Risk Factors for Implantable Defibrillator Lead Fracture in a Recalled and a Nonrecalled Lead

Risk Factors for ICD Lead Fracture. Introduction: The Medtronic Sprint Fidelis® implantable cardioverter defibrillator (ICD) lead was “recalled” in October 2007 after 268,000 implants worldwide due to increased failure risk. Manufacturer suggested monitoring has not been shown effective at preventing adverse events. Only limited data exist regarding clinical predictors of Fidelis® lead fracture. We sought to identify risk factors for Fidelis® fracture to guide clinical monitoring and compare its performance with a control lead. Methods: Fractured lead cases were retrospectively reviewed for demographic data, implant technique, radiographic appearance and clinical presentation was analyzed. Lead survival was compared using Kaplan‐Meir curves. Results: Study patients (n = 1314) experienced 18 Fidelis® and 6 Quattro? lead fractures. Patients with failed Fidelis® leads were younger than those with surviving leads (49.5 vs 64.6 years, P = 0.0066). Fidelis® lead fractures often occurred around the time of physical activity. No other measured demographic or technique related factors were associated with lead fracture. Fidelis® leads had significantly decreased survival compared with Quattro? leads (89.3 vs 98.9% at 30 months). Patients less than 50 years old had significantly decreased lead survival compared with those older than 50 in both Fidelis® (79.6% vs 96.5% at 24 months) and Quattro? (93.4 vs 99.8%, P < 0.001 at 24 months) leads. Conclusions: Patients under age 50, with either Fidelis® or Quattro? ICD leads, are at increased risk of lead fracture compared with patients over 50, particularly around the time of intense physical activity. Aggressive monitoring and advisory programming appears warranted in patients with Fidelis® leads as well as especially in younger patients. (J Cardiovasc Electrophysiol, Vol. 21, pp. 671‐677, June 2010)     

Acute Urinary Tract Toxicity of Tetraethylorthosilicate in Rats

Acute stomach, kidney, and bladder toxicity was evaluated inF344 rats after gastric gavage of tetraethylorthosilicate (TES)at daily doses of 0, 0.111, 0.223, and 0.333 g. Five rats ofeach sex at each dose were sacrificed after 1, 2, and 4 days.In TES-treated groups, silicate accumulated in the stomach glandsand the muscle layer of the forestomach and glandular stomach.Serum chemistries demonstrated acute onset of renal failure.In the kidneys, acute tubular necrosis, accumulation of silicates,and superficial necrotizing papillitis were observed. In therenal pelvis and bladder, there was urothelial simple hyperplasia,focal erosion of the mucosa, edema, and inflammation. Theseacute toxic changes were dose and time dependent, but significantsex differences were not observed. The microscopic changes inthe urothelium were similar to those observed following administrationof high doses of sodium saccharin to male rats in which urinarysilicate precipitate and crystals form.     

Aneurysm of the Left Main Coronary Artery

Aneurysms of the left main coronary artery are rare; the estimated incidence is < 0.1%. They are usually associated with atherosclerotic coronary artery disease, and are incidental discoveries at the time of cardiac catheterization for the evaluation of cardiac symptoms. This report describes the clinical course of a patient with an isolated left main coronary artery aneurysm and generalized atherosclerosis.     

Propofol reduces the incidence of vomiting after tonsillectomy in children

We compared the effect of a propofol-based anaesthetic to an isoflurane-based anaesthetic on the incidence of postoperative vomiting in children following tonsillectomy. Thirty-nine children were enrolled in the study and randomized to receive one of the proposed anaesthetics. All patients underwent a mask induction with halothane, nitrous oxide, and oxygen. Intravenous access was established and all children received fentanyl (2–4 μg·kg^-1) i.v., mivacurium (0.3 mg·kg^-1) i.v. and acetaminophen (10–15 mg·kg^-1) p.r. Following tracheal intubation, patients received either isoflurane (0.8–1.6%) or propofol (120–180 μg·kg^-1 min^-1) i.v. with nitrous oxide 70%/oxygen 30% for maintenance of anaesthesia. Vital signs were maintained within 20% of baseline. All patients were extubated in the operating room. PACU nursing staff recorded episodes of vomiting for 4–6 h prior to discharge. A telephone interview the following day was also used for data recovery. Age, sex, and duration of the procedure were not significantly different between the two study groups. Of 19 patients who received propofol, four vomited (21%); in contrast, of the 20 patients who received isoflurane, 11 vomited (55%). This difference is significant (P= 0.048 two-tailed Fisher's Exact Test). These data suggest that using propofol for anaesthesia can diminish the incidence of vomiting following tonsillectomy.     

Oral and Intravenous Amiodarone for Atrial Fibrillation-Flutter

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.     

Correlative Anatomy and Electrophysiology for the Interventional Electrophysiologist:

The cavotricuspid isthmus (CVTI) is the well-established location of atrial tissue critical for the maintenance of typical atrial flutter. The CVTI begins at the electrically inert tricuspid valve and includes the atrial myocardium up to the inferior vena cava (IVC).
In this article, we discuss relevant CVTI and right atrial anatomy of interest to the electrophysiologist. Critical questions that are considered include why ablation is sometimes difficult across the CVTI and how best to deal with anatomic variation including sub-Eustachian pouches or large pectinate muscles encroaching onto the isthmus. Important electroanatomic features of the right atrium (RA) including sites for naturally occurring conduction block and the anatomy of the "lower loop" are reviewed.
Following this discussion on the impact of the underlying anatomy for right atrial flutter ablation, an approach to dealing with difficulty when mapping or ablating this common arrhythmia is presented.     

Synthesis and secretion of immunoglobulin by spleen cells from resistant and susceptible mice infected with Trypanosoma brucei brucei GUTat 3.1

By 6 days after infection of susceptible C3H/He and resistant C57BL/6 mice with Trypanosoma brucei brucei GUTat 3.1, splenic plasma cell responses of both strains of mice were similar in terms of plasma cell number, intracellular Ig, Ig secretion, Ig class and Ig specificity for surface-accessible variant surface glycoprotein (VSG) epitopes on the infecting organisms, despite higher parasitaemia in the C3H/He mice. By 7 days after infection, however, although splenic plasma cells from both strains of mice had greatly amplified their Ig responses, those from C57BL/6 mice (which cleared parasites from their bloodstream between 6 and 7 days after infection) contained and secreted 3-5 times more Ig specific for exposed VSG epitopes on the infecting organisms than those from C3H/He mice which did not clear parasites from their bloodstream. In vitro, trypanosomes can absorb significant amounts of VSG-specific antibody produced by splenic plasma cells. However, differences in the detection of VSG-specific antibodies present in, and secreted by, splenic plasma cells of 7-day infected C3H/He and C57BL/6 mice were shown not to result from the presence of parasites in the cultures of C3H/He spleen cells. It is argued that between 6 and 7 days after infection, the C3H/He mice selectively lose the capacity to support development of plasma cells specific for exposed VSG epitopes on the infecting organisms and that this is a consequence rather than a cause of differences in the peak levels of first wave parasitaemia.     

Rate of Sickling of Red Cells during Deoxygenation of Blood from Persons with Various Sickling Disorders

The clinical severity of various sickle hemoglobinopathies was directlyrelated to the rate of increase of viscosity of blood during deoxygenation.The principal determinants of the rate were the concentration of hemoglobinS in the red cell and the degree of interaction between hemoglobins whenmore than one major type was present. There was a close correlation between the rate of change of viscosity of blood under the conditions employed and the minimum concentration of the deoxygenated hemolysaterequired for gelation. Hemoglobin D_Punjab showed the most marked interaction with hemoglobin S and hemoglobin F the least, accounting for thestriking clinical differences between S-D and S-F heterozygotes. Clinicalstatus of the patients and rate of increase of viscosity of partially deoxygenated blood were not closely correlated with the percentage of hemoglobinS in the hemolysate, the mean corpuscular sickle hemoglobin concentration,or the solubility of the hemoglobin. The viscosity of deoxygenated blood wasdirectly related to the proportion of sickled red cells, but filamentous formswere associated with a greater viscosity than holly leaf forms; accordingly,viscosity could not be predicted precisely from the percentage of sicklederythrocytes in a blood specimen. The viscosity of blood containing sicklederythrocytes was approximately proportional to the square of the hematocritvalue, an observation of relevance in explaining the frequent occurrence ofvascular occlusive manifestations in patients with certain heterozygous sickling disorders without appreciable anemia. The data of this study supportthe concept that all of the clinical manifestations of sickle cell disease areattributable to the consequences of intravascular sickling of erythrocytes.Clinical differences between patients whose red cells appear to be similarprobably can be explained by extracorpuscular factors influencing rates ofsickling.

Submitted on August 29, 1963 Accepted on January 6, 1964