Impact of Occluder Device Type on Success of Percutaneous Closure of Atrial Septal Defects–A Medium‐Term Follow‐up Study

Objective: To identify differences between various occluder types regarding thromboembolic event rates and existence of residual shunts during medium‐term follow‐up. Methods: Three hundred nine consecutive patients with presumed paradoxical embolism and scheduled for percutaneous closure of patent foramen ovale or atrial septal defect between 1997 and 2006 were considered for this study. Device implantation failed in seven patients (nonstable device position), so 302 patients (46 ± 12 years, 190 males) formed the study group using Amplatzer? (n = 208), Starflex? (n = 61), and Cardiastar? (n = 33) occluders. Follow‐up transesophageal echocardiography was performed 1, 3, and 6 months after implantation. Results: Periinterventional complications occurred in two patients (cardiac arrhythmias). There were more residual shunts in the Starflex? and Cardiastar? group than in the Amplatzer? group at 6‐month follow‐up (8/61 vs. 7/33 vs. 8/208, P = 0.0005). Performing logistic regression, the type of occluder device was a significant risk factor for the presence of residual shunt 6 months after implantation (P = 0.0033; Cardiastar? vs. Amplatzer? OR 6.346, 95% CI 1.998 – 20.156; Starflex? vs. Amplatzer? OR 4.369, 95% CI 1.444 – 13.222). During mean follow‐up of 31 ± 8 months 16 recurrent thromboembolic events occurred; the annual recurrence was 2.1% for combined end‐point stroke, TIA, and peripheral embolism (Amplatzer?: 1.3%, Starflex?: 3.9%, and Cardiastar?: 3.6%, P = 0.0467). The presence of an atrial septal aneurysm was the only significant risk factor (P = 0.0168, OR 3.664, 95% CI 1.263 – 10.630) for the occurrence of thromboembolic events. Conclusions: Percutaneous closure of patent foramen ovale or atrial septal defect is a safe procedure with little incidence of peri‐ and postprocedural complications. There is a significant difference between the Amplatzer?, Cardiastar?, and Starflex? occluders in regard to complete closure of the defects and annual recurrence of thromboembolic events.     

The Paclitaxel‐Eluting Coroflex™ Stent Study II (PECOPS II) Acute and 6‐Month Clinical and Angiographic Follow‐Up, 1‐Year Clinical Follow‐Up

Background and Objectives: Paclitaxel‐coated stents have proven their efficacy for reducing restenosis in de novo coronary artery lesions and in‐stent restenoses with superiority compared to bare metal stents. This study was performed to evaluate the procedural and 1 year results of the Paclitaxel‐eluting Coroflex? Please stent in coronary artery lesions. Methods: One‐hundred and twenty‐nine patients (66.2 ± 8.2 years, 31.0% diabetics, 20.2% unstable angina, 41.8% multivessel disease) were enrolled per protocol for elective single stent deployment into native de novo or post‐PTCA restenotic coronary lesions.The mean reference diameter was 2.84 ± 0.43 mm, the lesion length 12.51 ± 4.6 mm, and the minimal lumen diameter 0.75 ± 0.29 mm. Follow‐up was performed clinically in 129/129 (100%) after 6 and 12 months and angiographically in 120/129 (93%) patients after 6 months. Results: The success rates of the procedure and deployment were 100% and 95.3%, respectively. The in‐stent late loss and the late‐loss index were 0.27 ± 0.59 mm and 0.17 ± 0.40 resulting in binary in‐stent restenoses in 16/120 (13.3%) subjects and in‐segment restenoses in 20/120 (16.7%) subjects. Major adverse cardiac events occurred in 23/129 (17.8%) during the first 6 months of follow‐up with 3/129 (2.3%) myocardial infarctions, 1/129 (0.8%) secondary to stent thrombosis. From 6 to 12 months, 2/129 (1.6%) nonlesion related PCI were performed. Conclusion: The data of the Paclitaxel‐eluting Coroflex? Please stent evaluated in PECOPS II are within the range of the other currently available Paclitaxel‐eluting stent. (J Interven Cardiol 2010;23:160‐166)     

Can the Knemometer Shorten the Time for Growth Rate Assessment?

Hermanussen, M., Geiger-Benoit, K., Burmeister, J., and Sippell, W. G. (Endocrine Unit, Department of Paediatrics, Children's Hospital, and Institute for Jnformatics and Practical Mathematics, University of Kiel, Kiel, West Germany. Acta Paediatr Scand [Suppl] 337:30, 1987.
A total of 105 healthy children of both sexes and various ages were measured once or twice weekly by knemometry over periods of 161–202 days on 11–50 occasions. These data were used to calculate percentiles of the predictive error that occurred if short-term lower leg length differences were used to extrapolate half-annual growth rates. From these data, and observations on day-to-day variations of the lower leg length, it was concluded that growth rates derived from single differences between two consecutive lower leg length measurements are invalid and without predictive power for mean long-term lower leg increments. However, a novel statistical approach is presented, which results in the evaluation of daily lower leg growth rates to visualize quasi-continuous growth kinetics. Examples of successful and unsuccessful growth promoting therapeutic interventions are provided to demonstrate knemometric assessment of a significant modification of short-term growth kinetics.     

Ultrastructural Alterations in the Right and Left Ventricular Myocardium Following Multiple Low Energy Endocardial Countershocks in Anesthetized Dogs

Both high energy transthoracic and direct epicardial defibrillation can result in RV and LV myocardial damage, but little is known about the damage due to defibrillation using an endocardial RV electrode. Furthermore, disturbances in postdefibrillation oxidative metabolism have been reported and may be caused by primary injury of mitochondrial integrity and function, but information about ultrastructural mitochondrial alterations is rare. We therefore studied, in 13 fox hounds, RV and LV ultrastructural alterations following multiple low energy endocardial countershocks. Using an ICD and an endocardial defibrillation system a median of 54 (43–74) countershocks with a cumulative energy of 1,558 J (844–2,141 J) was delivered. After termination of countershocks, RV and LV myocardium was examined by electron microscopy. In both ventricles, severe myocardial alterations were found, including swollen mitochondria, disruption of mitochondrial crests, and loss of integrity of the mitochondrial inner and outer membranes. At the first time a semiquantitative score, originally developed for postischemic injury, was successfully used to grade the postcountershock mitochondrial alteration, which showed a more pronounced damage in the RV (2.69 ± 0.22 points) compared to the LV (2.18 ± 0.22; P = 0.021). We conclude that even the use of endocardial lead systems with low energy countershocks may lead to severe mitochondrial damage, especially in the RV.     

Angiographic Results and Elastic Recoil Following Coronary Excimer Laser Angioplasty with Saline Perfusion

Recent experiments have demonstrated that pressure waves of several hundred atmospheres, which occur during excimer laser coronary angioplasty (ELCA), are reduced while ablating in saline in comparison to blood or contrast medium. We report the procedural outcome of ELCA (XeCI laser operating at 308 nm, 25–40 Hz, 40–60 mJ/mm² fluence, and 135 nsec/pulse) performed with a modified saline infusion protocol (two operator technique, flush, and continuous application of saline through the guiding catheter immediately prior and during the whole losing procedure). We studied 48 patients (34 males, 14 females; mean age: 61 ± 6 years; 18 occlusions, 30 stenoses [> 60% diameter stenosis]) with 10 type A, 17 type B, and 21 type C lesions. Laser success (> 20% increase in minimal luminal diameter [MLD]) was achieved in 41 patients (85.4%), and procedural success (< 50% residual stenosis) in 44 patients (91.6%). The MLD increased from 0.37 ± 0.12 to 1.63 ± 0.35 mm (P < 0.001) following laser ablation, and to 2.30 ± 0.34 mm (P > 0.01) after percutaneous transluminal coronary angioplasty (PTCA). The mean percentage stenosis decreased from 81%± 6% (baseline) to 48%± 12% (P < 0.001) after laser ablation, and to 29%± 10% (P < 0.01) following PTCA. The mean diameter of the laser-catheter (LC) was 1.54 ± 0.2 and the mean diameter of the inflated balloon at maximum pressure was 2.7 ± 0.25 mm. Thus, the elastic recoil (ER) following balloon deflation was 15%± 9%, and below the reported ER for PTCA. Two major dissections occurred following ELCA; one patient required bypass surgery and developed a Q wave myocardial infarction (Ml), and one patient was successfully treated with stent implantation following abrupt closure. There were no in-hospital deaths, further Q wave MIs, and/or perforation. In conclusion, ELCA with concomitant saline infusion is effective, safe, and easy to perform. The use of this ablation procedure reduces the rate of significant dissections, favors effective tissue ablation, and thus may in part be responsible for a reduced amount of elastic recoil following additional balloon angioplasty. (J Interven Cardiol 1996;9:9–18)     

Sclerosing lymphangitis of the penis: a lymphangiofibrosis thrombotica occlusiva*

Three patients with so-called non-venereal sclerosing lymphangitis of the penis are presented. Light and electron microscopy of one case revealed a lymphatic collecting vessel with a fibrin thrombus in the process of recanalization and vessel wall fibrosis due to hyperplasia of smooth muscle cells and fibroblasts. The term ‘lymphangiofibrosis thrombotica occlusiva’ is proposed. Lymph stasis is suggested as a provoking factor for the dilatation and clinically striking firm thickening of the affected collecting vessel. No microorganisms were recognized. Within the fibrin thrombus, sprouts of endothelial cells showed intracellular vacuoles, probably indicating the first identifiable step in lymph capillary lumen formation. Signs of collagen remodelling were encountered in the thickened vessel wall.     

DYSKERATOSIS IN BOWEN''S DISEASE: THE ULTRASTRUOTURE AND FATE OF KERATINOCYTES WITH ALTERED TONO-FILAMENT-DESMOSOME COMPLEXES

Summary.— The ultrastructure of dyskeratotic cells in Bowen's disease has been studied. It has been found that, in the suprabasal layers in some keratino-cytes, all tonofilament-desmosome complexes (TFDC), as well as many cytoplasmic organelles, are altered. The earliest stage of TFDG alteration con-sisted in the separation and retraction of tonofilaments from the desmosomes. The consequence of this was the disappearance of the desmosomes and acantholytic separation of the involved keratinocyte. Our findings indicate that this was followed by the disintegration of the involved keratinocyte apart from the tonofilaments. These were released into the intercellular space and finally into the corium through breaks In the basal lamina. The Langerhans and some other dendritic epidermal cells are likely to play a role in the latter process.