High-Density Circumferential Pulmonary Vein Mapping with a 20-Pole Expandable Circular Mapping Catheter

The differentiation of pulmonary vein (PV) electrograms from atrial far-field signals during PV isolation (PVI) for atrial fibrillation (AF) may be difficult. In addition, owing to highly variable PV ostial sizes, current fixed-diameter circular PV mapping catheters may not yield optimal electrograms. We evaluated an expandable, circular 15–25 mm diameter, 20-pole mapping catheter for PV mapping during sustained AF in 25 patients. After selective PV angiography to define the ostial position and size, the catheter was introduced into each PV and withdrawn to the most stable proximal position, with optimal wall contact ensured by progressive loop expansion. At each PV ostium, electrograms recorded at high resolution (HR) were compared with those recorded at a resolution similar to that of a standard 10-pole Lasso catheter. After PVI performed during ongoing AF, the presence of residual far-field potentials (FFP) under both set-ups was compared. We mapped 97 PV, including 4 pairs with common ostia. In the HR recordings, the PV potentials had greater amplitude (0.5 ± 0.1 vs 0.3 ± 0.1 mV, P = 0.001) and fragmentation, whereas left atrial FFP were minimized. After successful isolation of all PV, FFP were observed in 33% of left superior and 28% of left inferior PV on the HR recordings, compared to 66% and 61%, respectively under normal resolution. Catheter stability and optimal wall contact, in combination with HR electrograms can optimize circumferential PV mapping during AF and improve the discrimination of FFP postablation.     

Melatonin treatment for rhythm disorder

Abstract We tried melatonin treatment in two patients with non-24 h sleep-wake syndrome, who did not respond to treatments by vitamin B₁₂, bright light therapy, or hypnotics. In one patient, melatonin 5–10 mg improved difficulty in falling asleep and in waking, although it failed to improve the sleep-wake rhythm. In another patient, melatonin 3 mg successfully changed the sleep-wake rhythm from free-running pattern to delayed sleep phase pattern. However, melatonin re-administration after a 4-month drug-free interval failed to improve his free-running sleep-wake rhythm. These results suggest that melatonin acted as a sleep inducer in one patient and as a phase setter in the other, although the effect on the latter patient was transient.     

Down-regulation of inducible nitric oxide synthase (iNOS) in rat with congenital hydronephrosis

BACKGROUND: Most of our knowledge concerning obstructive uropathy has been derived mainly from surgically manipulated animal models, and the pathogenesis of congenital obstructive hydronephrosis is not fully elucidated. Nitric oxide (NO) acts as an important biological modulator with diverse physiological functions, which can be either toxic or protective depending on the situation. NO is synthesized from l-arginine by nitric oxide synthase, and in the kidney iNOS is expressed spontaneously. The aim of our study is to investigate the expression of iNOS protein and its relationship with tubulointerstitial fibrosis and tubular cell apoptosis in congenital hydronephrosis. METHODS: We conducted histological studies on 18 kidneys of six-week-old-rats from an inbred colony of congenital hydronephrosis with reference to the histological grading of the affected kidney, tubulointerstitial fibrosis, renal tubular atrophy, and tubular cell apoptosis. Renal transforming growth factor-beta1 (TGF-beta1) level was determined by a sandwich ELISA assay and the expression of iNOS was analyzed by western blotting. RESULTS: Most of the hydronephrotic kidneys were markedly enlarged with dilatation of the collecting system, parenchymal thinning, tubular atrophy, interstitial infiltration and fibrosis. Renal TGF-beta1 level was higher in hydronephrotic kidneys than normal control kidneys (364.81 +/- 52.60 vs. 221.19 +/- 22.53 pg/mg protein, P < 0.05). Tubular apoptotic score in hydronephrotic kidneys was also significantly higher than in the normal control kidneys (1.97 +/- 0.42 vs. 0.14 +/- 0.02/HPF, P < 0.01). The expression of iNOS protein was lower in the affected kidneys compared with the normal control kidneys (8.79 +/- 0.78 vs. 14.00 +/- 0.83 arbitrary unit, P < 0.01). There was a negative correlation between iNOS expression and histological grading in congenital hydronephrosis. The iNOS expression also correlated negatively with renal interstitial fibrosis, TGF-beta1 level and tubular cell apoptosis. CONCLUSION: Our study confirmed the down-regulation of iNOS expression in affected kidneys from rats with congenital hydronephrosis, in which the cytoprotective effect of NO may be lost or weakened.     

Gadolinium-enhanced breath-hold three-dimensional time-of-flight MR angiography of the abdominal and pelvic vessels: The value of ultrafast MP-RAGE sequences

MR angiography (MRA) was performed in 50 consecutive subjects (mean age, 59 years), who had been referred for abdominal MRA, on a 1.5-T superconductive unit that used a body phased-array coil. Three breath-hold three-dimensional sequences were evaluated both in phantom and clinical studies: (a) standard fast three-dimensional gradient-echo sequence (TR = 15, TE = 6; imaging time, 32 seconds), (b) ultrafast three-dimensional gradient-echo sequence (TR = 8.2, TE = 3; imaging time, 18 seconds), and (c) ultrafast magnetization-prepared (MP) rapid acquisition gradient echo (RAGE) (TR = 5.8, TE = 2.9, inversion time [TI] = 20; imaging time, 15 seconds). The initial 30 patients were randomized into three groups by three separate sequences. For the remaining 20 patients, ultrafast-gradient-echo and ultrafast MP-RAGE sequences were performed. Conventional angiography was performed on 36 patients. Signal measurements of the phantom and clinical images of the aorta, visceral branches of the aorta, iliac arteries, inferior vena cavae, and portal veins were performed. The overall image quality and background fatty tissue contrast of the vessels were rated subjectively. Comparison of images between MRA and conventional angiography also was performed. The contrast between the vessels and background fatty tissue was significantly higher in the ultrafast MP-RAGE sequence in both quantitative and qualitative analysis, and image-quality ultrafast MP-RAGE was superior to the other two sequences (P < .01). The aorta and iliac arteries could be visualized in all pulse sequences, and abnormalities of these vessels were diagnosed correctly. The renal artery was visualized more clearly with the two ultrafast sequences.     

Time after excision and temperature alter ex vivo tissue relaxation time measurements

Previously unreported effects of tissue storage were recently observed in the authors' experimental magnetic resonance (MR) studies. To evaluate the effect of elapsed time after excision and storage temperature on tissue relaxation time measurements, tissue samples from the liver, pancreas, kidney, testis, spleen, and brain were obtained in rats. T1 and T2 were first measured within 5 minutes of excision, and between subsequent measurements, tubes were kept in a water bath at 40°C, at room temperature (28°C), or in an ice bath (4°C). Cellular and organellar integrity was assessed with electron microscopy and correlated with the MR findings. At 40°C (20-MHz spectrometer), the T1 of liver decreased from 280 msec ± 8 to 212 msec ± 10 during the first 60 minutes; the T1 of pancreas decreased from 276 msec ± 3 to 208 msec ± 2. Other tissues showed less than a 5% decrease in T1. T2 changes were smaller than T1 changes in all tissues. Electron microscopy of pancreatic acinar cells showed postmortem changes in mitochondria evolving over the first 60 minutes after death. Manganese loading experiments implicated mitochondrial manganese stores in the observed enhanced postmortem decrease in T1. This study calls into question reported relaxation time data for liver and pancreas. MR studies of excised tissues must account for time and temperature to prevent systematic experimental errors.     

Immunoadsorbent apheresis eliminates pathogenic IgG in childhood lupus nephritis

BACKGROUND: It is suggested that the highly cation-charged fraction of the IgG and IgG3 subclasses may play a pathogenic role in lupus nephritis. In contrast, immunoadsorbent therapy using a sodium dextransulfate fixed cellulose gel column-low invasive selective immunoadsorbent apheresis therapy (SDSC-IAT) has been applied to lupus nephritis with favorable results. However, elimination using pathogenic IgG by SDSC-IAT has never been investigated. METHOD: Two patients with diffuse proliferative lupus nephritis were treated using SDSC-IAT concomitant with immunosuppressive therapy. The eluates from the SDSC, and the patients' serum obtained before and just after SDSC-IAT were subjected to an IgG charge analysis using isoelectric focusing and immunoblotting, and also to laser nephelometry assay, which is used for measuring IgG subclass concentration. Indirect immunofluorescence staining was performed to detect IgG subclass deposition in the glomerulus. RESULTS: Both of the patients had an immediate decrease in anti-double-strand DNA antibody and in the circulating immune complex with a following clinical improvement. Repeated biopsies demonstrated improvement of glomerular lesions with a marked reduction of IgG and C3 deposition. The IgG of the SDSC eluates consisted of highly cation charged (isoelectric points: 9-10) fractions. In addition, IgG3 was specifically removed from the patients' serum using an SDSC among the IgG subclasses. The subclass of deposited IgG in the glomeruli showed IgG3 predominance. CONCLUSION: SDSC-IAT specifically removed the highly cation charged fractions of IgG and IgG3 from the patients' serum and the elimination of these fractions may have resulted in clinical improvement.     

Abnormal cardiac histology in severe intrauterine growth retardation infants

Four infants with severe intrauterine growth retardation (IUGR) weighing less than 1000 g at birth developed heart failure and died in our unit, where heart failure of IUGR infants is the main reason of death in extremely low birth-weight infants. The causes of their heart failure are one of the main themes in current neonatal medicine. The subjects of this study were four small for gestational age infants; all died due to heart failure 5 to 10 days after birth. Microscopic specimens of hearts from autopsies were evaluated with respect to the following characteristics: thickness of myocardial fibers, maturation of nuclei, presence of dysgenesis or necrosis in myocardium, and amount of glycogen in the heart. Neither dysgenesis nor infarction of the heart was found but hypoplasia in myocardial fibers and decreased glycogen levels were observed. Maturation delay in myocytes' nuclei did not appear to be severe. We conclude that these infants' hearts failed to adapt to postnatal hemodynamic changes because of inadequate myocardial function and inadequate glycogen reserves.