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Biomedical subjects

G C Brown

Publications and source records attributed to G C Brown.

At least 73 records · Page 4Linked to original sources
PubMed1999

Superoxide dismutase and hydrogen peroxide cause rapid nitric oxide breakdown, peroxynitrite production and subsequent cell death.

Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3. The breakdown of NO by this reaction was inhibited by cyanide (CN(-)) or by diethyldithiocarbamate (DETC), both Cu/Zn-SOD inhibitors, and the conversion of DHR to rhodamine-1,2,3 was inhibited by incubating Cu/Zn-SOD with either CN(-) or with high levels of H(2)O(2) or by including urate, a potent scavenger of ONOO(-). In the presence of phenol, the reaction of SOD, H(2)O(2) and NO caused nitration of phenol, which is known to be a footprint of ONOO(-) formation. H(2)O(2) addition to macrophages (cell line J774) expressing the inducible form of NO synthase (i-NOS) caused rapid breakdown of the NO they produced and this was also inhibited by CN(-) and by DETC. Subsequent ONOO(-) production by the macrophages, via this reaction, was inhibited by CN(-), high levels of H(2)O(2) or by urate. H(2)O(2) addition to i-NOS macrophages also caused cell death which was, in part, prevented by DETC or urate. We also found inhibition of mitochondrial respiration with malate and pyruvate as substrates, when isolated liver mitochondria were incubated with Cu/Zn-SOD, H(2)O(2) and NO. Inhibition of mitochondrial respiration was partly prevented by urate. The production of ONOO(-) by SOD may be of significant importance pathologically under conditions of elevated H(2)O(2) and NO levels, and might contribute to cell death in inflammatory and neurodegenerative diseases, as well as in macrophage-mediated host defence.

Animals↗
PubMed1999

Nitric oxide and mitochondrial respiration.

Nitric oxide (NO) and its derivative peroxynitrite (ONOO-) inhibit mitochondrial respiration by distinct mechanisms. Low (nanomolar) concentrations of NO specifically inhibit cytochrome oxidase in competition with oxygen, and this inhibition is fully reversible when NO is removed. Higher concentrations of NO can inhibit the other respiratory chain complexes, probably by nitrosylating or oxidising protein thiols and removing iron from the iron-sulphur centres. Peroxynitrite causes irreversible inhibition of mitochondrial respiration and damage to a variety of mitochondrial components via oxidising reactions. Thus peroxynitrite inhibits or damages mitochondrial complexes I, II, IV and V, aconitase, creatine kinase, the mitochondrial membrane, mitochondrial DNA, superoxide dismutase, and induces mitochondrial swelling, depolarisation, calcium release and permeability transition. The NO inhibition of cytochrome oxidase may be involved in the physiological regulation of respiration rate, as indicated by the finding that isolated cells producing NO can regulate cellular respiration by this means, and the finding that inhibition of NO synthase in vivo causes a stimulation of tissue and whole body oxygen consumption. The recent finding that mitochondria may contain a NO synthase and can produce significant amounts of NO to regulate their own respiration also suggests this regulation may be important for physiological regulation of energy metabolism. However, definitive evidence that NO regulation of mitochondrial respiration occurs in vivo is still missing, and interpretation is complicated by the fact that NO appears to affect tissue respiration by cGMP-dependent mechanisms. The NO inhibition of cytochrome oxidase may also be involved in the cytotoxicity of NO, and may cause increased oxygen radical production by mitochondria, which may in turn lead to the generation of peroxynitrite. Mitochondrial damage by peroxynitrite may mediate the cytotoxicity of NO, and may be involved in a variety of pathologies.

Animals↗
PubMed1999

On the mechanism by which vascular endothelial cells regulate their oxygen consumption.

Two enzymes, soluble guanylyl cyclase and cytochrome c oxidase, have been shown to be exquisitely sensitive to nitric oxide (NO) at low physiological concentrations. Activation of the soluble guanylyl cyclase by endogenous NO and the consequent increase in the second messenger cyclic GMP are now known to control a variety of biological functions. Cytochrome c oxidase, the terminal enzyme of the mitochondrial respiratory chain, is inhibited by NO. However, it is not clear whether NO produced by the constitutive NO synthase interacts with cytochrome c oxidase, nor is it known what the biological consequences of such an interaction might be. We now show that NO generated by vascular endothelial cells under basal and stimulated conditions modulates the respiration of these cells in response to acute changes in oxygen concentration. This action occurs at the cytochrome c oxidase and depends on influx of calcium. Thus, NO plays a physiological role in adjusting the capacity of this enzyme to use oxygen, allowing endothelial cells to adapt to acute changes in their environment.

Animals↗
PubMed1999

Release of cytochrome c from heart mitochondria is induced by high Ca2+ and peroxynitrite and is responsible for Ca(2+)-induced inhibition of substrate oxidation.

Prolonged heart ischaemia causes an inhibition of oxidative phosphorylation and an increase of Ca2+ in mitochondria. We investigated whether elevated Ca2+ induces changes in the oxidative phosphorylation system relevant to ischaemic damage, and whether Ca2+ and other inducers of mitochondrial permeability transition cause the release of cytochrome c from isolated heart mitochondria. We found that 5 microM free Ca2+ induced changes in oxidative phosphorylation system similar to ischaemic damage: increase in the proton leak and inhibition of the substrate oxidation system related to the release of cytochrome c from mitochondria. The phosphorylating system was not directly affected by high Ca2+ and ischaemia. The release of cytochrome c from mitochondria was caused by Ca2+ and 0.175-0.9 mM peroxynitrite but not by NO, and was prevented by cyclosporin A. Adenylate kinase and creatine kinase were also released after incubation of mitochondria with Ca2+, however, the activity of citrate synthase in the incubation medium with high and low Ca2+ did not change. The data suggest that release of cytochrome c and other proteins of intermembrane space may be due to the opening of the mitochondrial permeability transition pore, and may be partially responsible for inhibition of mitochondrial respiration induced by ischaemia, high calcium, and oxidants.

Animals↗
PubMed1999

The importance of qualitative vitreous examination in patients with acute posterior vitreous detachment.

OBJECTIVE: To determine whether patients with acute posterior vitreous detachment with pigmented vitreous granules or hemorrhage have a higher likelihood of retinal tear compared with those with qualitatively normal vitreous examination findings. METHODS: A multicenter cross-sectional study was performed in 3 peripheral ophthalmic clinics. Patients with acute posterior vitreous detachment were examined for the presence or absence of vitreous pigment granules, vitreous hemorrhage, and horseshoe retinal tear. RESULTS: Fifty-nine consecutive patients with acute posterior vitreous detachment met our eligibility criteria. Eight patients had a retinal tear, and thus its prevalence in our study was almost 14%. Thirteen patients (22%) had a high likelihood because they had evidence of either pigmented vitreous granules or hemorrhage. The prevalence of retinal tear in the setting of acute posterior detachment associated with vitreous hemorrhage alone, pigment alone, or vitreous hemorrhage and pigment was 54%. Patients with posterior vitreous detachment with pigmented vitreous granules or hemorrhage were significantly more likely to have a retinal tear (odds ratio, 52.0; 95% confidence interval, 5.4-497.0). Patients with a retinal tear were 7 times more likely to have pigmented vitreous granules or hemorrhage (LR + ve = 7.4, in which LR + ve indicates positive likelihood ratio; 95% confidence interval, 3.3-16.4). CONCLUSION: Patients with posterior vitreous detachment with vitreous pigment granules or hemorrhage are 52 times more likely to have a retinal tear compared with those who have normal findings on qualitative vitreous examination.

Acute Disease↗
PubMed1999

Utility values and diabetic retinopathy.

PURPOSE: To ascertain the utility values associated with diabetic retinopathy and varying degrees of visual loss. METHODS: One hundred consecutive patients with diabetic retinopathy and best-corrected visual acuity decreased to 20/40 or worse in at least one eye occurring primarily as a result of diabetic retinopathy were evaluated in a cross-sectional study. Utility values were ascertained in five groups using both the time trade-off and standard gamble methods: group 1 (best-corrected visual acuity in the better eye of 20/20 to 20/25), group 2 (best-corrected visual acuity in the better eye of 20/30 to 20/50), group 3 (best-corrected visual acuity in the better eye of 20/60 to 20/100), group 4 (best-corrected visual acuity in the better eye of 20/200 to 20/400), and group 5 (best-corrected visual acuity in the better eye of counting fingers to hand motions). RESULTS: The mean utility value for the diabetic retinopathy group as a whole was 0.77 (SD = 0.21; 95% confidence interval [CI], 0.73 to 0.81) with the time trade-off method and 0.88 (SD = 0.20; 95% CI, 0.84 to 0.92) with the standard gamble method. Employing the time trade-off method correlated with the best-corrected visual acuity in the better eye, the mean utility results were as follows: group 1 = 0.85 (95% CI, 0.75 to 0.95), group 2 = 0.78 (CI, 0.72 to 0.84), group 3 = 0.78 (CI, 0.67 to 0.89), group 4 = 0.64 (CI, 0.53 to 0.75), and group 5 = 0.59 (CI, 0.23 to 0.95). Thus, patients in group 1 (best-corrected visual acuity of 20/20 to 20/25 in the better eye) were willing to trade a mean of 15% of their remaining years of life in return for perfect vision in each eye, whereas those in group 5 (best-corrected visual acuity of counting fingers to hand motions in the better eye) were willing to trade a mean of 41% of their remaining years in return for perfect vision in each eye. There was no significant difference in mean utility values between patients who had decreased visual acuity from diabetic retinopathy for 1 year or less compared with those with decreased acuity for more than 1 year. There was also no significant difference in mean utility values between those with a 12th grade education or less compared with those with more than a 12th grade education. CONCLUSION: Visual loss occurring secondary to diabetic retinopathy is associated with a substantial decrease in patient utility value (and quality of life). The utility value is directly dependent on the degree of visual loss associated with the disease. The length of time of visual loss and amount of formal education do not appear to affect the utility value.

Adult↗
PubMed1999

Nitric oxide, cytochrome c and mitochondria.

Nitric oxide (NO) and its derivative, peroxynitrite (ONOO-), inhibit mitochondrial respiration, and this inhibition may contribute to both the physiological and cytotoxic actions of NO. Nanomolar concentrations of NO rapidly and reversibly inhibited cytochrome oxidase in competition with oxygen, as shown with isolated cytochrome oxidase, mitochondria, brain nerve terminals and cells. Cultured astrocytes and macrophages activated (by cytokines and endotoxin) to express the inducible form of NO synthase produced up to 1 microM NO, and inhibited their own respiration and that of co-incubated cells via reversible NO inhibition of cytochrome oxidase. NO-induced inhibition of respiration in brain nerve terminals resulted in rapid glutamate release, which might contribute to the neurotoxicity of NO. NO inhibition of cytochrome oxidase is reversible; however, incubation of cells with NO donors for 4 hours resulted in an inhibition of complex I, which was reversible by light and thiol reagents and may be due to nitrosylation of thiols in complex I. NO also caused the acute inhibition of catalase, stimulation of hydrogen peroxide production by mitochondria, and reaction with hydrogen peroxide on superoxide dismutase to produce peroxynitrite. Peroxynitrite inhibited complexes I, II and V (the ATP synthase), aconitase, creatine kinase, and increases the proton leak in isolated mitochondria. Peroxynitrite also caused opening of the permeability transition pore, resulting in the release of cytochrome c, which might then trigger apoptosis. Hypoxia/ischaemia also resulted in an acute reversible inhibition of cytochrome oxidase. Heart ischaemia caused the release of cytochrome c from mitochondria into the cytosol, and at the same time caspase-3-like-protease activity was activated in the cytoplasm. Addition of cytochrome c to non-ischaemic cytosol also caused activation of this protease activity, suggesting that caspase activation and consequent apoptosis is at least partly a result of this cytochrome c release.

Animals↗
PubMed1999

Evidence-based medicine, utilities, and quality of life.

Evidence-based medicine provides the highest quality of information for medical practitioners. At the top of the pyramid of evidence-based medicine are the prospective, randomized clinical trials and meta-analysis. Evidence-based medicine can be incorporated with quality-of-life parameters; the latter can be quantified using utility theory. With utility theory, utility values range from 0.0 (death state) to 1.0 (perfect health state). The higher the utility value, the better a person's quality of life. Interventional treatment can change the utility level experienced by a patient. A change in utility value induced by an interventional treatment can be amalgamated with the duration of the treatment effect to provide the number of quality-adjusted life-years (QALYs) gained by a specific treatment (QALYs = [gain in utility value] x [duration of treatment effect]). Thus, this formula takes into account both the improvement in quality of life and the improvement in length of life gained by a treatment. The number of QALYs gained by a treatment can then be incorporated with medical costs (discounted for the time value of money) to arrive at a final common denominator of $/QALY (cost per QALY). The parameter $/QALY can be used to compare the cost-effectiveness of interventional treatments across diverse specialties in medicine. In essence, this methodology allows a measure of the cost-effectiveness of a treatment that incorporates the highest quality of scientific information, clinical efficacy, patient quality-of-life preferences, and realistic costs.

Aged↗
PubMed1999

Cost-effectiveness of treatment for threshold retinopathy of prematurity.

OBJECTIVE: Retinopathy of prematurity (ROP) is a leading cause of adverse visual outcomes in premature infants. Both laser photocoagulation and cryotherapy have been demonstrated in clinical trials to be efficacious in reducing the incidence of visual loss occurring secondary to threshold ROP. Visual data recently have become available concerning the long-term clinical efficacy of both treatments, as have data concerning the utility value of visual states in general. Accordingly, we undertook an analysis to ascertain the cost-effectiveness of laser photocoagulation and cryotherapy in the treatment of threshold ROP. DESIGN: A computer simulation economic model is presented to evaluate the cost-effectiveness of cryotherapy and laser photocoagulation therapy, compared with the natural course of the disease, for treating premature infants with threshold ROP. The model applies long-term visual data from previous clinical trials, utility analysis, decision analysis, and economic principles, such as present value analysis, to account for the time value of money to arrive at a cost per quality-adjusted life-year (QALY) gained. OUTCOME MEASURES: Cost per QALY gained from laser therapy and cryotherapy. RESULTS: Laser photocoagulation therapy for threshold ROP costs $678 1998 US dollars (at a 3% discount rate to account for the time value of money) for each QALY gained from treatment. Cryotherapy for the same disease costs $1801 per QALY at a similar discount rate. CONCLUSIONS: From the point of view of cost-effectiveness, laser therapy seems to have an advantage over cryotherapy for the treatment of threshold ROP.

Computer Simulation↗
PubMed1999

Evidence-based medicine and cost-effectiveness.

Most available medical management techniques compare the practice patterns of providers with other providers but overlook the inherent value of interventional medical therapies to patients and society. The authors present a methodology for objectively evaluating the quality and cost-effectiveness of medical interventional therapies, and comparing them to each other using the common denominator of cost per quality-adjusted life-year ($/QALY). Advantages of this methodology include the fact that it: (1) compares the cost-effectiveness of different treatment regimens, (2) incorporates patient preferences, (3) employs evidenced-based medical data, information that is most reliable and reproducible, (4) factors in the effect of treatment on the quality of life and length of life, (5) offers an evaluation of the clinical efficacy of a treatment, (6) identifies both superior and marginal treatments, (7) maximizes the effective use of scarce resources, and (8) simplifies the understanding of health care procedures for consumers, payers, and providers.

Cost-Benefit Analysis↗
PubMed1999

Vision and quality-of-life.

OBJECTIVE: To determine the relationship of visual acuity loss to quality of life. DESIGN: Three hundred twenty-five patients with visual loss to a minimum of 20/40 or greater in at least 1 eye were interviewed in a standardized fashion using a modified VF-14, questionnaire. Utility values were also obtained using both the time trade-off and standard gamble methods of utility assessment. MAIN OUTCOME MEASURES: Best-corrected visual acuity was correlated with the visual function score on the modified VF-14 questionnaire, as well as with utility values obtained using both the time trade-off and standard gamble methods. RESULTS: Decreasing levels of vision in the eye with better acuity correlated directly with decreasing visual function scores on the modified VF-14 questionnaire, as did decreasing utility values using the time trade-off method of utility evaluation. The standard gamble method of utility evaluation was not as directly correlated with vision as the time trade-off method. Age, level of education, gender, race, length of time of visual loss, and the number of associated systemic comorbidities did not significantly affect the time trade-off utility values associated with visual loss in the better eye. The level of reduced vision in the better eye, rather than the specific disease process causing reduced vision, was related to mean utility values. The average person with 20/40 vision in the better seeing eye was willing to trade 2 of every 10 years of life in return for perfect vision (utility value of 0.8), while the average person with counting fingers vision in the better eye was willing to trade approximately 5 of every 10 remaining years of life (utility value of 0.52) in return for perfect vision. CONCLUSIONS: The time trade-off method of utility evaluation appears to be an effective method for assessing quality of life associated with visual loss. Time trade-off utility values decrease in direct conjunction with decreasing vision in the better-seeing eye. Unlike the modified VF-14 test and its counterparts, utility values allow the quality of life associated with visual loss to be more readily compared to the quality of life associated with other health (disease) states. This information can be employed for cost-effective analyses that objectively compare evidence-based medicine, patient-based preferences and sound econometric principles across all specialties in health care.

Adult↗
PubMed1998

Transcellular regulation of cell respiration by nitric oxide generated by activated macrophages.

A macrophage cell line (J774), activated with interferon-gamma and endotoxin to express the inducible form of NO synthase (iNOS), immediately inhibited the cellular respiration of co-incubated L-929 fibroblasts or non-activated J774 macrophages. The inhibition was potent, rapid and reversible when the NO was removed by adding oxyhaemoglobin or by inhibiting iNOS. Exogenously added NO also rapidly and reversibly inhibited cellular respiration over the same range of NO concentrations. This inhibition was competitive with oxygen and due to direct inhibition of cytochrome oxidase. Thus, NO generated by one cell can regulate the respiration of adjacent cells, supporting the hypothesis that NO may be a physiological and/or pathological regulator of cellular respiration, via its inhibition of cytochrome oxidase.

Animals↗
PubMed1998

Quantification of the relative contribution of parallel pathways to signal transfer: application to cellular energy transduction.

A simple mathematical formalism designed to quantify the relative contribution of parallel pathways to signal transduction is presented and applied to the regulation of the respiration rate by ATP, ADP and Pi concentrations in response to an increase of energy demand in isolated mitochondria. Theoretical studies were performed by means of the computer model of oxidative phosphorylation developed previously. Many earlier experimental studies have shown that externally-manipulated concentrations of all three metabolites can influence the respiration rate significantly. However, the effect of changes in [ATP], [ADP] and [Pi] that actually take place during an increased energy demand have not been determined in a quantitative way. It was shown in the present paper that [ADP] is the main regulatory factor which stimulates respiration during transition from state 4 to state 3 imposed by an addition of increasing amounts of an artificial ADP-regenerating system. Changes in [ATP] and [Pi] contribute to the respiration rate increase very weakly, and only in the nearest neighbourhood of state 3. Generally, changes in [ADP] are responsible for approx. 90% of the respiration rate increase during the state 4-->state 3 transition, while the remaining approx. 10% is due to changes in [Pi] and [ATP].

Adenosine Diphosphate↗
PubMed1998

Persistent inhibition of cell respiration by nitric oxide: crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione.

Both reversible and irreversible inhibition of mitochondrial respiration have been reported following the generation of nitric oxide (NO) by cells. Using J774 cells, we have studied the effect of long-term exposure to NO on different enzymes of the respiratory chain. Our results show that, although NO inhibits complex IV in a way that is always reversible, prolonged exposure to NO results in a gradual and persistent inhibition of complex I that is concomitant with a reduction in the intracellular concentration of reduced glutathione. This inhibition appears to result from S-nitrosylation of critical thiols in the enzyme complex because it can be immediately reversed by exposing the cells to high intensity light or by replenishment of intracellular reduced glutathione. Furthermore, decreasing the concentration of reduced glutathione accelerates the process of persistent inhibition. Our results suggest that, although NO may regulate cell respiration physiologically by its action on complex IV, long-term exposure to NO leads to persistent inhibition of complex I and potentially to cell pathology.

Animals↗
PubMed1998

Control of oxidative phosphorylation, gluconeogenesis, ureagenesis and ATP turnover in isolated perfused rat liver analyzed by top-down metabolic control analysis.

We have analyzed the control exerted by the pathways of oxidative phosphorylation, gluconeogenesis, ureagenesis, and maintenance ATP consumption over each other's rates in isolated, perfused rat liver using top-down metabolic control analysis. The livers from fasted rats were perfused with 3-hydroxybutyrate as respiratory substrate, lactate as substrate for gluconeogenesis, and ammonium as substrate for urea synthesis, in conditions where these pathways were only linked by their common intermediates: ATP, ADP, and Pi. The rates of oxygen consumption, glucose and urea synthesis were measured continuously. The pathways were perturbed either by adding specific inhibitors or by adding new pathways that consumed ATP, and the relative changes in pathway rates were used to calculate the flux control coefficients of each pathway over all pathway rates. When the liver was in a relatively inactive metabolic state, where ATP was only being used by the maintenance ATP-consuming pathways, then essentially all the control over ATP production and consumption was located in the maintenance ATP consumers with ATP production having no control. Whereas, when the liver was in a highly active state using extra ATP for both glucose and urea synthesis, then ATP production (from oxidative phosphorylation) had strong control over its own rate and the rates of glucose and urea synthesis, but gluconeogenesis and ureagenesis still had strong control over their own rates and negative control over each others rates, i.e. they competed for the limited ATP supply. The rate of the maintenance ATP consumers is remarkably insensitive to changes in ATP production and consumption, but exerts considerable control over all other pathways. These results indicate that the general assumption that the rates of ATP production and consumption are controlled exclusively by ATP consumers is false under conditions where a significant amount of ATP is used for biosynthetic processes, such as glucose and urea synthesis, and indicate that the latter processes may be partly controlled by regulators of ATP production and by other ATP-consuming pathways.

3-Hydroxybutyric Acid↗
PubMed1998

An interlaboratory study to find an alternative to the MPN technique for enumerating Escherichia coli in shellfish.

Nine laboratories in eight countries tested 16 batches of common mussels (Mytilus edulis) over a 32 week period in order to find an alternative to the Most Probable Number (MPN) technique to enumerate E. coli. The alternatives investigated included the 3M Petrifilm system, the Merck Chromocult agar method and a Malthus conductance technique. The Petrifilm was found to be unsuitable and was subsequently dropped from the trial. After 669 analyses, a correlation of 0.83 was observed for log E. coli counts between the MPN and Chromocult methods and there was no significant evidence that either method tended to give higher readings than the other. The MPN was slightly better than the Chromocult method for repeatability but the Chromocult was slightly better for reproducibility. However, the observed differences are probably too small to be of practical importance. On the basis of these data therefore, the two methods appear equally suitable for E. coli enumeration in shellfish. There were poor correlations between these methods and the Malthus technique. A small but significant number of samples tested positive on the Malthus instrument but were recorded negative on the MPN and Chromocult tests. Subsequent analysis positively identified E. coli from these Malthus assays. After statistical analysis, errors were noted in both the MPN and Chromocult methods but it was found that there would be no statistical differences if the Chromocult agar were used as an alternative to the MPN technique.

Colony Count, Microbial↗
PubMed1998

Does a visible retinal embolus increase the likelihood of hemodynamically significant carotid artery stenosis in patients with acute retinal arterial occlusion?

OBJECTIVE: To determine the value of visible retinal emboli as a diagnostic "test" for the detection of hemodynamically significant carotid artery stenosis in the setting of acute retinal artery occlusion. METHODS: A cross-sectional diagnostic accuracy study was performed in a tertiary North American center, with the results of the dichotomous diagnostic test (the presence or absence of visible retinal emboli) being placed against the dichotomous outcome of the presence or absence of hemodynamically significant carotid artery stenosis (defined as > or = 60%, or < 60%, carotid artery stenosis on either side). RESULTS: Forty-eight (18.7%) of our 256 patients had hemodynamically significant carotid artery stenosis. The sensitivity and specificity of retinal emboli for the detection of hemodynamically significant carotid artery stenosis were 39% and 68%, respectively. The presence of a visible retinal embolus generated a likelihood ratio of 1.24 (95% confidence interval, 0.84-1.86). This value corresponds to a patient with a pretest probability of 50% having a posttest probability of 55.3%. The absence of a visible retinal embolus generated a likelihood ratio of 0.88 (95% confidence interval, 0.68-1.15). CONCLUSIONS: The presence of a visible retinal embolus is a poor diagnostic test for the detection of hemodynamically significant carotid artery stenosis in the setting of acute retinal artery occlusion. Accordingly, the presence of an embolus should not influence the decision to perform carotid Doppler ultrasonography in patients with acute retinal arterial occlusion.

Adult↗