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C Bondy

Publications and source records attributed to C Bondy.

At least 19 recordsLinked to original sources

Androgen-responsive aspects of cognition in girls with Turner syndrome.

Turner syndrome (TS) represents a unique, sex hormone-deficient model in which to study the biological effects of androgen treatment (replacement) on cognition in females because TS girls have gonadal dysgenesis and absent ovarian androgen and estrogen production. We investigated the effects of androgen replacement therapy in TS girls, ages 10-14 yr, on cognitive function. A total of 64 TS girls were randomized to receive oxandrolone or placebo for 2 yr. They had a cognitive evaluation of four domains (verbal abilities, spatial cognition, executive function, and working memory) at baseline, 1, and 2 yr of the study. In addition, all subjects were examined for study safety every 6 months. Three of the four domains studied did not change significantly in response to oxandrolone treatment (verbal abilities, spatial cognition, and executive function). In contrast, the working memory summary score had a significant group by time interaction. The oxandrolone-treated group demonstrated improved performance after 2 yr, compared with the placebo group (P < 0.03). Minimal or no side effects were observed. In conclusion, oxandrolone treatment for 2 yr improves working memory in adolescent girls with TS. What this degree of improvement will mean in real life terms for TS girls remains to be determined.

Anabolic Agents↗

Persistent cognitive deficits in adult women with Turner syndrome.

BACKGROUND: Turner syndrome (TS) has a characteristic neurocognitive profile. Verbal abilities are, in general, normal; however, women with TS, as a group, have specific deficits in visual-spatial abilities, visual-perceptual abilities, motor function, nonverbal memory, executive function, and attentional abilities. Observed deficits could be caused by genetic or endocrine factors. OBJECTIVE: To evaluate the specific cognitive deficits that appear to persist in adulthood, are not estrogen-responsive, and may be genetically determined. METHODS: The cognitive performance of adult women with TS (n = 71) who were estrogen repleted was compared with verbal IQ- and socioeconomic status-matched female controls (n = 50). Sixty-one women with TS had ovarian failure and received estrogen replacement and 10 had preserved endogenous ovarian function and were not receiving estrogen replacement at the time of evaluation. RESULTS: Similar to children and adolescents with TS, adults with TS have normal verbal IQ but have relative difficulty on measures of spatial/perceptual skills, visual-motor integration, affect recognition, visual memory, attention, and executive function despite estrogen replacement. These deficits are apparent in women with TS despite apparently adequate estrogen effect, either endogenous or by hormone replacement. CONCLUSION: The cognitive phenotypes of adults with TS, with or without ovarian failure, are similar, indicating that estrogen replacement does not have a major impact on the cognitive deficits of adults with TS.

Adolescent↗

Granulosa cell proliferation is impaired in the Igf1 null ovary.

Insulin-like growth factor-I (IGF-I) expression is highly correlated with ovarian follicular growth and granulosa cell proliferation in both pre-pubertal and mature murine ovaries. Igf1 gene deleted mice are infertile, with ovarian follicles arrested at an early stage of development. To elucidate the cause of follicular dysfunction in Igf1 null mice, this study compared granulosa cell proliferation at baseline and in response to exogenous oestradiol (E2) in prepubertal Igf1 null and wild-type (WT) littermate mice. The basal granulosa cell mitotic index was 3.8+/-0.48 in WT and 1.3+/-0.7 in Igf1 null mice (P=0.03). After E2 treatment, WT granulosa mitotic index was 12.7+/-0.0 vs 5.5+/-0.8 for Igf1 null mice (P<0.001). Granulosal BRDU incorporation was also significantly reduced as were cyclin D2 and B1 immunoreactivities in Igf1 null compared with WT mice. The incidence of apoptosis was not increased in Igf1 null follicles, although BAX immunostaining was increased. These data suggest that IGF1 is essential for normal basal and oestrogen-induced granulosa cell proliferation and follicular growth.

Animals↗

The somatomedin hypothesis: 2001.

Since the original somatomedin hypothesis was conceived, a number of important discoveries have allowed investigators to modify the concept. Originally somatic growth was thought to be controlled by pituitary GH and mediated by circulating insulin-like growth factor-I (IGF-I, somatomedin C) expressed exclusively by the liver. With the discovery that IGF-I is produced by most, if not all, tissues, the role of autocrine/paracrine IGF-I vs. the circulating form has been hotly debated. Recent experiments using transgenic and gene-deletion technologies have attempted to answer these questions. In the liverspecific igf-1 gene-deleted mouse model, postnatal growth and development are normal despite the marked reduction in circulating IGF-I and IGF-binding protein levels; free IGF-I levels are normal. Thus, the normal postnatal growth and development in these animals may be due to normal free IGF-I levels (from as yet unidentified sources), although the role of autocrine/paracrine IGF-I has yet to be determined.

Animals↗

Distribution and mRNA expression of insulin-like growth factor system in pulmonary lymphangioleiomyomatosis.

BACKGROUND: Insulin-like growth factors (IGF-1 and IGF-2), the IGF-1 receptor (IGF-1R), and IGF-binding proteins (IGFBPs) are involved in normal pulmonary development and in the pathogenesis of smooth muscle cell tumors. METHODS: To evaluate the role of the IGF system in lymphangioleiomyomatosis (LAM), we used immunohistochemical and in situ hybridization techniques to characterize the expression of IGF-1, IGF-2, IGF-1R, and IGFBP-2, -4, -5, and -6 in lung tissue from 18 LAM patients. RESULTS: IGF-1, ICGF-2, IGF-1R, IGFBP-1, IGFBP-2, IGFBP-4, IGFBP-5, and IGFBP-6 were expressed by LAM cells. Reactivity and mRNA expression for IGF-2 were observed in LAM cells and resembled that found in normal smooth muscle cells during pulmonary development as well as in smooth muscle cell tumors. IGFBP-2, IGFBP-4, and IGFBP-6 were associated with spindle-shaped LAM cells, whereas IGFBP-5 was associated mainly with epithelioid LAM cells. CONCLUSIONS: These findings suggest that the IGFBPs modulate the effects of the IGFs on LAM cells. Thus, the patterns of localization and expression of components of the IGF system in LAM strongly suggest that these agents are involved in the proliferation of LAM cells.

Adult↗

Importance of the IGF system in early folliculogenesis.

In the primate ovary, androgens promote oocyte insulin-like growth factor (IGF) I expression as well as initiation of follicle development. In most other mammals, IGFs do not appear to be required for the entry of follicles into the pool of growing follicles and for their gonadotropin-independent development. In contrast, IGFs are involved in the increase in FSH-responsiveness of granulosa cells when follicles enter into the gonadotropin-dependent stages of follicular development (200 microm in mouse, 2 mm in sheep, 5 mm diameter in cattle). In the late stages of folliculogenesis, the decrease in IGFBPs participates in the increase in IGF bioavailability, leading to a further amplification of FSH action.

Animals↗

Localization and sex steroid regulation of androgen receptor gene expression in rhesus monkey uterus.

OBJECTIVE: To characterize the cellular sites and hormonal regulation of uterine androgen receptor gene expression in the monkey. METHODS: Ovariectomized rhesus monkeys (five in each group) were treated with placebo (the control group), estradiol (E2), E2 plus progesterone, or E2 plus testosterone by sustained-release pellets administered subcutaneously. After 3 days of treatment, uteri were removed and uterine sections were analyzed by in situ hybridization for androgen receptor messenger RNA (mRNA). RESULTS: Androgen receptor mRNA was detected in endometrial stromal cells and myometrial smooth muscle cells, with lesser expression in endometrial epithelial cells. Both E2 and E2 plus progesterone treatment doubled androgen receptor mRNA levels in stromal cells (P < .01), whereas E2 plus testosterone treatment increased stromal androgen receptor mRNA levels by about five-fold (P < .001) compared with placebo treatment. In the endometrial epithelium, E2 alone did not increase androgen receptor mRNA levels significantly. However, the E2 plus progesterone and E2 plus testosterone treatments increased epithelial androgen receptor mRNA levels by 4.3 and 5 times, respectively (P = .008 and P < .002, respectively). Androgen receptor mRNA was distributed homogeneously in smooth muscle cells across the myometrium. Estradiol treatment alone did not increase myometrial androgen receptor mRNA levels significantly, but the E2 plus progesterone and E2 plus testosterone treatments increased myometrial androgen receptor mRNA levels by 1.8 and 2 times, respectively (P = .001 and P < .001, respectively). CONCLUSION: Androgen receptor gene expression was detected in all uterine cell compartments where it was subject to significant sex steroid regulation. The fact that androgen receptor mRNA levels were consistently up-regulated by a combined E2 plus testosterone treatment while E2 treatment alone had little or no effect shows that a collaborative action of E2 and testosterone enhances androgen receptor expression in the monkey uterus.

Animals↗

Effects of Igf1 gene deletion on postnatal growth patterns.

This study documents the temporal and organ-specific effects of Igf1 gene deletion on postnatal growth patterns. Igf1-/- mice are 63+/-4% the size of wildtype (wt) littermates at birth and this ratio persists through postnatal day 20 (P20). After P20, Igf1-/- mice virtually stop growing, while wt littermates double in size from P20 to P40, after which their growth markedly decelerates. As a result, 'full-grown' Igf1-/- mice are less than one third the size of wt littermates. Igf1 gene deletion has disproportionate effects on organ growth. For example, at P10 and P40, Igf1-/- body weights are 63% and 31% of wt, respectively, while Igf1-/- lungs weigh only 34% and 22% of wt at these ages. In contrast, the Igf1-/- heart is disproportionately enlarged, representing approximately 85% of wt at P10 and approximately 56% at P40. Igf1-/- kidney, spleen and liver are slightly but significantly increased in size relative to the degree of reduction in Igf1-/- body weight. These data demonstrate that Igf1 has two major phases or modes of growth promotion. There is an early, growth hormone (GH)-independent Igf1 growth augmentation during perinatal development, responsible for about 35% of growth prior to P20. Then there are later effects due to GH-induced Igf1, which are responsible for increasing animal size by approximately 100% between P20 and 40. The fact that there is virtually no GH-induced growth in the Igf1-/- mice supports the view that Igf1 mediates GH's major effects on somatic growth. Finally, this study shows that Igf1 has discordant effects on pulmonary and cardiac growth parameters, with relative hypoplasia of Igf1-/- lungs and hypertrophy of Igf1-/- hearts.

Aging↗

Insulin-like growth factor I regulates gonadotropin responsiveness in the murine ovary.

The present study shows that insulin-like growth factor I (IGF-I) and FSH receptor (FSHR) mRNAs are selectively coexpressed in a subset of healthy-appearing follicles in murine ovaries, irrespective of cycle stage. Aromatase gene expression, a prime marker for FSH effect, is found only in IGF-I/FSHR-positive follicles, showing that these are healthy, gonadotropin-responsive follicles. Given the striking coexpression of FSHR and IGF-I, we hypothesized that FSH was responsible for follicular IGF-I expression. We found, however, that granulosa cell IGF-I mRNA levels are not reduced in hypophysectomized (+/-PMSG) or FSH knockout mice, indicating that FSH does not have a major role in regulation of granulosa cell IGF-I gene expression. To test the alternative hypothesis that IGF-I regulates FSHR gene expression, we studied ovaries from IGF-I knockout mice. FSHR mRNA was significantly reduced in ovaries from homozygous IGF-I knockout compared with wild type mice and was restored to control values by exogenous IGF-I treatment. The functional significance of the reduced FSHR gene expression in IGF-I knockout ovaries is suggested by reduced aromatase expression and by the failure of their follicles to develop normally beyond the early antral stage. In fact, IGF-I knockout and FSH knockout ovaries appear very similar in terms of arrested follicular development. In summary, we have shown that IGF-I and FSHR are selectively coexpressed in healthy, growing murine follicles and that FSH does not affect IGF-I expression but that IGF-I augments granulosa cell FSHR expression. These data suggest that ovarian IGF-I expression serves to enhance granulosa cell FSH responsiveness by augmenting FSHR expression.

Animals↗

Aquaporin-1 water channel expression in human kidney.

The pattern of aquaporin-1 water channel protein (AQP1) expression in the human kidney was analyzed by immunocytochemistry using semi-thin and optimized high-resolution immunoelectron microscopy based on freeze-substituted and Lowicryl HM20 embedded tissue. In addition, in situ hybridization was used to determine AQP1 mRNA distribution. Immunoblots revealed a 28-kd band and a 35- to 45-kd band corresponding to unglycosylated and glycosylated AQP1. Glomerular capillary endothelium exhibited extensive AQP1 labeling, whereas glomerular podocytes and Bowman's capsule epithelium were unlabeled. AQP1 was localized in the proximal tubule, including the neck region directly connected to the glomerulus. However, there was a marked difference in the level of expression between cross-sections of the convoluted part and the proximal straight tubules, the latter displaying the most intense labeling. AQP1 labeling continued uninterrupted from the proximal straight tubule into descending thin limbs in outer medulla. Abrupt transitions from heavily labeled to unlabeled segments of thin limbs were observed, primarily in the inner medulla. This may represent the transition from the water-permeable thin descending limb to the water-impermeable thin ascending limb. In addition, heavy labeling of fenestrated endothelium was also observed in peritubular capillaries in cortex, outer medulla, and inner medulla. Immunolabeling controls were negative. In situ hybridization documented a marked difference in AQP1 mRNA levels within the proximal tubule, with the greatest AQP1 mRNA expression in straight proximal tubules. Glomeruli also showed marked signals, and descending thin limbs exhibited extensive expression in exact concordance with the immunocytochemical results. It was concluded that: (1) AQP1 is present in all proximal tubule segments, including segment 1 and the neck region, but there is a pronounced difference in expression levels with respect to both protein and mRNA levels; (2) AQP1 labeling is observed in the endothelium of fenestrated peritubular capillaries, as well as fenestrated glomerular capillaries; (3) AQP1 labeling continues directly from proximal tubules to descending thin limbs; and (4) abrupt transitions from labeled to unlabeled thin limb epithelium are noted.

Aquaporin 1↗

Single lead VDD pacing: multicenter study.

Optimal treatment for patients with AV block and normal sinoatrial node (SA) function entails atrial sensing and ventricular pacing (VDD mode). Single-lead VDD pacing preserves AV synchrony, precludes the need to insert two leads, and makes the implanter's work simpler and quicker. Our objectives were to verify the performance of the Thera VDD pacing system (medtronic, Inc., Minneapolis, MN, USA), and evaluate the effectiveness of its atrial sensing and its ventricular sensing and pacing. In 165 patients, 150 adults (mean age 62 +/- 18 years) and 15 children (mean age 7 +/- 5 years) with 1 degree-3 degrees AV block and normal SA node function, a Thera VDD system (Models 8948 or 8968) was implanted. Intraoperative ventricular electrical measurements were not significantly different from those of VVI pacemakers. The mean amplitude of the atrial signal during implantation was 4.1 +/- 1.9 mV. Optimal atrial signals during implantation were usually obtained in the mid or lower part of the right atrium by using a special technique. Adequate atrial measurements remained stable throughout 24 months. There was no difference between serial measurements of atrial signal amplitudes at predischarge and during follow-up visits. Reposition of the lead was done in 2 patients (1.4%), and reprogramming to VVI in 7 patients: due to atrial fibrillation in 3 (1.8%) and due to atrial undersensing in 4 patients (2.4%). Thera VDD pacing is reliable and easy to manage with dependable atrial sensing and ventricular pacing. The survival rate of VDD pacing at 2 years was 96%.

Adolescent↗

Effects of an Igf1 gene null mutation on mouse reproduction.

Both sexes of adult mice homozygous for a targeted mutation of the Igf1 gene, encoding insulin-like growth factor 1, are infertile dwarfs (approximately 30% of normal size). The testes are reduced in size less than expected from the degree of dwarfism but sustain spermatogenesis only at 18% of the normal level. The epididymides are overall nearly allometric to the reduced body weight, but the distal regions of the duct, vas deferens, seminal vesicles, and prostate are vestigial. Despite the mutational impact on the epididymis, capacitated sperm are able to fertilize wild type eggs in vitro. It is hypothesized that the infertility of male mutants is caused by failure of androgenization resulting in absence of mating behavior, due to drastically reduced levels of serum testosterone (18% of normal). This hormonal deficiency was correlated with an ultrastructural analysis of mutant Leydig cells revealing a significant developmental delay, while assays in organ culture showed that the basal and LH-stimulated production of testosterone by testicular parenchyma is reduced in comparison with wild type controls. The female mutants fail to ovulate even after administration of gonadotropins, which is apparently the primary cause of their infertility, and possess an infantile uterus that exhibits a dramatic hypoplasia especially in the myometrium. The phenotypic manifestations of the mutation were correlated with the localization of transcripts for insulin-like growth factor I and its cognate receptor in wild type reproductive tissues by in situ hybridization.

Animals↗

Evaluation of a new rate adaptive ventricular pacemaker controlled by double sensors.

UNLABELLED: The LEGEND-PLUS, a new rate adaptive pacemaker that combines activity and minute ventilation sensing for automatic rate adaptation was implanted in the right ventricle (VVIR) in 11 patients (mean age 62 +/- 9 years). Initial programming was performed using the Programmer Exercise Protocol (a 3-minute walk). This programming was evaluated by treadmill tests, up-stairs and down-stairs walking, and Holter recordings. RESULTS: Following the final programming of LEGEND-PLUS, the mean upper activity rate was 102 +/- 7 beats/min (range 90-120 beats/min), while the mean upper minute ventilation rate was 125 +/- 16 beats/min (range 100-150 beats/min). The mean rate responses during the exercise protocol and the final programming in minute ventilation and activity sensing modes were 5.4 +/- 2.3 (range 1-9), versus 4 +/- 2.4 (range 1-8; P < 0.01) and 7.6 +/- 1.1 (range 5-9), versus 7.5 +/- 0.8 (range 6-9; P = 0.8), respectively. In the combined sensing mode, the acceleration rate was identical to the activity rate response and the deceleration rate mimicked the minute ventilation. CONCLUSION: Dual sensor VVIR pacemakers have the potential to improve rate adaptation to exercise. The rate response to exercise in patients fitted with activity and minute ventilation sensors, VVIR pacemakers closely mimics the physiological rate response.

Adult↗

Astrocytes upregulate glial fibrillary acidic protein (GFAP), but not insulin-like growth factor-I (IGF-I) during experimental autoimmune neuritis (EAN).

T cell-mediated autoimmune neuritis produces rapid activation of spinal cord microglia. To determine whether this microglial response upregulates astrocytic expression of IGF-related proteins, we induced EAN and used in situ hybridization and immunocytochemistry to examine the mRNAs and peptides for glial fibrillary acidic protein (GFAP), insulin-like growth factor-I (IGF-I), IGF-I receptor (IGFR-I) and IGF binding protein-2 (IGFBP-2). Relative levels of GFAP mRNA and peptide were highest in the lumbar spinal cord 4-10 d following T cell transfer and significant GFAP elevations were still present after three weeks. The astrocytes expressing GFAP mRNA and peptide were localized around motoneurons which were related topographically to axons in peripheral nerve inflammatory lesions. In the nucleus gracilis, where terminals of dorsal root ganglion neurons are located, astrocytic levels of GFAP mRNA and peptide rose later and did not reach their highest levels until 21 d after T cell transfer. Even though microglia were activated in both locations 2-4 d after transfer, astrocytic levels of IGF-I, IGFR-I and IGFBP-2 mRNA and peptide did not differ significantly from those observed in controls. The dissociation of GFAP and IGF-I expression in EAN suggests that these astrocytic responses may be independently regulated. We also suggest that the type and severity of remote neuronal injury are probably more important inducers and regulators of these astrocytic responses than microglial cell activation.

Animals↗

Expression of insulin-like growth factor binding proteins in the rat kidney: effects of long-term diabetes.

Recent studies have shown that the renal synthesis of insulin-like growth factor binding proteins (IGFBPs) is altered in insulin-deficient diabetes mellitus, suggesting that these changes may be implicated in the alterations in renal function and morphology that accompany diabetes. To investigate the time course and the precise cellular distribution of changes in IGFBP expression, we used quantitative in situ hybridization to analyze renal IGF-I and IGFBP-1 to -5 messenger RNA (mRNA) localization and levels from 2 days to 6 months after the onset of streptozotocin-induced diabetes. There was an immediate sharp decline in IGF-I mRNA levels in the outer medulla that persisted for up to 3 months and a much smaller reduction in IGF-I mRNA levels in the medullary thick ascending limbs (MTALs). In nondiabetic animals, IGFBP-1 mRNA is most abundant in the MTALs. Immediately after the induction of diabetes, however, there was a greater than 2-fold increase in cortical IGFBP-1 mRNA and a 75% decrease in IGFBP-1 mRNA in MTALs. These changes persisted for up to 6 months in the diabetic animals. In contrast, IGFBP-5 mRNA levels were increased in the outer medulla and decreased in the cortex of diabetic kidneys. No significant changes in renal IG-FBP-2 mRNA levels or distribution were noted, and changes in IG-FBP-3 and -4 mRNA levels were subtle. In summary, streptozotocin-induced diabetes is associated with very prominent and complex alterations in renal IGF system gene expression, including robust increases in cortical IGFBP-1 and profound decreases in cortical IG-FBP-5 mRNA and medullary IGF-I mRNA levels. The divergent changes in IGFBP-1 and -5 mRNA levels in cortex vs. outer medulla indicate that regulation of IGFBP mRNA levels is quite complex.

Albuminuria↗

Granulosa cell DNA synthesis is strictly correlated with the presence of insulin-like growth factor I and absence of c-fos/c-jun expression.

Insulin-like growth factor I (IGF-I) mRNA is selectively expressed by a subset of rat ovarian follicles. To elucidate the biological role and regulation of follicular IGF-I, we have analyzed individual follicles with respect to IGF-I production, DNA synthesis, and c-fos and c-jun expression, since AP-1 complex components have been implicated both in regulation of IGF-I gene expression and cell proliferation. IGF-I mRNA localization, bromodeoxyuridine (BRDU) incorporation, and c-fos and c-jun immunoreactivity were compared in serial sections from prepubertal and mature rat ovaries. BRDU incorporation is exclusively concentrated in IGF-I-expressing follicles in both prepubertal and mature rats, with further intrafollicular correlation between local concentrations of BRDU-positive granulosa cells and IGF-I mRNA. Furthermore, there is a striking negative correlation between IGF-I mRNA localization and follicular fos/jun immunoreactivity. Both c-fos and c-jun are readily detected in granulosa cells of luteinized follicles where IGF-I mRNA is never found. Immunoreactive c-jun but not c-fos is detected in granulosa cells of atretic follicles, while neither c-fos nor c-jun is detected in IGF-I mRNA-positive granulosa cells. These data implicate IGF-I in granulosa cell proliferation and the fos/jun heterodimer in granulosa cell luteinization, while expression of c-jun in the absence of c-fos may be implicated in programmed granulosa cell death.

Animals↗

The effect of overdrive pacing rate and duration on ventricular escape rhythms in patients with chronic complete atrioventricular block.

The effect of overdrive (OD) pacing rate and duration on subsidiary pacemakers was evaluated in 54 patients with third-degree AV block. They had a permanent pacemaker implanted 61 +/- 56 months earlier because of complete AV block in 38 patients and, in 16 patients because of second-degree AV block, which in the interim advanced to complete AV block. The patients had a reliable infranodal escape rhythm, with a mean cycle length of 2,022 +/- 603 msec, upon discontinuation of the ventricular OD pacing, at a rate of 40 beats/min. The escape interval and escape rhythm cycle length was evaluated after OD pacing at 40, 50, 60, 70, 90, and 100 beats/min for 30 seconds, at each rate. In 100% of the patients the subsidiary pacemaker recovered after OD pacing at 40 and 50 beats/min and the number decreased to 59% at a rate of 100 beats/min. The escape interval prolonged gradually between OD pacing at 40 and 100 beats/min, by 56%. The effect of OD pacing duration at 50 and 70 beats/min was evaluated. At an OD pacing rate of 70 beats/min there was a significant effect of the pacing duration on the escape interval. There were significant differences in the escape interval duration and escape rhythm cycle length between males and females, patients with or without coronary artery disease, and patients with narrow or wide QRS escape. However, the increase in the OD pacing rate had a similar effect on the escape interval in the above mentioned groups. There was no effect on the paced QRS duration and sinus cycle length at each OD pacing rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Clinical evaluation of a new single pass lead VDD pacing system.

UNLABELLED: Twenty-five patients with second- to third-degree AV block and normal sinus function (16 males, mean age 60 +/- 18; range 15-78 years) underwent implantation of VVD pacemakers (THERA VDD, Medtronic, Inc.) with a single pass (SP) lead. RESULTS: During implantation the mean amplitude of the atrial (A) signal was 3.9 +/- 1.4 mV (range 2.0-7.8 mV). Stable, acceptable A-signals during implantation were usually observed in the mid- or lower part of the right atrium. The lead tip electrical parameters were not compromised in any patient in order to obtain an acceptable A-signal. To verify VDD device function, patients underwent pacing system analysis on the second day and again 1, 3, and 6 months after implantation. Acute and chronic electrical measurements in the ventricle were similar to those with regular steroid leads. During follow-up tests, stable atrial sensing (A > or = 0.7 mV) was found in all but one patient (in whom A was 0.25-0.5 mV and an intermittent loss of atrial sensing occurred). There was no difference between serial measurements of A-signal amplitudes on the second day or 1, 3, and 6 months after implantation: 1.9 +/- 1.3 mV, 1.5 +/- 0.6 mV, 1.3 +/- 0.8 mV, and 1.5 +/- 1.1 mV, respectively. The mean implantation time was 54.0 +/- 17 minutes and the mean fluoroscopy time was 3.2 +/- 1.3 minutes. CONCLUSIONS: SP lead VDD pacing is reliable and easy to manage with dependable atrial sensing and ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗