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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 9 (1998), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lidocaine's Effect on Defibrillation Depends on Lead System. Introduction: Epicardial and endocardial defibrillation electrode systems affect myocardial electrophysiology and sympathetic function differently. Thus, we postulate that antiarrhythmic drugs will interact with these electrode systems differently. Methods and Results: Defibrillation energy requirements (DER) at 20% (ED20), 50% (ED50), and 80% (ED80), success were measured at baseline and during lidocaine (10 mg/kg per hour) or D5W treatment for epicardial and endocardial electrodes. Pigs were randomized to treatment (lidocaine or D5W) and electrode system, which resulted in four experimental groups: (1) epicardial electrode + D5W; (2) epicardial electrode + lidocaine; (3) endocardial electrode + D5W; and (4) endocardial electrode + lidocaine. ED50 DER (mean ± SEM) values at baseline for groups 1–4 were 10.6 ± 1, 8.5 ± 1, 12.6 ± 1, and 12.3 ± 1 J, respectively. DER values for groups 1 and 3 during D5W were similar to baseline. Conversely, lidocaine increased ED50 DER values from 8.5 ± 1 to 13.5 ± 2 J (P 〈 0.05) in group 2 animals (epicardial electrodes). When lidocaine was administered to group 4 animals (endocardial electrodes), however, ED50 DER values remained similar to baseline values (12.3 ± 1 to 14.3 ± 2 J, P = NS). Lidocaine increased ED50 DER values by 59% with the epicardial electrode system, which was significantly greater than the 16% increase with the endocardial electrode system (P 〈 0.05). Electrophysiologic response and electrode impedance were similar between electrode systems. Conclusion: Lidocaine increases DER values to a greater extent when using epicardial versus endocardial electrode system. Thus, drug-device interactions are dependent on the electrode system. These data suggest that the electrophysiologic milieu created by endocardial defibrillation mitigates the effects that lidocaine has on DER values.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: The Medtronic ICD-AT has atrial/ventricular therapies, which can be programmed to deliver atrial defibrillation during sleep, intended to potentially decrease shock anxiety/pain and lifestyle disruption. However, these shocks may diminish sleep quality. This study examined atrial shock characteristics (i.e., mode, frequency), AF symptoms, and psychological factors as determinants of sleep quality. Methods and Results: The 96 ICD-AT patients were mostly men (72%; M age 65 ± 12 years) and implanted for 1.6 years (SD = 0.8 years). Patients were divided into shock groups based on the proportion of mode (≥90%) of total atrial shocks received. Patients were grouped into either automatic-nocturnal shock group (8 P.M.–8 A.M.; n = 35) or manual-awake shock group (n = 42). Psychological measures included Pittsburgh Sleep Quality Index (PSQI), Center for Epidemiology Studies-Depression Scale, State-Trait Anxiety Inventory, and Illness Intrusiveness Rating Scale. Atrial fibrillation disease burden was assessed via atrial symptom score and atrial shock use. PSQI global scores were similar between manual (7.67 ± 2.53) and automatic shock (8.20 ± 2.93) groups. A multiple hierarchical regression analysis indicated that no atrial shock variables were predictive of sleep quality; yet, both AF symptom (B = 0.226, P = 0.040) and depression (B = 0.392, P = 0.034) scores predicted diminished sleep quality, accounting for 42% of the variance in global sleep quality (P 〈 0.001). Conclusion: These results suggest that atrial defibrillation therapy does not have a deleterious impact on sleep. However, the significance of AF symptoms and depression indicate that comprehensive care of both physical and psychological symptomatology may improve sleep quality in ICD-AT patients. (J Cardiovasc Electrophysiol, Vol. 14, pp. 960-964, September 2003)
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 13 (2002), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Pericardial Procainamide Delivery. Introduction: Procainamide delivery into the pericardial space may produce a greater and more prolonged electrophysiologic effect, particularly in thin superficial atrial tissue, compared with intravenous delivery. Methods and Results: Swine were randomized to sequential procainamide doses delivered intravenously (n = 6) or into the pericardial space (n = 7). The cumulative pericardial doses were 0.5, 1.5, and 3.5 mg/kg, and the intravenous doses were 2, 10, and 26 mg/kg. Pericardial procainamide prolonged right atrial effective refractory period from baseline by 22% (P 〈 0.01) but only at the 3.5 mg/kg cumulative dose. This dose slowed interatrial conduction time by 14% (P 〈 0.05) and raised atrial fibrillation threshold by 70 mA (P 〈 0.05). Pericardial procainamide had minimal effect on ventricular electrophysiology. Similar results occurred with a single 2 mg/kg pericardial dose in a closed chest model. Intravenous 10 and 26 mg/kg cumulative doses prolonged atrial effective refractory period from baseline by 24% and 18% (P 〈 0.01), respectively. The 26 mg/kg cumulative intravenous dose slowed interatrial and atrial-ventricular conduction times by 27% and 17%, respectively (P 〈 0.05), raised atrial fibrillation threshold, and slowed ventricular conduction time by 29% (P 〈 0.05). Pericardial procainamide produced pericardial fluid concentrations ranging from 250 to 1,500 μg/mL, but plasma concentrations were 〈 1 μg/mL. Intravenous procainamide doses produced pericardial fluid concentrations similar to plasma trough concentrations 0 to 12 μg/mL. Conclusion: The single 2 mg/kg and 3.5 mg/kg cumulative pericardial procainamide doses prolonged atrial refractoriness and raised atrial fibrillation threshold similar to the 26 mg/kg cumulative intravenous dose, but the duration of effect was similar between delivery methods. Pericardial procainamide did not affect global or endocardial ventricular electrophysiology nor was it associated with ventricular proarrhythmia.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 15 (2004), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: The Medtronic Jewel AF 7250 is an implantable cardioverter defibrillator with atrial and ventricular therapies (ICD-AT). The ICD-AT is effective in managing atrial tachyarrhythmias (atrial fibrillation [AF]), but patient acceptance remains an issue. This aim of this study was to measure ICD-AT acceptance. Methods and Results: ICD-AT acceptance was evaluated in 96 patients enrolled in the “Jewel AF-AF-Only Study” for ≥3 months of follow-up (mean 19 months). Patients were mostly men (72%; age 65 ± 12 years). Clinical data and a written survey (75% response rate) were used to quantify demographics, AF frequency and symptoms, atrial defibrillation therapy, quality of life (QOL), psychosocial distress, and ICD-AT therapy acceptance. From implant to survey, AF symptom and severity scores decreased by 18% (P ≤ 0.05), and QOL (SF-36) scores increased by 15% to 50% (P ≤ 0.05). ICD-AT therapy acceptance was high, with 71.3% of patients scoring in the 75th percentile on the Florida Patient Acceptance Survey. ICD-AT acceptance was correlated with the Physical Component Scale and Mental Health Component Scale scores of the SF-36 (r = 0.28 and 0.35, respectively). ICD-AT acceptance was negatively correlated with depressive symptomatology (r =–0.59), trait anxiety (r =–0.48), illness intrusiveness (r =–0.55), and AF symptom and severity scores (r =–0.26). ICD-AT acceptance did not correlate with preimplant cardioversions, number of atrial shocks, AF episodes detected by the device, or device implant duration. Conclusion: Most patients accepted ICD-AT therapy. Patients were more likely to accept ICD-AT if they had less psychosocial distress, greater QOL, and lower AF symptom burden. (J Cardiovasc Electrophysiol, Vol. 15, pp. 286-291, March 2004)
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Regional Hyperkalemia and Defibrillation. Introduction: Increased spatial electrical heterogeneity has heen associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity. Methods and Results: We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo In the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P 〈 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient. Conclusion: Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 12 (2001), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lidocaine and Shock Proarrhythmia. Introduction: Lidocaine increases monophasic shock defibrillation energy requirement (DER) values but does not alter biphasic shock DER values. However, the mechanism of this drug/shock waveform interaction is unknown. It may be that lidocaine increases the proarrhythmic actions of monophasic shocks but not biphasic shocks. Thus, lidocaine may increase monophasic shock DER values by increasing myocardial vulnerability to shock-induced ventricular fibrillation. Methods and Results: Area of myocardial vulnerability (AOV), defined by a two-dimensional grid according to shock strength (y-axis) and shock coupling interval (x-axis), was assessed for biphasic shocks (n = 11) and monophasic shocks (n = 13) in intact swine hearts. Shocks were randomly delivered during right ventricular pacing at 10 shock strengths (50 to 500 V) and five coupling intervals (160 to 240 msec). AOV was defined as the number of points within the test grid that induced ventricular fibrillation. AOV, upper limit of vulnerability (ULV), and DER values were determined at baseline and during systemic infusion of lidocaine (10 mg/kg/hour). Lidocaine increased AOV, ULV, and DER values by 35%, 23%, and 36%, respectively, for monophasic shocks. However, lidocaine did not alter AOV, ULV, or DER values for biphasic shocks. Conclusion: Lidocaine increases the AOV to monophasic shocks, which is directly related to changes in ULV and DER values. This implies that lidocaine increases the proarrhythmic activity of monophasic shocks but not biphasic shocks. This may explain why lidocaine increases monophasic shock DER values.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148-5018 , USA and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Pacing and clinical electrophysiology 28 (2005), S. 0 
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with a variety of symptoms such as dizziness, palpitations, shortness of breath, and other signs of heart failure, which in turn impact quality of life (QOL). Implantable cardioverter defibrillators with atrial therapies (ICDs-ATs) have been shown to reduce AF symptoms and improve QOL in select AF samples. Method: This study examined the strength of relationships between objective (device-detected AF events) versus subjective (emotional symptoms) data and AF symptoms (number) reported as part of the Patient Atrial Shock Survey of Acceptance and Tolerance Study (N = 96, 72% men, M age = 65, SD = 12). Depression and anxiety were assessed via the Center for Epidemiological Studies—Depression Scale and the-State Trait Anxiety Inventory. AF disease burden was measured via a number of device-detected AF episodes and the Atrial Tachyarrhythmia Symptom Severity Scale. Results: Hierarchical multiple regression analysis indicated that negative emotions accounted for a significant 13.2% of unique variance in AF symptom score (F change (1, 54) = 9.625, P = 0.003). On the other hand, the number of device-detected AF episodes accounted for non-significant 8.2% of unique variance in the AF symptom score (P = 0.167). The full model explained 25.7% of the variance in AF symptom score (F(6, 54) = 3.110, P = 0.011). Specifically, greater number of treated AF episodes (β= 0.251, P = 0.043) and higher levels of negative emotions (β= 0.369, P = 0.003) predicted greater number of reported AF symptoms. Conclusion: Therefore, psychological distress may be a significant confounding factor affecting patient's report of AF symptoms rather than the actual experience of recurrent AF episodes.
    Type of Medium: Electronic Resource
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