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  • 1
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Annals of noninvasive electrocardiology 8 (2003), S. 0 
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Although arrhythmogenesis of Brugada syndrome is still unknown, it has been reported to be associated with conduction disturbances. Two ST-segment morphologies (coved and saddle-back patterns) have been described in this syndrome. No study has sought to determine which morphology has stronger conduction disturbances, thereby associating with life-threatening events. Methods: Forty-six patients who presented the Brugada-type ECG with either of a characteristic coved (n = 25) or saddle-back (n = 21) pattern of ST-segment morphology underwent signal-averaged ECG (SAECG). SAECG parameters, and the history of life-threatening events defined as syncope or aborted sudden death, were compared between groups. Results: Although filtered QRS duration did not differ between groups, the incidence of late potentials in the coved group was higher than in the saddle-back group (22 patients (88%) versus 4 patients (19%); P 〈 0.01), showing lower RMS40 and longer LAS40. Life-threatening events occurred in 17 patients (68%) in the coved group and 7 patients (33%) in the saddle-back group (P = 0.02). Conclusion: The coved pattern of ST segment was more closely related to conduction disturbances than the saddle-back pattern in patients with Brugada-type ECG. Life-threatening events were more common in patients with the coved ST-segment elevation. Conduction disturbances in the coved pattern of ST segment may reflect a substrate of arrhythmogenesis in Brugada syndrome.
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  • 2
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Microvolt T-wave alternans (TWA) has been proposed as a useful index to identify patients at risk of ventricular tachyarrhythmias. Recent studies have demonstrated that antiarrhythmic drugs, such as amiodarone and procainamide, decrease the prevalence of TWA. In this study, we tested whether TWA in patients on antiarrhythmic pharmacotherapy significantly predicts the recurrence of ventricular tachyarrhythmias in patients with dilated cardiomyopathy.Methods: To evaluate the ability to predict the recurrence of ventricular tachyarrhythmias, determinate TWA and left ventricular ejection fraction (LVEF) were prospectively assessed in 49 patients with ischemic or nonischemic dilated cardiomyopathy on antiarrhythmic pharmacotherapy for sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). The pharmacotherapy consisted of class I (17 patients), III (29 patients), and IV (3 patients) antiarrhythmic drugs. The study endpoint was the first recurrence of sustained VT or VF on treatment during the follow-up period.Results: TWA was positive on antiarrhythmic pharmacotherapy in 30 patients (61%). During a follow-up of 13 ±; 11 months, the sustained VT or VF recurred in 21 of the 41 patients (51%) with available follow-up data. The sensitivity of TWA and LVEF for predicting recurrence of ventricular tachyarrhythmias was 76 and 38%, specificity was 60 and 70%, positive predictive value was 67 and 57%, and negative predictive value was 71 and 52%. Kaplan-Meier event-free analysis revealed that TWA was a significant risk stratifier (P = 0.02), whereas LVEF was not.Conclusions: This prospective study suggests that TWA significantly predicts the recurrence of ventricular tachyarrhythmias, even on antiarrhythmic pharmacotherapy, in patients with dilated cardiomyopathy. TWA may also be a useful marker for evaluating the efficacy of antiarrhythmic drugs for ventricular tachyarrhythmias. A.N.E. 2001; 6(3):203–208
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  • 3
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2XG , UK . : Blackwell Publishing, Inc.
    Annals of noninvasive electrocardiology 10 (2005), S. 0 
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Recent studies suggest that the Brugada-type electrocardiogram (ECG) is much more prevalent than the manifest Brugada syndrome. Although invasive electrophysiologic investigations have been proposed as a risk stratifier, their value is controversial, and alternative noninvasive techniques may be preferred. We sought a noninvasive strategy to detect a high-risk group in a long-term follow-up study of subjects with a Brugada-type ECG, and no history of cardiac arrest. Methods: This study enrolled 124 consecutive subjects with a Brugada-type ECG. Prognostic indices included: age, sex, a family history of sudden death, syncopal episodes, a spontaneous coved-type ST-segment elevation, maximal magnitude of ST-segment elevation, a spontaneous change in ST segment, a mean QRS duration, maximal QT interval, QT dispersion, late potentials (LP) by signal-averaged ECG, and microvolt T-wave alternans. Results: Of the 124 subjects, 20 consenting subjects had an implantable defibrillator before follow-up. During a 40 ± 19-month follow-up, 12 subjects (9.7%) reached one of the endpoints (sudden death or ventricular tachyarrhythmia). Of the 12 risk indices, a family history of sudden death, syncopal episodes, a spontaneous coved-type ST-segment elevation, a spontaneous change in ST segment, and LP had significant values. In multivariate analysis, a spontaneous change in ST segment had the most significance (a relative hazard, 9.2; P = 0.036). Combined assessment of this index and other significant indices obtained higher positive predictive values (43–71%). Conclusions: A spontaneous change in ST segment is associated with the highest risk for subsequent events in subjects with a Brugada-type ECG. The presence of syncopal episodes, a history of familial sudden death, and/or LP may increase its value.
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of noninvasive electrocardiology 7 (2002), S. 0 
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Brugada syndrome is a primary electrical disease of the heart that causes sudden cardiac death or life-threatening ventricular arrhythmias, especially in younger men. Genetic analysis supports that this syndrome is a cardiac ion channel disease. A typical electrocardiographic finding consists of a right bundle branch block pattern and ST-segment elevation in the right precordial leads. The higher intercostal space V1 to V3 lead electrocardiogram could be helpful in detecting Brugada patients. Although two types of the ST-segment elevation are present, the coved type is more relevant to the syndrome than the saddle-back type. These patterns can be present permanently or intermittently. Recent data suggest that the Brugada-type electrocardiogram is more prevalent than the manifest Brugada syndrome. Asymptomatic individuals have a much lower incidence of future cardiac events than the symptomatic patients. Although risk stratification for the Brugada syndrome is still incomplete, the inducibility of sustained ventricular arrhythmias has been proposed as a good outcome predictor in this syndrome. In noninvasive techniques, some clinical evidence supports that late potentials detected by signal-averaged electrocardiography are a useful index for identifying patients at risk. The available data recommend prophylactic implantation of an imptantabie cardioverter defibrillator to prevent sudden cardiac death. This review summarizes recent information of the syndrome by reviewing most of new clinical reports and speculates on its risk stratification. A.N.E. 2002;7(3):251–262
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  • 5
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Transmembrane action potentials (TAPs) were recorded during simultaneous mapping of a reentrant wavefront induced in canine isolated atria. The activation pattern was visualized dynamically using a high resolution electrode catheter mapping system. During functional reentry (spiral wave), cells in the core of the spiral wave remained quiescent near their resting membrane potential. Cells away from the core progressively gained TAP amplitude and duration, and at the periphery of the spiral wave the cells generated TAPs with full height and duration. During anatomical reentry, when the tip of the wavefront remained attached to the obstacle (a condition of high source-to-sink ratio), the TAP near the obstacle had normal amplitude and duration. However, when the tip of the wavefront detached from the obstacle (condition of lowered source-to-sink ratio) the TAP lost amplitude and duration. These results are consistent with the theory that the source-to-sink ratio determines the safety factor for wave propagation and wave block near the core. With decreasing source-to-sink ratio, TAP progressively decreases in amplitude and duration. In the center of the core, the cells, while excitable, remain quiescent near their resting potential. This decrease reflects a progressive decrease in the source-to-sink ratio. TAP vanishes in the core where cells remain quiescent near their resting potential. Functional and meandering reentrant wavefronts are compatible with the spiral mechanism of reentry where block at the rotating point is provided by the steep curvature of the wave tip.
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  • 6
    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: It has been reported that electrical stimulation can control spiral wave (SW) reentry. However, previous research does not account for the effects of stimulus-induced virtual electrode polarization (VEP) and the ensuing cathode-break (CB) excitation. The aim of the present study was to examine the interaction of VEP with SW reentry in a bidomain model of electrical stimulation and thus provide insight into the mechanistic basis of SW control. Methods and Results: We conducted 3,168 simulations of localized stimulation during SW reentry in an anisotropic bidomain sheet. Unipolar cathodal 2-ms stimuli of strengths 4, 8, 16, and 24 mA were delivered at 99 locations in the sheet. The interaction between stimulus-induced VEP and SW reentry resulted in 1 of 3 possible outcomes: SW shift, SW breakup, or no effect. SW shift, which could be instrumental in SW termination at an anatomic or functional line of block, resulted from CB rather than cathode-make excitation. Stimulus timing, site, and strength all were important factors in VEP-mediated SW control. Furthermore, we found that the number of episodes of SW shift across the fibers was more sensitive to stimulus strength than that of SW shift along the fibers. SW shift can be explained by the interaction between the four VEP-induced wavebreaks and the wavebreak of the SW, ultimately resulting in termination of the original SW and the survival of one of the VEP-induced wavebreaks. This establishes a new SW reentry. Conclusion: This study provides new mechanistic insight into SW control. (J Cardiovasc Electrophysiol, Vol. 15, pp. 226-233, February 2004)
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  • 7
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148 , 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 ventricular apex has a helical arrangement of myocardial fibers called the “vortex cordis.” Experimental studies have demonstrated that the first postshock activation originates from the ventricular apex, regardless of the electrical shock outcome; however, the related underlying mechanism is unclear. We hypothesized that the vortex cordis contributes to the initiation of postshock activation. To clarify this issue, we numerically studied the transmembrane potential distribution produced by various electrical shocks. Methods and Results: Using an active membrane model, we simulated a two-dimensional bidomain myocardial tissue incorporating a typical fiber orientation of the vortex cordis. Monophasic or biphasic shock was delivered via two line electrodes located at opposite tissue borders. Transmembrane potential distribution during the monophasic shock at the center of the vortex cordis showed a gradient high enough to initiate postshock activation. The postshock activation from the center of the vortex cordis was not suppressed, regardless of the initiation of spiral wave reentry. Spiral wave reentry was induced by the monophasic shock when the center area of the vortex cordis was partially excited by the nonuniform virtual electrode polarization. Postshock activation following the biphasic shock also originated from the center of the vortex cordis, but it tended to be suppressed due to the narrower excitable gap around the center of the vortex cordis. The electroporation effect, which was maximal at the center of the vortex cordis, is another possible mechanism of postshock activation. Conclusion: Our simulations suggest that the vortex cordis may cause postshock activation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 295-302, March 2003)
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  • 8
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Breakthroughs in VF Depend on Rotational Anisotropy. Introduction: The left ventricle (LV) and right ventricle (RV) are characterized by specific fiber orientation known as “rotational anisotropy.” However, it remains unclear whether the LV and RV are different with regard to the effect of rotational anisotropy on the dynamics of scroll waves during ventricular fibrillation (VF). To resolve this issue, we used a computation-based model to study scroll wave behavior. Methods and Results: We composed an environment of simulated three-dimensional ventricular wall slabs, with optional ratios of fiber rotation to wall thickness (0°, 6°, and 12°/mm thickness; LV 10 mm, RV 5 mm), using Luo-Rudy phase I equations. When rotational anisotropy was not incorporated into the LV wall slab (θendo˜θepi= 0°), most scroll waves rotated around the filaments perpendicular to the tissue surface, with only a few accompanying breakthrough waves. In a twisted LV model (θendo˜θepi= 60° and 120°), the scroll waves were demonstrated as multiple wavelets scattered spatiotemporally, frequently accompanied by breakthrough waves that were promoted by rotational anisotropy. In a twisted RV model (θendo˜θepi= 30° and 60°), single scroll waves and/or figure-of-eight reentrant waves appeared, with comparatively few breakthrough waves, regardless of the degree of fiber twist. Conclusion: The proportion of electrical effects of rotational anisotropy and tissue boundaries plays an important role in the genesis of breakthrough waves during VF, and the difference in wave propagating patterns and frequency spectrum of the ventricles may arise, in part, from the number of breakthrough waves promoted by rotational anisotropy.
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  • 9
    ISSN: 1089-7682
    Source: AIP Digital Archive
    Topics: Physics
    Notes: In support of the spiral wave theory of reentry, simulation studies and animal models have been utilized to show various patterns of spiral wave tip motion such as meandering and drifting. However, the demonstration of these or any other patterns in cardiac tissues have been limited. Whether such patterns of spiral tip motion are commonly observed in fibrillating cardiac tissues is unknown, and whether such patterns form the basis of ventricular tachycardia or fibrillation remain debatable. Using a computerized dynamic activation display, 108 episodes of atrial and ventricular tachycardia and fibrillation in isolated and intact canine cardiac tissues, as well as in vitro swine and myopathic human cardiac tissues, were analyzed for patterns of nonstationary, spiral wave tip motion. Among them, 46 episodes were from normal animal myocardium without pharmacological perturbations, 50 samples were from normal animal myocardium, either treated with drugs or had chemical ablation of the subendocardium, and 12 samples were from diseased human hearts. Among the total episodes, 11 of them had obvious nonstationary spiral tip motion with a life span of 〉2 cycles and with consecutive reentrant paths distinct from each other. Four patterns were observed: (1) meandering with an inward petal flower in 2; (2) meandering with outward petals in 5; (3) irregularly concentric in 3 (core moving about a common center); and (4) drift in 1 (linear core movement). The life span of a single nonstationary spiral wave lasted no more than 7 complete cycles with a mean of 4.6±4.3, and a median of 4.5 cycles in our samples. Conclusion: (1) Patently evident nonstationary spiral waves with long life spans were uncommon in our sample of mostly normal cardiac tissues, thus making a single meandering spiral wave an unlikely major mechanism of fibrillation in normal ventricular myocardium. (2) A tendency toward four patterns of nonstationary spiral tip motion was observed. © 1998 American Institute of Physics.
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  • 10
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Electroporation in a Model of Cardiac Defibrillation. Introduction: It is known that highstrength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as “electroporation.” However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock. Methods and Results: Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the highstrength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation. Conclusion: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.
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