Search PubMed⌕ Search

Biomedical subjects

N X Nguyen

Publications and source records attributed to N X Nguyen.

85 records · Page 5Linked to original sources
PubMed1989

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↗
PubMed1989

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↗
PubMed1989

[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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1986

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↗
PubMedDate not supplied

[A clinical comparative study of tyndallometry using 2 laser flare meters].

BACKGROUND: The laser flare meter FM-500 (Kowa, diode laser, 670 nm) is a simplified version of the laser flare-cell meter FC-1000 (Kowa, He-Ne laser, 632.8 nm). the aim of this study was to compare flare measurements of the laser flare meter FC-500 with the established laser flare-cell meter FC-1000 and to determine the reproducibility of both instruments in vivo. PATIENTS AND METHODS: Ten eyes of 10 normal subjects (mean age 32.2 +/- 8.0 y) and 21 eyes of 21 patients (mean age 36.7 +/- 17.2 y) with various forms of uveitis were included in the study. Aqueous flare was quantified using the laser flare-cell meter FC-1000 and the laser flare meter FM-500 by one examiner under comparable conditions. The selection of eyes as well as the order of the examinations were done in a randomized fashion. Measurements with both instruments were repeated the following day in normal eyes. Statistical analysis was done using linear regression analysis, intraclass correlation and U-test. RESULTS: Flare values (photon counts/ms) did not differ significantly between the instruments either for normal eyes (3.3 +/- 0.4 vs 3.5 +/- 0.6) or for eyes with uveitis (16.2 +/- 9.0 vs 16.4 +/- 8.7). A high correlation of flare counts between both instruments was observed in normal eyes (r = 0.73, p < 0.001) and a very high correlation in eyes (R = 0.99, p < 0.0001) with mildly to moderately increased counts (< 50 photon counts/ms). Differences between flare values of both instruments were -0.17 +/- 0.4, range -0.8 +/- 0.6 in the normal eyes and -0.23 +/- 1.38, range -3.1 +/- 3.4 in the patients with mildly to moderately increased flare counts. However, flare counts differed for very high aqueous flare in one patient with acute fibrinous iridocyclitis with the FM-500 indicating higher values. The intraclass correlation coefficients were 0.70 for the FC-1000 and 0.76 for the FM-500 in normal eyes and 0.99 for both instruments in eyes with uveitis. CONCLUSIONS: In eyes without or with mild to moderate breakdown of the blood-aqueous barrier, the two instruments give comparable results. However, measurements may differ in eyes with high flare readings.

Adult↗
PubMedDate not supplied

Impact of increased intraocular pressure on long-term corneal endothelial cell density after penetrating keratoplasty.

PURPOSE: Besides immunological graft rejection, persistently increased intraocular pressure (IOP) is among the most important causes for graft failure after penetrating keratoplasty (PK). The purpose of this study was to assess the longitudinal development of IOP after PK and to investigate possible correlations with corneal endothelial cell density. METHODS: This longitudinal prospective study included 209 eyes after PK with a complete follow-up at 3 months, 6 months, before first suture removal (16 +/- 5 months) and after complete suture removal (21 +/- 5 months). At each examination, IOP was measured by Goldmann applanation tonometry. Endothelial cell density was assessed by specular microscopy (EM 1100, Tomey). The indications for PK were 48% keratoconus, 34% Fuchs' dystrophy, 5.4% stromal dystrophies, 8.6% secondary bullous keratopathy and 4% corneal scars. An iridotomy was performed routinely during PK. The postoperative treatment with topical steroids was standardized. RESULTS: Preoperatively, the mean IOP was 13.6 +/- 2.9 mm Hg with increased IOP (>21 mm Hg) in 2.0% of eyes. After 3 months, the incidence of increased IOP (24.5 +/- 4.6 mm Hg) was highest (6.7%) and decreased thereafter to 3.0% after complete suture removal. No patients showed IOP higher than 30 mm Hg. A persistently increased IOP for more than 3 months was seen in 2% of patients. At 3 months postoperatively, the mean endothelial cell density was 1,977 +/- 496/mm(2) and did not decrease significantly (p > 0.05) until 6 months (1,771 +/- 507 cells/mm(2)). At the end of the follow-up period, the mean endothelial cell density was significantly reduced (1,347 +/- 501 cells/mm(2)). There was no significant correlation between IOP and mean endothelial cell density at any postoperative examination stage (p > 0.24). Patients with persistently increased IOP for more than 3 months did not have significantly different endothelial cell densities in comparison with those without increased IOP. CONCLUSION: From 6 months after PK, the incidence of increased IOP was not higher than the preoperative level. Mild to moderate temporary IOP elevations after PK do not seem to affect the endothelial cell density of the graft until complete suture removal. Further long-term studies are necessary to assess the clinical relevance of these observations.

Cell Count↗
PubMedDate not supplied

What do PPS margins mean? Different things to different groups.

Since the inception of Medicare's prospective payment system (PPS) in 1983, the interpretation of Medicare PPS operating margins has generated much debate and confusion. Numerous estimates often show considerable range from the highest to the lowest within roughly the same time periods. In almost all instances the reason for these differences is attributable to elements of the study design. In this article adapted from a paper he wrote for The Catholic Health Association, Allen Dobson identifies and describes the legitimate reasons for differences among studies of Medicare PPS operating margins. His paper provided a useful framework for reviewing studies of this type. He determined that three sets of factors--statistical, methodological, and interactive--influence the magnitude of margin estimates. Dr. Dobson concluded that the various margin estimates all show essentially the same thing: Margins under PPS have fallen significantly and are likely to continue to do so as long as actual case costs rise more rapidly than actual case revenues. By PPS year 6, few types of hospitals are likely to receive adequate funds from Medicare to cover their expenses.

Costs and Cost Analysis↗