The prognostic impact of fluctuating levels of C-reactive protein in Brazilian haemodialysis patients: a prospective study.

BACKGROUND: A single elevated C-reactive protein (CRP) value predicts mortality in haemodialysis (HD) patients, but the relative importance of repeated vs occasional positive systemic inflammatory response findings is not known. METHODS: To assess the influence on survival of occasional inflammation, CRP, serum albumin (S-Alb) and fibrinogen were analysed bimonthly in 180 HD patients (54% male, 49+/-14 years). Clinically significant inflammation was defined as CRP >5.1 mg/l, based on the receiver operating characteristics curve for CRP as predictor of death. Based on four consecutive measurements of CRP, patients were assigned into three groups: group 1 (n = 74; 41%), no inflammation (CRP < or = 5.1 mg/l in all measurements); group 2 (n = 65; 36%), occasional inflammation (1-3 measurements of CRP > 5.1 mg/l); and group 3 (n = 41; 23%), persistent inflammation (all measurements of CRP >5.1 mg/l). The nutritional status was evaluated by subjective global assessment (SGA) and body mass index (BMI), and the survival (21 months of follow-up) by Kaplan-Meier curve and Cox model. RESULTS: The median and range of CRP values (mg/l) for group 1, 2 and 3 were: 3.2 (3.2-5.1), 3.6 (3.2-54.9) and 13.8 (5.2-82), respectively (P<0.001), whereas the prevalence of malnutrition, assessed by SGA and BMI, did not differ significantly between the groups. The survival rate by Kaplan-Meier analysis was significantly different among the groups (chi2 = 12.34; P = 0.0004). Patients in group 3 showed the highest mortality (34%; P = 0.001), compared with group 1 (8%) and group 2 (14%; P = 0.01), respectively, whereas there was no significant difference in mortality between groups 1 and 2. Age, CRP, S-Alb level and SGA were independent predictors of mortality. CONCLUSION: The patients with a persistent elevation of CRP had a higher mortality rate than the patients with occasional CRP elevation. Thus, persistent, rather than occasional, inflammation is an important predictor of death in HD patients.     

Comparison of Asymmetry in Cerebral Blood Flow Between Brain Hemispheres Using Digital Subtraction Angiography

BACKGROUND AND PURPOSE: Recently, endovascular techniques have gained significant therapeutic potential for both treatment and prevention of stroke. Cerebral angiography, which is an essential component of these procedures, has been used to provide morphological information regarding condition of blood vessels. In this study, we propose to determine the possibility of acquiring information regarding cerebral blood flow (CBF) in addition to morphologic information from data routinely available during angiography. METHODS: Digital subtraction angiography sequences were obtained for eight patients having occlusive disease in internal carotid artery (ICA) territories. Two regions-of-interest (ROIs) corresponding to the two brain hemispheres on AP view were delineated. For each image, the average pixel value within each ROI was calculated and used to generate time-density curves. Indices obtained from each curve were compared with each other and with the results obtained from the single photon emission computed tomography (SPECT) studies performed a pre- or postangiography procedure. RESULTS: Comparison between ICA stenosis and cerebral perfusion measurements revealed that cerebral perfusion deficit can be independent of arterial occlusive disease. The indices obtained from the time-density curves exhibit a correlating trend with the results from SPECT studies. However, lack of sufficient sample data prevented any meaningful statistical analysis to be conducted. CONCLUSIONS: We have developed a technique for utilizing the angiographic data for the important task of routinely and easily measuring CBF. Availability of CBF measurements during cerebral angiography may favorably impact upon the appropriate use of endovascular procedures and potentially contribute to the reduction of morbidity and mortality associated with stroke.     

Total anomalous pulmonary venous drainage. Seventeen-year surgical experience

Between 1968 and 1985, 80 children underwent correction of total anomalous pulmonary venous drainage. There were 47 boys and 33 girls whose ages ranged from 3 days to 16 years (median 2 months, interquartile range 5 years). Seventy (87.5%) were less than 1 year of age at operation. Fifty-eight (72.5%) weighed less than 5 kg, the range being 1.6 to 42 kg (median 3.7 kg, interquartile range 2.4 kg). Forty-five (56%) patients had supracardiac, 14 (17.5%) cardiac, 15 (19%) infracardiac, and 6 (7.5%) had mixed total anomalous pulmonary venous drainage. Follow-up was complete in 78 (97.5%) and ranged from 6 to 189 months (median 58 months, interquartile range 59 months). There were 14 (17.5%) early and six (7.5%) late deaths. Analysis by various factors revealed year of operation as the only factor to affect survival at the 5% level of significance. Early mortality was 29% between 1968-1977 and 11% between 1978-1985 (p = 0.04). Postoperative pulmonary venous obstruction occurred in five (6%) patients between 6 weeks and 3 months after operation. All 5 died, three after reoperation. Five (6%) other children had reoperations, four for residual shunts and one for superior vena caval obstruction.     

Carotid Stent-Supported Angioplasty via Radiobrachial Route

Endovascular stent-supported angioplasty is a treatment option for atherosclerotic disease of the cervical internal carotid artery in high-risk patients. The traditional transfemoral approach is not suitable for patients who suffer from common femoral artery or abdominal aorta atheropathy. We report a case of carotid stent deployment using the radial route in a 68-year-old man with type B aortic dissection, having severe right internal carotid artery origin stenosis, presenting with ipsilateral retinal ischemic events. Technical aspects of carotid stenting via the radial approach are described and the related literature is discussed.     

Comparison of Methodologies for Calculating Quality Measures Based on Administrative Data versus Clinical Data from an Electronic Health Record System: Implications for Performance Measures

New reimbursement policies and pay-for-performance programs to reward providers for producing better outcomes are proliferating. Although electronic health record (EHR) systems could provide essential clinical data upon which to base quality measures, most metrics in use were derived from administrative claims data. We compared commonly used quality measures calculated from administrative data to those derived from clinical data in an EHR based on a random sample of 125 charts of Medicare patients with diabetes. Using standard definitions based on administrative data (which require two visits with an encounter diagnosis of diabetes during the measurement period), only 75% of diabetics determined by manually reviewing the EHR (the gold standard) were identified. In contrast, 97% of diabetics were identified using coded information in the EHR.The discrepancies in identified patients resulted in statistically significant differences in the quality measures for frequency of HbA1c testing, control of blood pressure, frequency of testing for urine protein, and frequency of eye exams for diabetic patients. New development of standardized quality measures should shift from claims-based measures to clinically based measures that can be derived from coded information in an EHR. Using data from EHRs will also leverage their clinical content without adding burden to the care process.     

A new scheme for grading the quality of scientific reports that evaluate imaging modalities for cerebrovascular diseases.

Imaging of head and neck vasculature continues to improve with the application of new technology. To judge the value of new technologies reported in the literature, it is imperative to develop objective standards optimized against bias and favoring statistical power and clinical relevance. A review of the existing literature identified the following items as lending scientific value to a report on imaging technology: prospective design, comparison with an accepted modality, unbiased patient selection, standardized image acquisition, blinded interpretation, and measurement of reliability. These were incorporated into a new grading scheme. Two physicians tested the new scheme and an established scheme to grade reports published in the medical literature. Inter-observer reliability for both methods was calculated using the kappa coefficient. A total of 22 reports evaluating imaging modalities for cervical internal carotid artery stenosis were identified from a literature search and graded by both schemes. Agreement between the two physicians in grading the level of scientific evidence using the new scheme was excellent (kappa coefficient: 0.93, p<0.0001). Agreement using the established scheme was less rigorous (kappa coefficient: 0.39, p<0.0001). The weighted kappa coefficients were 0.95 and 0.38 for the new and established schemes, respectively. Overall agreement was higher for the newer scheme (95% versus 64%). The new grading scheme can be used reliably to categorize the strength of scientific knowledge provided by individual studies of vascular imaging. The new method could assist clinicians and researchers in determining appropriate clinical applications of newly reported technical advances.     

CD14 is not involved in Rhodobacter sphaeroides diphosphoryl lipid A inhibition of tumor necrosis factor alpha and nitric oxide induction by taxol in murine macrophages.

Taxol, a microtubule stabilizer with anticancer activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages in vitro. Recently, it was shown that taxol-induced macrophage activation was inhibited by the LPS antagonist Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA). To investigate the mechanisms of taxol-induced macrophage activation, the present study focused on the interaction of LPS, RsDPLA, and taxol in the activation of and binding to macrophages. Taxol alone induced murine C3H/He macrophages to secrete tumor necrosis factor alpha (TNF) and to produce nitric oxide (NO) with kinetics similar to that of LPS. Macrophages from LPS-hyporesponsive C3H/HeJ mice, in contrast, did not yield any detectable TNF and NO production in response to LPS or taxol. RsDPLA inhibited taxol-induced TNF and NO production from C3H/He macrophages in a dose-dependent manner. The inhibition by RsDPLA was specific for LPS and taxol in that RsDPLA did not inhibit heat-killed Listeria monocytogenes- or zymosan-induced TNF production. Polymyxin B blocked the inhibitory effect of RsDPLA on taxol-induced TNF production. The inhibitory activity of RsDPLA appeared to be reversible since macrophages still responded to taxol in inducing TNF production after the RsDPLA was washed out with phosphate-buffered saline prior to the addition of taxol. Taxol-induced TNF production was not inhibited by colchicine, vinblastine, or 10-deacetylbaccatine III. A mutant cell line, J7.DEF3, defective in expression of a CD14 antigen, responded equally well to taxol by producing TNF as did the parent J774.1 cells. This suggested that the activation of macrophages by taxol does not require CD14. Taxol-induced TNF production by the mutant cells was also inhibited by RsDPLA. 125I-labeled LPS and 3H-labeled taxol was reported to bind to J774.1 cells predominantly via CD14 and microtubules, respectively. The binding of 125I-labeled LPS to J7.DEF3 cells was about 30 to 40% of that to J774.1 cells. The binding of 125I-LPS to J774.1 cells was inhibited by unlabeled LPS and RsDPLA but not by taxol. On the other hand, 3H-labeled taxol bound to both J774.1 cells and J7.DEF3 cells in similar time- and dose-dependent manners. The binding of [3H]taxol to these cells was inhibited by taxol but not by LPS or RsDPLA. Although the binding studies failed to examine cross competition for binding to macrophages, a possible explanation of these results is that LPS, RsDPLA, and taxol share the same molecule(s) on murine macrophages for their functional receptor(s), which is neither CD14 nor tubulin.