Several Unsuccessful Internal and External Defibrillations During Active Can ICD Implantation in a Patient with Pneumothorax

During implantable cardioverter defibrillator (ICD) implantation of an active can ICD several defihrillations with 20 J and 34 J as well as 360 J externally were ineffective. The implant criteria were finally met with a second defibrillation lead and reversed polarity. A left-sided pneumothorax due to subclavian vein puncture was detected soon after ICD implantation. It is assumed that especially in the active can alignment the developing pneumothorax made defibrillation current flow more difficult. In case of several unsuccessful defibrillations during active can ICD implantation in which the subclavian vein was punctured, the possibility of a pneumothorax should be considered.     

CHANGES IN HISTAMINE CONTENT FOLLOWING PHARMACOLOGICALLY-INDUCED MAST CELL DEGRANULATION IN THE RAT CONJUNCTIVA

Compound 48/80 was applied into one eye of male Wistar rats and a drop of vehicle into the contralateral eye. Another group of rats received sodium cromoglycate in both eyes every 6 h for a period of 48 h. One eye was challenged with compound 48/80 30 min after the end of treatment with sodium cromoglycate. The eyes were monitored clinically and the histamine content of the conjunctiva was determined fluorometrically. The basal histamine levels in rat conjunctival homogenates were quantified. Pharmacologically-induced mast cell degranulation by a single application of 0.1 g ml(-1)of compound 48/80 resulted in significant decreases of conjunctival histamine levels 1, 12 and 24 h after challenge. Sodium cromoglycate prevented the effect of compound 48/80 when administered into the eye prior to the challenge with the non-immunogenic histamine releaser. Upon termination of the application, the membrane stabilizer was unable to reverse the reduced histamine levels in the conjunctival homogenates.     

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.     

Catheter Ablation of Electrical Storm Due to Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy: Acute Results and Its Effect on Long‐Term Survival

Background: Electrical storm due to recurrent ventricular tachycardia (VT) in patients with implantable cardioverter defibrillator (ICD) can adversely affect their long‐term survival. This study evaluates the efficiency of the radiofrequency catheter ablation of electrical storm due to monomorphic VT in patients with idiopathic dilated cardiomyopathy (DCM) and assesses its long‐term effects on survival. Methods and Results: Between April 2004 and October 2008, 13 consecutive patients (nine men, mean age 56.8 ± 17.8 years) with DCM and electrical storm due to monomorphic VT who had ICD underwent 17 catheter ablation procedures, including four epicardial, at our center. Acute complete success was defined as the lack of inducibility of any VT at the end of procedure during programmed right ventricular stimulation and was achieved in eight patients (61.5%). During a median follow‐up of 23 months (range 3–63 months) nine patients (69%) were alive and eight patients (61.5%) were free from VT recurrence. Among those with acute complete (n = 8) and partial (n = 5) success, seven patients (87.5%) and one patient (20%) were free from any VT recurrence and ICD therapy, respectively (P = 0.025). Among those with acute complete and partial success, seven patients (87.5%) and two patients (40%) were alive, respectively (Mantel‐Cox test P = 0.082). Among those who had an initially failed endocardial ablation (n = 8), four underwent further epicardial ablation that was completely successful in three patients (75%). Conclusion: Catheter ablation in patients with DCM and electrical storm due to monomorphic VT who had an ICD prevents further VT recurrence in 61.5% of the patients. Complete successful catheter ablation may play a protective role and was associated with reduced mortality during the follow‐up period. More aggressive ablation strategies in patients with initially failed endocardial ablation might improve the long‐term survival of these patients; however, further studies are needed to clarify this issue. (PACE 2010; 33:1504–1509)     

IDIOPATHIC APLASTIC ANAEMIA IN CHILDREN

The results of treatment of 19 children with idiopathic aplastic anaemia is reported. Initially the patients received testosterone-prednisone therapy. When a satisfactory haemoglobin level had been reached metandienon was substituted for testosterone and the corticosteroids withheld. 8 patients died without signs of response, 2 patients responded initially but died later. The remaining 9 patients are alive but in only 3 of them was it possible to discontinue all therapy without signs of relapse. The rate of remission varied considerably. One patient required 23 months of combined therapy to achieve a normal haemoglobin level. A moderate hypoplasia of the bone^marrow at the start of therapy was the most favourable prognostic sign in this series. Therefore, it may be concluded that every effort should be made to diagnose the disease before the bone-marrow changes have progressed to severe hypoplasia.     

Acid Instillation Increases Gastric Luminal Prostaglandin E2 Output in Man

ABSTRACT. The capacity of the gastroduodenal mucosa to maintain integrity when exposed to acid and pepsin may require formation of endogenous prostaglandins (PG). The gastric mucosa is capable of PG biosynthesis, and PGE₂ is present in the gastric contents of man. The purpose of this study was to examine if acidification of the human stomach affects the output of PGE₂. Gastric perfusion was made with 150 mM HC1 in seven healthy subjects pretreated with a histamine-2-receptor blocker (ranitidine). Gastric luminal PGE₂ was measured by gas chromatography-mass spectrometry. Basal output of PGE₂ was 1.42 ± 0.24 pmol/min (mean+SEM), which increased to 5.37 ± 0.91 pmol/min (p < 0.02) during acid perfusion. Gastric acidification did not cause mucosal damage as judged by luminal DNA. We conclude that PGE₂ is synthesized in the gastric mucosa even during nearly complete inhibition of parietal cell secretion. Luminal acid, a likely physiological stimulator of mucosal defense, induces a fivefold increase in PGE₂ output from the intact mucosa.