Cerebral hemodynamics during sensorimotor activation in humans.

We studied the time course and magnitude of cerebral blood flow velocity (CBFV) changes in the middle cerebral artery (MCA) and the regional cerebral blood flow (rCBF) in the MCA territory during stimulation of the left sensorimotor cortex. Healthy right-handed male subjects were examined during performance of right-hand finger movement sequences, vibratory stimulation, and somatosensory discrimination. In somatosensory discrimination there were significant increases of the mean CBFV (4.8 +/- 9.9 cm/s; P < 0.01) and the mean rCBF (10.2 +/- 4.2 ml.100 g-1.min-1; P < 0.01), whereas no significant changes of the mean CBFV and rCBF occurred in finger movement sequences or vibratory stimulation. During all stimulation sessions the mean CBFV changes increased rapidly and reached a first maximum 3.3 +/- 0.3 s after stimulation onset. Simultaneous measurements of relative mean CBFV changes in both MCAs revealed left-right differences during voluntary finger movement sequences (left MCA, 14.3 +/- 10.6%; right MCA, 0.9 +/- 11.6%; P < 0.001) corresponding to a higher mean rCBF change in the left MCA territory. In the two tasks involving finger movements there was an increase of the respiratory rates (4.3 +/- 3.8 breaths/min; P < 0.05) and the pulse rates (11.6 +/- 5.5 beats/min; P < 0.05), respectively. Our data demonstrate a correspondence of mean CBFV and rCBF changes evoked by sensorimotor activation in the human brain. Furthermore, cerebral hemodynamic changes related to motor activity are accompanied by cardiorespiratory effects.

Spontaneous oscillations in cerebral blood flow velocity in normal humans and in patients with carotid artery disease.

Spontaneous oscillations in cerebral blood flow velocity (CBFV) in normals and in patients with stenoses or occlusions of the internal cerebral artery were measured using transcranial Doppler sonography. In normal subjects, large oscillations of up to +/- 30% from the mean CBFV were found with low frequencies between 0.4 and 9 cycles/min. No correlations between CBFV oscillations and systemic circulatory parameters were detected. In patients with carotid artery obstructions the CBFV oscillations were significantly reduced in the middle cerebral artery ipsilaterally to a hemodynamically significant lesion, but not contralaterally. Our results support the hypothesis that spontaneous oscillations (B-waves) of small pial vessels are responsible for the CBFV fluctuations.

Characteristics and clinical value of an intravenous echo-enhancement agent in evaluation of high-grade internal carotid stenosis.

Although ultrasound is a highly useful tool for clinical diagnosis, it has certain limitations in accurately quantifying internal carotid stenosis or diagnosing internal carotid occlusion. However, these limitations can be overcome by increasing the echogenicity of flowing arterial blood by use of echo-enhancement agents. Two phase III studies assessed the usefulness of the IV transpulmonary echo enhancer Levovist (SH U 508A) in improving characterization and quantification of severe internal carotid stenosis on ultrasound scans. In addition, Levovist-induced enhancement characteristics of the Doppler frequency spectrum have been analyzed. To be included in the study reviewed here, patients had to have a high-grade (> or = 70%) stenosis or occlusion of an internal carotid artery (ICA), as judged by conventional angiography or by standard cervical Doppler ultrasound. Patients were excluded from consideration if they were pregnant or nursing, had a history of galactosemia, or had received an ionic contrast medium within 24 hours before or after the intended administration of Levovist. Written informed consent was obtained from all patients before entry into the study. Of 32 patients (14 women, 18 men, median age 64 yr) who were included in this study, high-grade stenosis was verified in 30 ICA vessels and occlusion was verified in two vessels. After admission into the study, the carotid bifurcation was insonated in all patients using a 7.5-MHz linear array transducer for color Doppler-assisted duplex imaging and a 4-MHz pulsed-wave Doppler for velocity spectrum measurements before and after injection of the echo enhancement agent Levovist. Levovist-induced increases in carotid blood echogenicity began 11 +/- 2 seconds (mean +/- SD) after the start of injection, peaked at 21 +/- 2 dB, and had a half-life of 75 seconds. A fast Fourier transform of the original Doppler velocity spectrum demonstrated Levovist-induced enhancement throughout the entire velocity spectrum, with an increase in ICA blood flow velocity paralleling an increase in reflected ultrasound energy. Quantitative vascular measurements (cross-sectional luminal area reduction and plaque length) obtained before and during echo enhancement were highly correlated (r > 0.90). However, visualization of the entire length of the intrastenotic residual flow lumen, was significantly improved by Levovist enhancement (52% versus 83%; p = 0.01). Levovist considerably increased interpretable data by improving image quality in patients with high-grade carotid stenosis. Furthermore, the significant improvement in visualization of the residual flow lumen suggests that echo-enhancement agents may be most useful in improving the ultrasonography-based diagnosis of internal carotid occlusion.

Injuries related to all-terrain vehicular accidents: a closer look at head and neck trauma.

Morbidity and mortality associated with all-terrain vehicular accidents is climbing at a steady rate. These accidents frequently result in multiorgan system trauma. A retrospective study of all victims involved in three-wheel motor vehicle accidents admitted to the UCSD Trauma Unit between July 1980 and July 1985 is presented. Injury severity was assessed using the Abbreviated Injury Scale (AIS) and the Injury Severity Score (ISS). The average patient age was 23.3 years with 30% under 16 years of age. There was a male to female ratio of 14:1. The average hospital stay was 12.4 days. Six percent died as a result of their injuries. Injuries to the head and neck were sustained by 83.3% of patients, facial injuries by 46.6%, injuries to the chest by 13.3%, and injuries to the pelvis and abdomen by 13.3%. Thirty percent suffered injuries to the extremities and over 50% had abrasions, contusions, and/or lacerations. Physicians, the public, and state and federal agencies are urged to promote safer use of these recreational vehicles.