Speed of normalization of right ventricular volume overload after transcatheter closure of atrial septal defect in children and adults.
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Publications and source records attributed to Q L Cao.
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Catheter closure of secundum atrial septal defect (ASD) using the Amplatzer septal occluder (ASO) is a potential alternative for open surgical repair. However, the large profile of the device obtained immediately after closure continues to raise some concerns regarding its long-term safety. To evaluate the changes in the profile of the device after being deployed, transesophageal echocardiography was performed in 70 patients (17 men and 53 women) who underwent catheter closure of ASDs immediately after and at 6-month follow-up. The median age at closure was 16 years (range 1.9 to 75) and the median size of the ASD as assessed by transesophageal echocardiography was 14 mm (range 3 to 25). The thickness (profile) of the device was assessed in the 4-chamber, short- and long-axis views of the interatrial septum, and measured at its middle and at the junction of the waist with the disc at its 2 ends. Seventy-three devices were deployed in the 70 patients. The median size of the device was 19 mm (range 8 to 34). Complete closure was achieved in 81.4% and 91.4% immediately after and at 6-months follow-up, respectively. The thickness of the device at its middle decreased from 12.2 +/- 4.3, 12.2 +/- 3.7, and 12.5 +/- 4.3 mm in the 4-chamber, short- and long-axis views to 6.5 +/- 2.0, 6.3 +/- 1.9, and 6.5 +/- 2.2 mm, respectively. The thickness of the device at its superior, inferior, anterior, and posterior edges also decreased by 41.8% +/- 14.0% to 43.7% +/- 9.8%. The changes in the thickness were related to device size. Larger devices were thicker after being deployed. We conclude that the thickness of the ASO decreases by 42% to 48% within 6 months after deployment, resulting in a lower profile.
Embryonic day 14 rat cerebral cortex-derived precursors were expanded with FGF2 and labeled with BrdU prior to being transplanted into the kainic acid-lesioned adult rat spinal cord. While these precursors give rise to cells with neuronal, astrocytic and oligodendroglial phenotypes vitro, they remained largely undifferentiated up to 12 weeks in vivo. Numerous BrdU-labeled cells were found in injured gray matter, and also lining the dilated central canal that sometimes accompanies these lesions. BrdU-labeled cells never co-expressed Map2ab, rarely co-expressed GFAP but often co-expressed nestin, even after 12 weeks in vivo. These observations suggest that the environment of the kainic acid-injured spinal cord is not hostile to transplanted embryonic cerebral cortex-derived precursors, but also is not conducive to their neuronal differentation.
Proliferating populations of undifferentiated neural stem cells were isolated from the embryonic day 14 rat cerebral cortex or the adult rat subventricular zone. These cells were pluripotent through multiple passages, retaining the ability to differentiate in vitro into neurons, astrocytes, and oligodendrocytes. Two weeks to 2 months after engraftment of undifferentiated, BrdU-labeled stem cells into the normal adult spinal cord, large numbers of surviving cells were seen. The majority of the cells differentiated with astrocytic phenotype, although some oligodendrocytes and undifferentiated, nestin-positive cells were detected; NeuN-positive neurons were not seen. Labeled cells were also engrafted into the contused adult rat spinal cord (moderate NYU Impactor injury), either into the lesion cavity or into the white or gray matter both rostral and caudal to the injury epicenter. Up to 2 months postgrafting, the majority of cells either differentiated into GFAP-positive astrocytes or remained nestin positive. No BrdU-positive neurons or oligodendrocytes were observed. These results show robust survival of engrafted stem cells, but a differentiated phenotype restricted to glial lineages. We suggest that in vitro induction prior to transplantation will be necessary for these cells to differentiate into neurons or large numbers of oligodendrocytes.
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Surgical closure of multiple muscular ventricular septal defects (MVSDs) is associated with mortality and morbidity; therefore, both surgeons and cardiologists welcome a nonsurgical safe approach. We report our initial results of catheter closure of MVSD using the new Amplatzer muscular VSD occluder delivered via the venous or arterial routes. Eight patients with MVSD underwent closure of their VSDs using the Amplatzer VSD occluder under general endotracheal anesthesia. The mean +/- SD of age was 5.4 +/- 3.1 years (2-10 years) and mean weight was 18.4 +/- 6.5 kg (11.5-29 kg). All patients had left ventricular volume overload with mean Qp/Qs ratio of 1.7 +/- 0.6 (1.4-3). The location of the VSD was mid muscular in four, anterior in two, apical in one, and posterior in one. The systolic pulmonary artery pressure ranged from 25 to 85 mm Hg (mean, 39.9 +/- 18.8 mm Hg). The device was implanted successfully in all eight patients. In five patients (four mid muscular and one apical), the deployment of the device was anterograde from the right internal jugular vein and in three patients (two anterior and one posterior VSD), the initial attempt at anterograde deployment was unsuccessful due to kinking in the delivery sheath; therefore, retrograde deployment was attempted successfully. The size of the device used ranged from 6 to 14 mm (the size of the connecting waist). In patients with elevated pulmonary artery pressure, repeat measurements immediately after closure revealed normalization in all. There was immediate complete closure of the defect in two patients and six patients had trivial residual shunt (foaming through the device), which disappeared completely within 24 hr in five and at 6-month follow-up in the sixth patient. The mean fluoroscopy time was 37.1 +/- 13 min (11.7-55 min). Complications encountered included transient junctional rhythm in one patient. No blood transfusion was required. On follow-up evaluation, there has been no episode of endocarditis, thromboembolism, hemolysis, or wire disruption. we conclude that the Amplatzer MVSD occluder is a safe and effective device for closure of MVSDs up to 12 mm in diameter. Further clinical trials with this device are underway. Cathet. Cardiovasc. Intervent. 49:167-172, 2000.
We present a series of four patients with orthodeoxia-platypnea who underwent successful transcatheter closure of their patent foramen ovale using the Amplatzer devices (Amplatzer septal occluder/Amplatzer PFO occluder). The average saturation increased from 81% to 96% with complete resolution of symptoms. The Amplatzer devices are safe and effective treatment options for patients with orthodeoxia-platypnea.
UNLABELLED: Conduction abnormalities and arrhythmias may occur in patients following secundum atrial septal defect (ASD) closure using the Amplatzer septal occluder (ASO). Therefore, the aim of this study was to prospectively perform ambulatory ECG monitoring to assess the electrocardiographic effects of transcatheter closure (TCC) of ASD using the ASO device. From 5/97 to 3/99, 41 patients with secundum ASD, underwent TCC using the ASO device at a median age of 9.2[emsp4 ]y. (0.5-87[emsp4 ]y.) and median weight of 34[emsp4 ]kg (5. 6-88[emsp4 ]kg.). Ambulatory Holter monitoring was performed pre- and immediately post TCC. Holter analysis included heart rate (HR), ECG intervals, supraventricular ectopy (SVE), ventricular ectopy (VE), and AV block. No change in baseline rhythm was noted in 37 patients (90%). Changes in AV conduction occurred in 3 patients (7%), including intermittent second degree AV block type II, and complete AV dissociation post closure. SVE was noted in 26 patients (63%) post closure, ranging from 5-2207 supraventricular premature beats (SVPB), including 9 patients (23%) with non-sustained supraventricular tachycardia (SVT), 3 of whom had short runs of SVT prior to closure. A significant increase in post-closure number of SVPB per hour (p=0.047) was noted. No significant difference was noted in PR interval, ventricular premature beats per hour, or QRS duration. CONCLUSIONS: Based on ambulatory ECG analysis, TCC of ASD with the ASO device is associated with an acute increase in SVE and a small risk of AV conduction abnormalities, including complete heart block. Long term follow-up studies will be necessary to determine late arrhythmia prevalence and relative frequency compared with standard surgical ASD repair.
Although balloon pulmonary valvuloplasty (BPV) has been advocated as a means of palliating patients with tetralogy of Fallot (TOF), the results of this procedure were not uniformly good in this patient population. The purpose of this study was to review our institutionOs experience with BPV in patients with TOF, and to determine whether echocardiographic criteria exist that may be used to identify patients likely to derive prolonged benefit from this procedure. Between 1991 and 1999, nine patients with TOF, ages 0. 4Eth 26.1 weeks (mean, 7.4 +/- 7.6 weeks) underwent BPV due to cyanosis and other associated medical conditions (e.g., coronary artery anomalies, small size) that rendered immediate surgical intervention undesirable. Data from the catheterization and pre-BPV echocardiograms were analyzed. All patients had at least transient improvement in oxygen saturation. However, 4 patients (Group 1) required intervention (1 open-heart repair, 3 palliative shunts) within 5 weeks of BPV due to recurrent desaturation. In the remaining 5 patients (Group 2), open-heart repair was delayed 8Eth 36 weeks (mean, 23 +/- 13 weeks). Groups 1 and 2 did not differ regarding pulmonary valve annulus, main pulmonary artery or branch pulmonary artery diameter. However, the diastolic diameter of the right ventricular outflow tract (RVOT) was significantly smaller in Group 1 (18.3 +/- 3.5 mm/m2 versus 24.4 +/- 4.1 mm/m2 in Group 2; p < 0.05). Four out of five patients with a RVOT diameter < 23 mm/m2 were in Group 1, and all patients with RVOT diameter greater than 25 mm/m2 were in Group 2. We conclude that BPV can effectively palliate patients with TOF whose RVOT diastolic diameter is > 25 mm/m2. However, patients with a diastolic RVOT diameter < 23 mm/m2 are unlikely to have sustained improvement following BPV.
Expression of the growth and plasticity associated protein GAP-43 is closely related to synaptogenesis and synaptic remodeling in the developing as well as in the mature nervous system. We have studied the postnatal development of GAP-43 mRNA expression in the auditory brainstem and determined the time course of its reexpression following deafening through cochlear ablation using a digoxigenin-coupled mRNA probe. By the first postnatal day, GAP-43 mRNA was expressed at high levels in all auditory brainstem nuclei. But whereas GAP-43 mRNA is almost entirely lost in most of these nuclei in the adult animal, significant levels of this molecule are retained in the inferior colliculus and, most notably, in the lateral and medial superior olivary nucleus. As a consequence of unilateral cochleotomy, GAP-43 mRNA rose dramatically in some neurons of the ipsilateral lateral superior olive, whereas the hybridization signal decreased in others. Using double staining protocols, we found that those olivary neurons that increase their level of GAP-43 mRNA appear to be identical with the cells developing strong GAP-43 immunoreactivity after cochleotomy. By combining axonal tracing with in situ hybridization, we proved that at least some of the cells with increased levels of GAP-43 mRNA and protein are the cells of origin of olivocochlear projections. A substantial decrease of the level of GAP-43 mRNA took place in the inferior colliculus contralateral to the lesioned cochlea. Our results led us to suggest that neurons in the superior olivary complex may play a crucial role in orchestrating auditory brainstem plasticity.
Coil closure of patent ductus arteriosus (PDA) has become an accepted alternative to surgical closure in most pediatric cardiac centers. However, little is known about the mid-to long-term outcome of this procedure. Therefore, we evaluated the immediate, short-, and long-term outcome of transcatheter coil closure (TCC) of PDA using single or multiple Gianturco coils or the Gianturco-Grifka Vascular Occlusive Device (GGVOD). One hundred forty-nine patients underwent an attempt at TCC of their PDAs at a median age of 2.4 years (2 weeks to 55 years) and median weight of 13.5 kg (2.3-87 kg). There were 33 patients < 1 year of age. The median PDA minimal diameter was 2 mm (0.4-7 mm) with 26 patients whose PDA minimal diameter was > 4 mm. A 4 Fr catheter was used for coil deployment in 136 patients, a 3 Fr in 4, and an 8 Fr in 4 patients who received the GGVOD. A single coil was used in 77 patients and multiple coils (2-6) were used in 66 patients. One hundred forty-six patients had successful closure (142 had immediate complete closure and 4 had residual shunt), 3 patients failed the initial attempt (2 underwent surgical ligation and 1 had a successful second attempt a year later). Of the four patients with residual shunt, three underwent a second procedure with implantation of 1-3 coils resulting in complete closure in all and one patient had spontaneous resolution of the residual shunt. Complications were encountered in nine patients: six had coil migration with successful retrieval in four; two had left pulmonary artery stenosis (2.4 kg and 6.3 kg infants), and one patient had loss of femoral arterial pulse. The median fluoroscopy time was 16 min (2-152 min). One hundred forty-two patients had the procedure as an outpatient, five patients stayed greater than 24 hr, and two of these patients were in hospital for 1 month for noncardiac reasons. At a median follow-up interval of 3.0 years (1 month to 5.1 years), there were no episodes of delayed coil migration, delayed recanalization, thromboembolic episodes, or bacterial endocarditis. Lung perfusion scans performed at a median follow-up interval of 1.6 years in 31 patients who received multiple coils revealed 45% +/- 5% blood flow to the left lung. Long-term follow-up of coil closure of PDA indicates that the technique is safe and effective for most patients with PDA up to a diameter of 7 mm.
A 35-year-old female patient with a large residual shunt following transcatheter closure of a large secundum atrial septal defect using the Das-Angel Wings device underwent successful complete closure of the residual shunt using a 15-mm Amplatzer Septal Occluder. Transesophageal (two- and three-dimensional) echocardiography was of great help during the closure procedure. Cathet. Cardiovasc. Intervent. 48:184-187, 1999.
BACKGROUND: The positions, sizes, and shapes of ventricular septal defects (VSDs) can be difficult to assess by 2-dimensional echocardiography (2DE). Volume-rendered 3-dimensional echocardiography (3DE) can provide unique views of VSDs from the left ventricular (LV) side, allowing complete assessment of their circumference and spatial orientations to other anatomic structures. METHODS AND RESULTS: Seventeen experimentally created defects of various locations, sizes, and shapes were imaged and reconstructed in 9 explanted porcine hearts. From an en face projection, major and minor axis diameters of the defects were measured, and these data were compared with direct anatomic measurements. Optimal reconstructions of the VSDs were obtained in all heart specimens, accurately depicting their positions and shapes. The correlations between 3DE and anatomy for the VSD major and minor axis diameters were y=1.0x+0.3 (r=0.88, P<0.001) and y=1.0x-1.4 (r =0.89, P<0.001), respectively. Good agreement between the 2 methods was demonstrated for all measurements. Our experience from the in vitro model was then applied to patient studies. Optimal LV en face reconstructions were obtained in 45 of 51 patients, permitting detailed assessment of the positions, sizes, and shapes of the VSDs. In the 25 patients with comparative surgical measurements, the correlations between 3DE and surgery for the VSD major and minor axis diameters were y =0. 81x+2.1 (r=0.92, P<0.001) and y=0.73x+2.0 (r=0.91, P<0.001), respectively. Good agreement was demonstrated between measurements made by 3DE and those obtained at surgery. CONCLUSIONS: 3DE provides excellent visualization of various types of VSDs. From an LV en face projection, the positions, sizes, and shapes of VSDs can be accurately determined. Such precise imaging will be beneficial for surgical and catheter-based closure of difficult perimembranous and singular or multiple muscular VSDs.
Two-dimensional echocardiography (2-DE) and Doppler methods are generally used for assessing mechanisms and severity of mitral regurgitation (MR). Recently, 3-dimensional echocardiography (3-DE) has been applied successfully in various cardiac disorders, but its value in evaluating the mechanism and the severity of MR are not known. We studied 30 patients with MR using 2-DE and 3-DE. Volume-rendered gray-scale 3-DE images of the mitral valve apparatus and MR jets were reconstructed. Maximal volume of the MR jet by 3-DE was compared with mitral regurgitant volume and fraction, regurgitant jet area and the ratio of jet area to left atrial area, and semiquantitative grading derived from 2-DE methods. Our results demonstrated that 3-DE aided in a better depiction of the mitral apparatus and its abnormalities in 70% of the patients. The origin, direction, and morphology of the MR jet were better delineated in 3-DE volumetric display. Quantitative analysis, however, showed only a weak to moderate correlation between 3-DE maximal MR jet volume and 2-DE mitral regurgitant volume (y = 0.5x + 11.4, r = 0.7), regurgitant fraction (y = 0.5x + 8.2, r = 0.65), mitral regurgitant jet area (y = 0.2x + 5, r = 0.51), jet area to left atrial area ratio (y = 0.53x + 7.6, r = 0.54), and semiquantitative grading of MR (y = 9.1x - 1.8, r = 0.74). In conclusion, 3-DE aids in a better understanding of the mechanisms of MR and morphology of the regurgitant jets. Its quantitative ability, when reconstruction of the jet alone is used, may be limited.
A neonate with pulmonary atresia with intact ventricular septum (PA/IVS) underwent successful retrograde transcatheter perforation of the pulmonary valve, using a 2 Fr radio-frequency catheter with subsequent anterograde balloon dilation of the valve. Due to persistent hypoxemia, the neonate underwent placement of a 4-mm modified Blalock-Taussig shunt. Transcatheter retrograde transductal perforation of the pulmonic valve in PA/IVS is feasible and may be a potential alternative to anterograde perforation.
A 9-year-old patient with a large coronary arteriovenous fistula (circumflex-right atrium) underwent successful complete percutaneous closure, using the new Amplatzer Duct Occluder (ADO) inserted via a 6 Fr sheath.
A 6 1/2-year-old (weight 20 kg) patient was found to have significant cavo-atrial obstruction and significant right-to-left shunt via multiple large fenestrations in the baffle, with oxygen saturation of 81% 3 1/2 yr after a fenestrated Fontan operation. In one session, this patient had undergone placement of a Palmaz stent at the cavo-atrial narrowing in order to increase anterograde venous return into the pulmonary artery. This was unsuccessful in improving the oxygen saturation because of the large leak in the baffle. Therefore, at a second catheterization session, two telescoping dacron-covered experimental vascular self-expanding stents were placed from the right atrial origin (distal to the hepatic veins) into the pulmonary artery connection delineated by the Palmaz stent, with complete reconstruction of the baffle and improvement in oxygen saturation to 95%.
BACKGROUND: Two-dimensional echocardiography is useful for estimating the extent of infarct-related wall motion abnormalities. Such estimation, however, is based on a few selected views and extrapolated for the whole left ventricle (LV). This approach does not provide us with the actual amount of dysfunctional myocardium. Volume-rendered three-dimensional echocardiography (3DE) might overcome these limitations. In this study we explored (1) how well volume-rendered 3DE delineates regional dysfunction of the infarcted LV and (2) how well dysfunctional myocardial mass quantified by 3DE reflects the actual anatomic infarct mass. METHODS AND RESULTS: 3DE was performed before and 3 hours after coronary occlusion in 16 dogs. With the LV viewed in equidistant short-axis slices, the region of dysfunction was demarcated, and the dysfunctional myocardial mass was derived from this. With triphenyltetrazolium chloride staining, anatomic infarct regions were delineated, dissected, and weighed. The anatomic infarct mass was 16.3+/-7.7 g (mean+/-SD) (range, 6.4 to 31.4 g); the dysfunctional mass estimated by 3DE was 17.4+/-9.1 g (range, 5.2 to 39.0 g). The mean difference was 1.0 g. The correlation between dysfunctional mass (y) and infarct mass (x) was y=l.lx-0.6, r=.93 (P<.0001). The percentage of LV involved in infarction was 18.2+/-5.8% (range, 9.1% to 26.1%); the percentage of LV involved in regional dysfunction was 18.3+/-6.9% (range, 7.9% to 31.2%). The mean difference was 0.1%. The correlation between percentage of LV involved in infarction (x) and percentage of LV involved in dysfunction (y) was y=1.0x-1.1, r=.92 (P<.0001). CONCLUSIONS: Volume-rendered 3DE crisply displays regional dysfunction of infarcted LV. 3DE-measured dysfunctional mass accurately reflects the anatomic infarct mass.