Aqueous flare in eyes with choroidal malignant melanoma.
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Aqueous Humor↗
Biomedical subjects
N X Nguyen
Publications and source records attributed to N X Nguyen.
Quantitative assessment of aqueous flare and aqueous 'cells' in pseudoexfoliation syndrome.
We used the laser flare-cell meter to measure aqueous flare and aqueous 'cells' in 38 eyes of 38 patients with pseudoexfoliation, in 36 normal control eyes of 36 subjects, and in 19 eyes of 19 patients with chronic open-angle glaucoma unrelated to pseudoexfoliation. In pseudoexfoliation eyes, both aqueous flare (0.61 +/- 0.55 mg/ml human albumin equivalent) and aqueous 'cells' (mean 10.70, range 0-50.6 cells/0.075 mm3) were significantly higher than in the normal control group (flare 0.15 +/- 0.06 mg/ml, 'cells' 0.43, range 0-2, P less than 0.0001) and in the glaucoma group without pseudoexfoliation (flare 0.19 +/- 0.08 mg/ml, 'cells' 0.80, range 0-2.4, P less than 0.0001 and P less than 0.005). No significant difference could be found between the flare and cell counts of normal eyes and glaucoma eyes without pseudoexfoliation (P greater than 0.09, P greater than 0.05) and between PSX eyes with (18 eyes) and without (20 eyes) open-angle glaucoma (P greater than 0.99, P greater than 0.4). Our findings indicate that the blood-aqueous barrier is impaired in eyes with pseudoexfoliation, and that the laser flare-cell meter may be a useful tool to quantify these changes. These alterations of the blood-aqueous barrier need to be considered in medical therapy and intraocular surgery.
Aged↗
Quantitative measurement of aqueous flare and aqueous "cells" in eyes with diabetic retinopathy.
In order to evaluate the applicability of the laser flare-cell meter to diabetic oculopathy, we measured aqueous flare and aqueous "cells" in 84 diabetic eyes of 84 patients and 50 normal control eyes of 50 age-matched subjects. Using fluorescein angiography, diabetic retinopathy was divided into background retinopathy (11 eyes), preproliferative retinopathy (38 eyes), and proliferative retinopathy (35 eyes). In diabetic eyes, the occurrence of both aqueous flare (0.73 +/- 0.39 mg/ml human albumin equivalent) and aqueous cells (mean 2.96, range 0-35.7 cells/0.075 mm3) was significantly greater than in the normal control group (flare 0.14 +/- 0.06 mg/ml, cells 0.39, range 0-2 cells/0.075 mm3, P < 0.0001 and P < 0.0002, respectively). The flare values also showed differences between the diabetic subgroups, with flare values being higher in more advanced stages of diabetic retinopathy. No significant correlation could be found between the flare values and the kind of diabetic therapy, the duration of the diabetes, and the number of or the time interval since previous retinal laser coagulations. A flare value of more than 0.5 mg/ml was found to represent probably a "critical value" indicating a tendency towards preproliferative and or proliferative changes. The laser flare-cell meter is a valuable instrument for noninvasive, quantitative assessment of alterations of the blood-aqueous barrier in diabetes. The increase of flare values seems to parallel the progression of diabetic retinopathy.
Adult↗
[Neuroretinal rim in eyes with simple optic atrophy].
In comparison with normal eyes, eyes affected by glaucomatous optic nerve damage are characterized by a decreased neuroretinal rim area and an increased optic cup size. This study was performed to find whether eyes with nonglaucomatous optic nerve atrophy and normal eyes differ with respect to the neuroretinal rim. In all, 143 eyes with nonglaucomatous descending optic nerve atrophy and 563 normal eyes were biomorphometrically examined. The area and form of the neuroretinal rim and optic cup and the horizontal and vertical cup-to-disc ratios did not differ significantly between the two groups. These results are in part not supported by data in the literature. If they are confirmed by further studies, they will indicate that measurement of the neuroretinal rim and estimation of the cup-to-disc ratios will not be useful for the diagnosis of damage to the descending nonglaucomatous optic nerve. It will be helpful for the differentiation of eyes with glaucomatous and nonglaucomatous optic nerve atrophy.
Adult↗
Role of intravenous isoproterenol in the electrophysiologic induction of atrioventricular node reentrant tachycardia in patients with dual atrioventricular node pathways.
To assess the role of intravenous isoproterenol for the facilitation of electrophysiologic induction of atrioventricular (AV) node reentrant tachycardia, 20 patients with dual AV node pathways who lacked inducible AV node reentrant tachycardia at control study had a constant isoproterenol infusion administered and underwent repeat study. Six (30%) of 20 patients (group I) had inducible AV node reentrant tachycardia during isoproterenol infusion whereas the other 14 (70%) patients (group II) did not. Paroxysmal supraventricular tachycardia was clinically documented in all 6 group I patients compared to 3 (21%) of 14 group II patients (p = 0.002). The sensitivity and specificity of isoproterenol-facilitated induction of AV node reentrant tachycardia were 67 and 100%, respectively. The isoproterenol-facilitated induction of sustained AV node reentry was mediated by resolution of the weak link in anterograde slow pathway in 2 (33%) patients, in retrograde fast pathway in 3 (50%) and in both anterograde slow and retrograde fast pathways in 1 (17%) patient. Four group I patients were given intravenous propranolol, 0.2 mg/kg body weight, and had complete suppression of isoproterenol-facilitated induction of AV node reentry. Thus, intravenous isoproterenol is a rather sensitive and highly specific adjunct to electrophysiologic induction of AV node reentrant tachycardia in patients with dual AV node pathways but without inducible sustained AV node reentry.
Adrenergic beta-Antagonists↗
Electrophysiologic manifestations of the excitable gap of orthodromic atrioventricular reciprocating tachycardia demonstrated by single extrastimulation.
To assess the electrophysiologic characteristics of the excitable gap, 12 patients with orthodromic atrioventricular (AV) reciprocating tachycardia were studied. During tachycardia, 8 patients used a left-sided and 4 patients a right-sided anomalous bypass tract for retrograde conduction. QRS complex-synchronized single extrastimuli were delivered from high right atrium, right ventricular apex and coronary sinus, respectively, scanning the whole cycle length of tachycardia. An excitable gap was determined to be present if tachycardia resetting or tachycardia termination occurred. The duration of the excitable gap varied among different pacing sites and occupied 0 to 48% (mean 17 +/- 16) of basic tachycardia cycle length (240 to 480 ms, mean 327 +/- 70). Three patterns of tachycardia resetting were observed: the sum of coupling interval and return cycle being (1) less than a fully compensatory pause in 12 of 12 patients, (2) more than a fully compensatory pause in 5 of 12 patients and (3) equal to a fully compensatory pause in 2 of 12 patients, depending on extent of AV nodal conduction delay exhibited in return cycle. Tachycardia termination was possible when extrastimuli were delivered from right ventricular apex and coronary sinus but not from high right atrium, and only when basic tachycardia cycle length was greater than or equal to 290 ms in 7 of 12 patients. Tachycardia termination was accounted for by development of orthodromic conduction block in AV node in 7 of 7 patients and in bypass tract in 2 of 7 patients. Therefore, site of extra-stimulation and basic tachycardia cycle length affect electrophysiologic manifestations of excitable gap. Further, functional properties of the AV node influence patterns of tachycardia resetting and are primarily responsible for tachycardia termination during programmed single extrastimulation.
Adult↗
The retinal nerve fiber layer in normal eyes.
The retinal nerve fiber layer is different in normal and glaucomatous eyes. The authors used red-free photographs to examine the retinal nerve fiber layer in 234 normal eyes. The retinal nerve fiber layer was most visible in the inferior temporal arcade, followed by the superior temporal arcade, then by the temporal macular area, and finally the nasal area. This distribution was significantly (P less than 0.0001) correlated to (1) the configuration of the neuroretinal rim, which was significantly broadest at the inferior disc pole followed by the superior one, (2) the juxtapapillary caliber of the retinal vessels, which were significantly wider in the inferior temporal arcade than in the superior temporal arcade, and (3) the location of the foveola 0.53 +/- 0.34 mm inferior to the middle point of the vertical optic disc axis. The retinal nerve fiber layer decreased with age. No correlation occurred with sex or right or left eye. No localized retinal nerve fiber layer defects were seen. These features of the normal retinal nerve fiber layer are important for diagnosis of retinal nerve fiber layer changes secondary to optic nerve damage in the diseased eye.
Adolescent↗
[The retinal nerve fiber layer in normal eyes and in glaucoma. I. Semiquantitative data of 398 eyes with glaucoma].
Atrophy of the optic nerve is associated with changes of the retinal fiber layer (RNFL). Using red-free photographs the authors examined the RNFL of 398 eyes with chronic primary open-angle glaucoma and compared it with the RNFL of 234 normal eyes. The glaucoma group was divided into five stages and the fundus into four sectors. Differences between the normal and glaucoma eyes were: (1) The sequence of the sectors, with regard to the best visibility of the retinal nerve fiber bundles, was changed. In the normal eyes the nerve fiber bundles were most often best visible in the inferior temporal sector, followed by the superior temporal sector, the temporal horizontal area and finally the nasal region. In the glaucoma group the nerve fiber bundles were significantly more often best detectable in the superior temporal sector and the temporal horizontal area. (2) The degree of visibility of the retinal nerve fibers decreased significantly with increasing glaucoma stage. (3) Localized defects were seen in 15% of the eyes with glaucoma and none of the normal eyes. The specificity of this qualitative parameter was, therefore, 100%. The defects were found most often in the superior and inferior temporal regions. These differences between normal and glaucomatous eyes were also significant for the first glaucoma stage of this study. The localization of the foveola below the optic disk center (0.53 +/- 0.34 mm in the glaucoma group and 0.55 +/- 0.29 mm in the normal eyes) was not significantly different.
Adolescent↗
[The retinal nerve fiber layer in normal and glaucomatous eyes. II. Correlations].
The retinal nerve fiber layer is different in normal and glaucomatous eyes. We correlated semi-quantitative data of the retinal nerve fiber layer of 398 eyes with chronic primary open-angle glaucoma and of 234 normal eyes with the intra- and parapapillary morphometric signs and with the perimetric indices. The three parameters "sequence of the fundus sectors concerning the best visibility of the retinal nerve fiber bundles", "visibility of the nerve fiber bundles", and "localized defects" were significantly (p less than 0.001) correlated to 1) area of the neuroretinal rim as a whole and in four different optic disc sectors, 2) neuroretinal rim width determined every 30 degrees, 3) optic cup area, diameters and form, 4) horizontal and vertical cup/disc ratios and the quotient of the horizontal to vertical cup/disc ratio, 5) area and width of zone "Alpha", zone "Beta", and the total parapapillary chorio-retinal atrophy, 6) diameter of the retinal vessels, 7) grade of a "tesselated fundus", and 8) the visual field loss. If only the inferior temporal and the superior temporal sectors were considered, the retinal nerve fiber bundles were less visible in that sector with the largest notch in the neuroretinal rim, the smaller neuroretinal rim area and width, the thinner retinal vessels, and the larger zone "Alpha", zone "Beta", and total parapapillary chorio-retinal atrophy. The glaucomatous changes in the retinal nerve fiber layer are correlated in time and location with the intra- and parapapillary and the perimetric alterations. Evaluation of the retinal nerve fiber layer is a useful method to detect a glaucomatous optic nerve damage.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Optic disc morphometry in simple optic nerve atrophy.
This study was undertaken to evaluate the optic disc changes in eyes with non-glaucomatous optic nerve damage. The intra- and parapapillary region was evaluated morphometrically in 106 eyes of 56 patients with simple optic nerve atrophy (SONA) and in 107 normal eyes of 57 subjects. Colour stereo optic disc diapositives were used. Only one randomly chosen eye per subject and patient was taken for statistical analysis. Characteristics of SONA were: decreased visibility of the parapapillary retinal nerve fibers, diminished retinal vessel diameter, and area with pallor larger than area with cupping. Size and form of the optic disc, neuroretinal rim, peripapillary scleral ring, and zone Alpha and Beta of the parapillary chorioretinal atrophy were not significantly different. Also, distinctness of a tesselated fundus, frequency of optic disc haemorrhages and frequency of bared circumlinear or bared cilioretinal vessels did not differ significantly. These morphologic features are helpful in the diagnosis and differential diagnosis of SONA.
Adult↗
Non-quantitative morphologic features in normal and glaucomatous optic discs.
Glaucoma is associated with changes of the optic disc topography. Using color stereo photographs we examined non-quantitative signs in 584 optic discs of 308 patients with chronic primary open-angle glaucoma and in 383 optic discs of 236 age and refraction matched normal subjects. Only one eye per patient and normal subject was chosen for statistical analysis. Highest predictive value to differentiate between normal and glaucoma eyes had the parameters 'changes in the juxtapapillary retinal nerve fiber layers' (86.7%), 'abnormal size (79.8%) and abnormal location (68.6%) of the parapapillary chorio-retinal atrophy', 'smallest neuroretinal rim part outside of the temporal horizontal disc sector' (78.5%), and area with cupping larger than area with pallor' (68.2%). Characteristics with high specificity and low sensitivity were 'optic disc haemorrhages', 'bared cilioretinal arteries', and 'bared circumlinear vessels'. With their evaluation being independent of sophisticated techniques the non-quantitative parameters are helpful for the ad hoc diagnosis of glaucomatous optic nerve damage.
Adult↗
[Planimetry of glaucomatous, para-papillary, chorio-pigment epithelial retinal atrophy].
Glaucomatous optic nerve damage is associated with changes in the parapapillary region. These changes were measured on 15 degrees color stereo slides of the optic nerve head. We examined 450 eyes of 330 patients suffering from chronic primary open-angle glaucoma and 200 eyes of 161 normal subjects. The glaucoma group was divided into five stages according to the neuroretinal rim configuration. In the parapapillary region, the "alpha" zone characterized by irregular hypo- and hyperpigmentation, and the "beta" zone (large visible choroidal vessels and visible sclera) were differentiated. Zone "beta" was located between the optic disc and zone "alpha". Both zones were significantly larger in the total glaucoma group (p less than 0.00001, Mann-Whitney-test), and in each of the five glaucoma stages, than in the normal subjects. Zone "beta" increased in size more than zone "alpha". The parapapillary region deserves special attention in the diagnosis of glaucoma.
Adult↗
Effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability in patients with paroxysmal supraventricular tachycardia.
To assess the effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability, the electrophysiologic properties of the atrium were studied before and during intravenous infusion of isoproterenol at 2 to 5 micrograms/min in 11 patients with paroxysmal supraventricular tachycardia exhibiting atrial latency during programmed atrial extrastimulation. In all patients, the isoproterenol infusion reduced the extent of maximum atrial latency (from 86 +/- 19 to 62 +/- 16 ms, p less than 0.001). This was accompanied by a significant shortening of both effective and functional refractory periods of the atrium (from 213 +/- 31 to 174 +/- 40 ms, p less than 0.005 and from 259 +/- 31 to 215 +/- 29 ms, p less than 0.001, respectively). The intra-atrial and interatrial conduction times were also significantly reduced (from 24 +/- 15 and 63 +/- 17 to 15 +/- 10 and 48 +/- 15 ms, p less than 0.005, respectively). In 3 patients with demonstrable atrial vulnerability, the isoproterenol infusion abolished the inducibility of repetitive atrial responses or atrial flutter, or both. Although the clinical significance of the suppressive action of beta-adrenergic stimulation on atrial vulnerability remains to be determined, the present study has demonstrated that beta-adrenergic stimulation significantly reduces atrial latency.
Adult↗
Spontaneous conversion of atrial flutter to antidromic atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome.
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Adult↗
Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias.
To assess effects of beta-adrenergic blockade on ventricular tachycardia (VT) of various mechanisms, electrophysiology studies were performed before and after intravenous infusion of propranolol (0.2 mg/kg) in 33 patients with chronic recurrent VT, who had previously been tested with intravenous verapamil (0.15 mg/kg followed by 0.005 mg/kg/min infusion). In the verapamil-irresponsive group, 10 patients (group IA) had VT that could be initiated by programmed ventricular extrastimulation and terminated by overdrive ventricular pacing, and 11 patients (group IB) had VT that could be provoked by isoproterenol infusion (3-8 micrograms/min) but not by programmed electrical stimulation, and that could not be converted to a sustained sinus rhythm by overdrive ventricular pacing. Notably, in the group IA patients, all 10 patients had structural heart disease (coronary arteriosclerosis or idiopathic cardiomyopathy); beta-adrenergic blockade accelerated the VT rate in one patient but exerted no effects on the VT rate in the remaining 9 patients, and VT remained inducible in all 10 patients. By contrast, in the group IB patients, 7 of the 11 patients had no apparent structural heart disease; beta-adrenergic blockade completely suppressed the VT inducibility during isoproterenol infusion in all 11 patients. There were 12 patients with verapamil-responsive VT (group II). 11 of the 12 patients had no apparent structural heart disease. In these patients, the initiation of VT was related to attaining a critical range of cycle lengths during sinus, atrial-paced or ventricular-paced rhythm; beta-adrenergic blockade could only slow the VT rate without suppressing its inducibility. Of note, 14 of the total 33 patients had exercise provocable VT: two in group IA, five in group IB, and seven in group II. Thus, mechanisms of VT vary among patients, and so do their pharmacologic responses. Although reentry, catecholamine-sensitive automaticity, and triggered activity related to delayed afterdepolarizations are merely speculative, results of this study indicate that beta-adrenergic blockade is only specifically effective in a subset group (group IB) of patients with VT suggestive of catecholamine-sensitive automaticity.
Adolescent↗
Verapamil and ventricular tachyarrhythmias.
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Arrhythmias, Cardiac↗
Postexertional cardiac asystole in a young man without organic heart disease.
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Adult↗
Reversal of left ventricular intracavitary gradient with intracavitary diastolic regurgitation in hypertrophic obstructive cardiomyopathy.
A 73 year old man presented with angina and nonsustained ventricular tachycardia. Cardiac catheterization revealed the dynamic systolic intracavitary gradient of hypertrophic obstructive cardiomyopathy. Abnormal isovolumetric relaxation resulted in the development of a diastolic gradient from the left ventricular outflow tract to the left ventricular apex accompanied by intracavitary regurgitation of contrast material from the outflow tract to the left ventricular body during left ventriculography. This case provides hemodynamic and angiographic confirmation of abnormal isovolumetric relaxation in this syndrome and insight into its mechanism.
Aged↗