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  • 1
    Electronic Resource
    Electronic Resource
    Ventricular Arrhythmias Following Exposure of Failing Hearts to Oxidative Stress in Vitro (2005)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 16 (2005), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: There is experimental evidence that heart failure (HF) is an oxidative stress and that HF myocytes may be damaged by oxygen-derived free radicals. However, the arrhythmogenicity of these radicals has not been studied in HF. Methods and Results: Isolated perfused hearts were obtained from sham-operated (SHAM, n = 6), and fast pacing (250 ms, 2 weeks)-induced heart failure porcines (HF, n = 8). Epicardial conduction was mapped in the longitudinal and transverse directions and ventricular arrhythmias were closely monitored after perfusion of 100, 300, and 1000 μmol/L H2O2. Left ventricular epicardium was sampled for action potentials recordings in the same conditions. Myocardial levels of thiobarbituric acid reactive substances and antioxidant enzymatic capacity were also assessed. Epicardial conduction velocities were unaffected by H2O2 in both groups. Isolated ventricular premature beats and runs of slow ventricular rhythm with H2O2 more frequently occurred in HF compared to SHAM despite an increased antioxidant capacity including Cu/Zn and Mn superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. Sustained arrhythmias were not observed. Higher thiobarbituric acid reactive substances levels were found in HF confirming endogenous oxidative stress. Action potential duration at plateau level was increased following H2O2 in SHAM but not in HF epicardial fibers where a toxic effect developed at 1000 μmol/L. Conclusion: Oxidative stress with concomitant increase in antioxidant capacity develops in this HF model. There is a greater proclivity to oxidative stress-mediated arrhythmias in HF. These arrhythmias are mainly extrasystoles or slow ventricular rhythms and not dependent on abnormal myocardial conduction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2005.40584.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanisms of Onset of Atrial Fibrillation: (2003)
    350 Main Street , Malden , MA 02148-5018 , U.S.A . : Blackwell Publishing
    Pacing and clinical electrophysiology 26 (2003), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The aim of this study was to analyze the onset mechanisms of atrial tachyarrhythmias using a dedicated diagnostic system in 83 recipients of DDDR pacemakers implanted for standard clinical indications. The pulse generator was programmed in DDD mode, at 60 beats/min, and the diagnostic instrument was programmed to document atrial tachyarrhythmic episodes at rates 〉200 beats/min. Onset mechanism was defined as the combination of ambient rhythm and trigger. Various underlying rates and rhythms patterns, including tachycardia, increasing frequency of premature atrial complex (PAC), underlying heart rate increase, restart, and no specific underlying rhythm, and various triggers, including single, multiple, or short runs of PACs, sudden rate decrease, and sudden onset of atrial tachyarrhythmia were included in the combined classification. Atrial tachyarrhythmic episodes were documented on one follow-up interrogation in 48 of the 83 patients. The pacing indications consisted of high degree atrioventricular block in 19 patients, bradycardia-tachycardia syndrome in 22, and isolated sinus node dysfunction in 6 patients. The onset mechanisms of 318 episodes were recorded and analyzed. A variety of triggers were observed in 33 of the 48 patients, and 39 patients had various ambient rhythms. Among 20 documented onset mechanisms, the most common were increasing frequency of PAC + short runs (17%), no specific ambient rhythm + sudden onset (24%), and increasing frequency of PAC + sudden onset (12%). There were wide intra- and interpatient variations in onset mechanisms, suggesting that state-of-the-art pacemakers should represent versatile diagnostic tools and offer flexible pacing methods to refine the management of atrial tachyarrhythmias. (PACE 2003; 26:1336–1341)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2003.t01-1-00191.x
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  • 3
    Electronic Resource
    Electronic Resource
    Pacemaker Lead Extraction with the Needle's Eye Snare for Countertraction via a Femoral Approach (2002)
    Oxford, UK : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 25 (2002), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: KLUG, D., et al.: Pacemaker Lead Extraction with the Needle's Eye Snare for Countertraction via a Femoral Approach. Femoral approach pacemaker lead extraction is described as a safe and efficacious procedure. When the lead can not be removed from its myocardial insertion, the “Needle's eye snare” has become available, and it allows a femoral approach traction associated with a countertraction . Between May 1998 and May 2000, 222 lead extraction procedures were performed in 99 patients using the femoral approach. This article reports the results of the 70 lead extractions requiring the use of the Needle's eye snare for femoral approach countertraction in 39 patients with a total of 82 leads. The indications were infection, accufix leads and lead dysfunction in 56, 1 and 6 leads, respectively. The age of the leads was 113 ± 56 months. Sixty-one (87.2%) leads were successfully extracted, the extraction was incomplete in 3 (4.3%) cases and failed in 6 (8.5%) cases. The failures were due to leads totally excluded from the venous flow for four leads, the impossibility of advancing the 16 Fr long sheath through the right and left iliac veins for one lead and one traction induced a nontolerated ventricular arrhythmia. In these cases, an extraction by a simple upper traction had been attempted in another center several months before. The complications included two deaths and one transient ischemia of the right inferior limb. Despite the selection of a series of leads for which an extraction by a simple traction on the proximal end of the lead was impossible or unsuccessful, femoral countertraction seems to be a safe and efficacious procedure. The failure of this technique occurred in patients with damaged leads due to a previous extraction procedure performed in centers with limited experience in lead extraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2002.01023.x
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  • 4
    Electronic Resource
    Electronic Resource
    Identification of Ventricular Tachycardia of Epicardial Origin from Unipolar Potentials Obtained at the Endocardial Surface: Is It Feasible? (2002)
    Oxford, UK : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 25 (2002), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: LACROIX, D., et al.: Identification of Ventricular Tachycardia of Epicardial Origin from Unipolar Potentials Obtained at the Endocardial Surface: Is It Feasible? VT late after myocardial infarction usually originates from the endocardial surface; subepicardial substrates are also possible. The identification of these atypical locations with endocardial mapping remains unresolved even with new mapping technologies. This study compared isopotential maps, signal morphology, and activation patterns around left endocardial breakthroughs recorded in VTs originating from the subepicardium or subendocardium after remote myocardial infarction. These results were extracted from a database of 111 tachycardias obtained at surgery in 34 patients. Mapping was performed with a 128-unipolar electrode system using an epicardial mesh and a left ventricular endocardial balloon. Subepicardial (n = 7) and subendocardial VTs (n = 10) were defined as complete superficial reentry and/or as tachycardias with a ≥ 25-ms delay between the earliest activity and the breakthrough of activation on the opposite surface. A positive potential distribution covering the area of initial endocardial activity was observed in a single subepicardial VT but in none of the subendocardial ones (P = NS). R waves were observed on the earliest endocardial unipolar signals in two subepicardial VTs and five subendocardial VTs (P = NS). The area covered by the first 5-ms or 10- ms isochrone at the endocardial level was larger in subepicardial VTs than in subendocardial VTs but the difference was not significant. In conclusion, despite a wider endocardial area of early activity in VTs of subepicardial origin, no reliable criteria can be proposed to identify these tachycardias from mapping data restricted to the endocardial surface. This is probably due to highly nonuniform anisotropic propagation around the scarred tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2002.01561.x
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