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Ventricular Fibrillation (ventricular + fibrillation)
Kinds of Ventricular Fibrillation Selected AbstractsAnalysis of the Pattern of Initiation of Sustained Ventricular Arrhythmias in Patients with Implantable DefibrillatorsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2000ERIC TAYLOR M.D. Initiation of Sustained Ventricular Arrhythmias. Introduction: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease. Methods and Results: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating heat of all ventricular arrhythmias was 523 ± 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty-two (85%) of the arrhythmia episodes were initiated by a late-coupled premature beat, 33 (13%) were initiated by an early-coupled premature beat, and 5 episodes (2%) were initiated with a short-long-short sequence. The patttern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias. Conclusion: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late-coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia. [source] A Model of Ischemically Induced Ventricular Fibrillation for Comparison of Fixed-dose and Escalating-dose Defibrillation StrategiesACADEMIC EMERGENCY MEDICINE, Issue 6 2004James T. Niemann MD Abstract Objectives: Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. Methods:Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J,300 J,360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with ,3 shocks. Results: VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with ,3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with ,3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with ,3 shocks ranging from 200 to 360 J. Conclusions: In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks. [source] Spontaneous Onset of Ventricular Fibrillation during Atrioventricular Nodal Reentrant TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2009CHRISTIAN VON BARY M.D. No abstract is available for this article. [source] Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Simulation Study Using a Dynamic Mechanoelectric Model of Ventricular TissueJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008SATOKO HIRABAYASHI master of environment Introduction: To investigate the mechanisms underlying the increased prevalence of ventricular fibrillation (VF) in the mechanically compromised heart, we developed a fully coupled electromechanical model of the human ventricular myocardium. Methods and Results: The model formulated the biophysics of specific ionic currents, excitation,contraction coupling, anisotropic nonlinear deformation of the myocardium, and mechanoelectric feedback (MEF) through stretch-activated channels. Our model suggests that sustained stretches shorten the action potential duration (APD) and flatten the electrical restitution curve, whereas stretches applied at the wavefront prolong the APD. Using this model, we examined the effects of mechanical stresses on the dynamics of spiral reentry. The strain distribution during spiral reentry was complex, and a high strain-gradient region was located in the core of the spiral wave. The wavefront around the core was highly stretched, even at lower pressures, resulting in prolongation of the APD and extension of the refractory area in the wavetail. As the left ventricular pressure increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated the wave breakup and meandering of tips through interactions between the wavefront and wavetail. Conclusions: This simulation study indicates that mechanical loading promotes meandering and wave breaks of spiral reentry through MEF. Mechanical loading under pathological conditions may contribute to the maintenance of VF through these mechanisms. [source] Predictors of All-Cause Mortality for Patients with Chronic Chagas' Heart Disease Receiving Implantable Cardioverter Defibrillator TherapyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2007AUGUSTO CARDINALLI-NETO M.D., Ph.D. Background: Implantable Cardioverter Defibrillators (ICD) have sporadically been used in the treatment of either Sustained Ventricular Tachycardia (VT) or Ventricular Fibrillation (VF) in Chagas' disease patients. This study aimed at determining predictors of all-cause mortality for Chagas' disease patients receiving ICD therapy. Methods and Results: Ninety consecutive patients were entered the study. Mean left ventricular ejection fraction was 47 ± 13%. Twenty-five (28%) patients had no left ventricular systolic dysfunction. After device implantation, all patients were given amiodarone (mean daily dose = 331, 1 ± 153,3 mg), whereas a B-Blocking agent was given to 37 (40%) out of 90 patients. Results: A total of 4,274 arrhythmias were observed on stored electrogram in 64 (71%) out of 90 patients during the study period; SVT was observed in 45 out of 64 (70%) patients, and VF in 19 (30%) out of 64 patients. Twenty-six (29%) out of 90 patients had no arrhythmia. Fifty-eight (64%) out of 90 patients received appropriate shock, whereas Antitachycardia Pacing was delivered to 58 (64%) out of 90 patients. There were 31 (34%) deaths during the study period. Five patients were lost to follow up. Sudden cardiac death affected 2 (7%) out of 26 patients, whereas pump failure death was detected in the remaining 24 (93%) patients. Number of shocks per patient per 30 days was the only independent predictor of mortality. Conclusion: Number of shocks per patient per 30 days predicts outcome in Chagas' disease patients treated with ICD. [source] Ventricular Fibrillation Induced by Stretch Pulse: Implications for Sudden Death Due to Commotio CordisJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2006FRANK BODE M.D. Introduction: Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity. Methods: We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. Results: Sudden balloon inflation induced VF when pressure pulses of 208,289 mmHg were applied within a window of 35,88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 ± 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 ± 3% to 26 ± 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation. Conclusions: Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis. [source] Types of Ventricular Fibrillation:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004or 300 No abstract is available for this article. [source] Asynchronous Ventricular Pacing Triggering Ventricular FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2004ETIENNE DELACRETAZ M.D. [source] Repolarization Abnormality in Idiopathic Ventricular Fibrillation:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2004Assessment Using 24-Hour QT-RR, QaT-RR Relationships Introduction: We evaluated the characteristics of QT-RR and QaT (apex of T wave)-RR relationships in patients with idiopathic ventricular fibrillation (IVF) compared with control subjects. We hypothesized that IVF patients have unique repolarization dynamics related to a reduced fast Na current and a prominent transient outward current. Methods and Results: The study group consisted of 9 men (age 47 ± 10 years) with IVF (6 with Brugada type and 3 with non-Brugada type) who had experienced nocturnal episodes of VF. The control group consisted of 28 healthy age-matched men (age 44 ± 12 years). The relationships between QT and RR intervals and between QaT and RR intervals were analyzed from 24-hour Holter ECG data using an automatic measurement system. Both QT and QaT at RR intervals of 0.6, 1.0, and 1.2 seconds were determined from QT-RR and QaT-RR linear regression lines. Both QT-RR and QaT-RR slopes were lower in the IVF group than in the control group (QT-RR: 0.092 ± 0.023 vs 0.137 ± 0.031, P < 0.001; QaT-RR: 0.109 ± 0.025 vs 0.153 ± 0.028, P < 0.001). QT at an RR interval of 0.6 second did not differ between two groups, but QT at RR intervals of either 1.0 or 1.2 seconds was significantly shorter in the IVF group than in the control group (RR 1.0 s: 0.384 ± 0.018 vs 0.399 ± 0.017, P < 0.05; RR 1.2 s: 0.402 ± 0.019 vs 0.426 ± 0.020, P < 0.01). QaT at RR intervals of either 1.0 or 1.2 seconds also was shorter in the IVF group (RR 1.0 s: 0.289 ± 0.022 vs 0.312 ± 0.021, P < 0.01; RR 1.2 s: 0.311 ± 0.024 vs 0.343 ± 0.024, P < 0.01). In four patients, oral administration of disopyramide (300 mg/day) was effective in suppressing VF episodes and increased slopes of QT-RR and QaT-RR relationships. Conclusion: IVF patients had lower slopes of QT-RR and QaT-RR regression lines and impaired prolongation of QT and QaT at longer RR intervals compared with control subjects. These unique repolarization dynamics may be related to the frequent occurrence of VF episodes at night. (J Cardiovasc Electrophysiol, Vol. 15, pp. 59-63, January 2004) [source] Shock-Induced Epicardial and Endocardial Virtual Electrodes Leading to Ventricular Fibrillation via Reentry, Graded Responses, and Transmural ActivationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2004FREDERICK G. EVANS Ph.D. Introduction: The mechanism of ventricular fibrillation (VF) induction by T wave shocks has been attributed to reentry, propagated graded responses (PGR), and triggered activity. The limitation of recording transmembrane potential (Vm) from only a single surface has hampered efforts to elucidate the relative role of these phenomena and their relationship to shock-induced virtual electrodes. Methods and Results:Vm patterns from epicardial and endocardial surfaces of isolated sheep right ventricles were recorded with two CCD cameras for monophasic (M) and biphasic (B) shocks delivered at various coupling intervals (CI) from a unipolar mesh electrode on the epicardium. VF was induced via (1) the formation of reentry following make or break excitation; (2) propagated graded responses during apparent isoelectric window; and (3) breakthrough activation patterns coincident with endocardial-to-epicardial gradients in Vm. M shocks depolarized both surfaces at long CIs and polarized epicardial and endocardial surfaces oppositely at short CIs. At intermediate CIs, postshock Vm patterns could lead to reentry on one surface or endocardial-to-epicardial gradients resulting in breakthrough. B induced VF less than M for short and intermediate CIs due to more homogeneous end-shock Vm patterns. However, at long CIs these homogeneous patterns resulted in more VF induction because B left the tissue closer to the Vm threshold for propagation. Conclusion: Postshock activity occurred either immediately via epicardial or endocardial reentry, or after a delay caused by transmural propagation or propagated graded responses. These findings could explain the isoelectric window and focal activation patterns observed on the epicardium following VF induction shocks. (J Cardiovasc Electrophysiol, Vol. 15, pp. 79-87, January 2004) [source] Spatiotemporal Correlation Between Phase Singularities and Wavebreaks During Ventricular FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2003YEN-BIN LIU M.D. Introduction: Phase maps and the detection of phase singularities (PSs) have become a well-developed method for characterizing the organization of ventricular fibrillation (VF). How precisely PS colocalizes with wavebreak (WB) during VF, however, is unknown. Methods and Results: We performed optical mapping of 27 episodes of VF in nine Langendorff-perfused rabbit hearts. A WB is a point where the activation wavefront and the repolarization waveback meet. A PS is a site where its phase is ambiguous and its neighboring pixels exhibit a continuous phase progression from ,, to +,. The correlation coefficient between the number of WBs and PSs was 0.78 ± 0.09 for each heart and 0.81 for all VF episodes (P < 0.001), indicating a significant temporal correlation. We then superimposed the WBs and PSs for every 100 frames of each episode. These maps showed a high degree of spatial colocalization. To quantify spatial colocalization, the spatial shifts between the cumulative maps of WBs and PSs in corresponding frames were calculated by automatic alignment to obtain maximum overlap between these two maps. The spatial shifts were 0.04 ± 0.31 mm on the x-axis and 0.06 ± 0.27 mm on the y-axis over a 20 × 20 mm2 mapped field, indicating highly significant spatial correlation. Conclusion: Phase mapping provides a convenient and robust approach to quantitatively describe wave propagation and organization during VF. The close spatiotemporal correlation between PSs and WBs establishes that PSs are a valid alternate representation of WB during VF and further validated the use of phase mapping in the study of VF dynamics. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1103-1109, October 2003) [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Electrical Restitution and Ventricular Fibrillation: Negotiating a Slippery SlopeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2002ROBERT F. GILMOUR Jr. Ph.D. [source] Restitution, Ventricular Fibrillation, and Drugs: Where Are We Now?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2002HAROLD C. STRAUSS M.D. [source] Pilsicanide-Induced Marked T Wave Alternans and Ventricular Fibrillation in a Patient with Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2002MASAHIKO TAKAGI M.D. [source] Prevention of Ventricular Fibrillation by Cilostazol, an Oral Phosphodiesterase Inhibitor, in a Patient with Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2002TAKESHI TSUCHIYA M.D. Cilostazol and Brugada Syndrome. We report the case of 67-year-old man with Brugada syndrome, in whom daily episodes of ventricular fibrillation (VF) occurred every early morning for 4 days. The episodes of VF were completely prevented by an oral administration of cilostazol, a phosphodiesterase inhibitor. This effect was confirmed by the on-and-off challenge test, in which discontinuation of the drug resulted in recurrence of VF and resumption of the drug again prevented VF. This effect may be related to the suppression of Ito secondary to the increase in heart rate and/or to an increase in Ca2+ current (ICa) due to an elevation of intracellular cyclic AMP concentration via inhibition of phosphodiesterase activity. This drug might have an anti-VF potential in patients with Brugada syndrome. [source] Role of Structural Complexities of Septal Tissue in Maintaining Ventricular Fibrillation in Isolated, Perfused Canine VentricleJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001TAKANORI IKEDA M.D. Tissue Structure and VF.Introduction: It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle. Methods and Results: Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2-mm resolution) with 120-msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and "figure-of-eight" stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls. Conclusion: VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle. [source] Pacing During Ventricular Fibrillation: Factors Influencing the Ability to CaptureJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001JONATHAN C. NEWTON M.S. Pacing During Ventricular Fibrillation.Introduction: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated. Methods and Results: A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10× diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10× diastolic pacing threshold delivered by the second or third train. Conclusion: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters. [source] Laplacian Electrograms and the Interpretation of Complex Ventricular Activation Patterns During Ventricular FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2000PH.D., RUBEN CORONEL M.D. Laplacian Electrograms and Ventricular Fihrillation. Introduction. During ventricular fibrillation (VF) interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicabillity of Laplacian electrograms for detection of the moment of local activation during VF. Methods and Results. From isolated perfased porcine infact heart, 247 local unipolar electrograms were recorded simultaneously (13 × 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF, Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms ane its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation iodicted by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance, Following epicardial stimulation, Laplacian amplitude was significantly larger than during complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearancce of acitivity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of substanined episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). Conclusion. Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied toe automatic sensing devices, such its the internal defibrillator, may optimize defibrtilation success. (J Cardiovasc Electrophysiol, Vol. 11, pp. 1119-1128, October 2000) [source] Clinical Characteristics of Patients With Spontaneous or Inducible Ventricular Fibrillation Without Apparent Heart Disease Presenting with J Wave and ST Segment Elevation in Inferior LeadsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000MASAHTKO TAKAGI M.D., Ph.D. Ventricular Fibrillation with J Wave in Inferior Leads. Introduction: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. Methods and Results: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. Conclusion: These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome. [source] Role of Left Ventricular Scar and Purkinje-Like Potentials During Mapping and Ablation of Ventricular Fibrillation in Dilated CardiomyopathyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2009ANIL-MARTIN SINHA M.D., D.Phil. Background: Purkinje-like potentials (PLPs) have been described as important contributors to initiation of ventricular fibrillation (VF) in patients with normal hearts, ischemic cardiomyopathy, and early after-myocardial infarction. Methods: Of the 11 consecutive patients with VF storm, nonischemic cardiomyopathy (68 ± 22 years, left ventricular ejection fraction 28 ± 8%) who were given antiarrhythmic drugs and/or heart failure management, five had recurrent VF and underwent electrophysiology study (EPS) and catheter ablation. Results: At EPS, frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia did not occur. With isoproterenol, VF was induced in three patients, and sustained monomorphic PVCs were induced in one patient. Three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, CA) revealed posterior wall scar in four of the five patients. PLP in sinus rhythm were recorded around the scar border in these four patients, and radiofrequency ablation targeting PLP was successfully performed at these sites. The patient without PLP did not undergo ablation. During follow-up (12 ± 5 months), only the patient without PLP had four VF recurrences requiring implantable cardioverter-defibrillator (ICD) shocks. Conclusion: In patients with VF and dilated cardiomyopathy, left ventricular posterior wall scar in the vicinity of the mitral annulus seems to be a common finding. Targeting PLP along the scar border zone for ablation seems to efficiently prevent VF recurrence in these patients. [source] Coronary Blood Flow Produced by Muscle Contractions Induced by Intracardiac Electrical CPR during Ventricular FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009HAO WANG M.D. It has been reported that transthoracic electrical cardiopulmonary resuscitation (ECPR) generates coronary perfusion pressures (CPP) similar to manual chest compressions (MCC). We hypothesized that intracardiac ECPR produces similar CPP. Methods: ECPR pulse train protocols were applied for 20 seconds in a porcine model following 10 seconds of ventricular fibrillation (VF), using a defibrillator housing electrode and a right ventricular coil (IC-ECPR). Each protocol consisted of 200-ms electrical pulse trains applied at a rate of 100 pulse trains/min. The protocols were grouped in skeletal-based versus cardiac-based stimulation measurements. CPP was recorded and compared to historical MCC values generated by a similar experimental design. CPP > 15 mm Hg at 30 seconds of VF following the application of an IC-ECPR protocol was defined as successful. Results: Mean CPP for all intracardiac ECPR pulse train protocols at 30 seconds of VF was 14.8 ± 3.8 mm Hg (n = 39). Mean CPP in seven successful skeletal-based IC-ECPR protocols was 19.4 ± 3.2 mm Hg, and mean CPP in 10 successful cardiac-based IC-ECPR protocols was 17.4 ± 2.1 mm Hg. Reported CPP for 15 MCC experiments at 30 seconds of VF was 22.9 ± 9.4 mm Hg (P = 0.35 compared to skeletal-based IC-ECPR, P = 0.08 compared to cardiac-based IC-ECPR). Conclusions: Intracardiac applied electrical CPR produced observable skeletal muscle contractions, measurable pressure pulses, and coronary perfusion pressures similar to MCC during a brief episode of untreated VF. [source] Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff-Parkinson-White SyndromePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2008ROBERT J. KIM M.D. We report the case of a young man who presented with a rapid, narrow-complex atrial fibrillation. A few hours after being administered intravenous metoprolol and diltiazem for rate control, he developed intermittent ventricular preexcitation on the electrocardiogram (ECG) and experienced ventricular fibrillation, from which he was successfully defibrillated. A subsequent electrocardiogram in sinus rhythm demonstrated previously unknown Wolff-Parkinson-White pattern. A left lateral accessory pathway was successfully ablated. Wolff-Parkinson-White syndrome should be included in the differential diagnosis when a young patient presents with atrial fibrillation, even if the ventricular complexes on the ECG are not preexcited. [source] Influence of Drive Cycle Length on Initiation of Ventricular Fibrillation During Implantable Cardioverter Defibrillator Threshold TestingPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2006NEIL K. SANGHVI Background: Programmed electrical stimulation of the heart as a method to induce tachyarrhythmias has been described since the 1960s. To date, no study has examined optimal drive cycle length in the induction of ventricular fibrillation (VF) during defibrillation threshold testing after implantable cardioverter-defibrillator placement. We hypothesized that longer drive cycle length, by means of the longer action potential duration, would promote intramyocardial phase 2 reentry and facilitate induction of VF. Methods: Fifty consecutive implants were randomized in a prospective crossover format for this study. The group consisted of 40 men and 10 women, with each patient receiving either a 400 or 600 ms initial drive train prior to 1.2 J internal shock on the T wave with a goal to induce ventricular fibrillation. The timing of the T wave shock was determined by measuring the interval from the beginning of the QRS to the apex of the T wave in lead II. Successful inductions were defibrillated via the cardioverter defibrillator. Patients were then crossed over and the protocol repeated. Results: Twenty of 23 (87%) patients were successfully induced into VF in the initial 400 ms drive train arm whereas 22 of 27 (81%) were successfully induced in the 600 ms arm. Thus, a total of 44 (88%) patients were successfully induced at 400 ms, 41 (82%) patients were successfully induced at 600 ms, and 2 (4%) patients were not inducible at either cycle length, but were inducible with 50 Hz ventricular stimulation. However, no significant difference was noted between the two groups. Conclusion: No investigation to date has questioned whether a relationship exists between drive cycle length and initiation of ventricular fibrillation. Our study addresses this question, though negative for difference between 400 and 600 ms drive trains. Further research into optimal strategies for inducing ventricular fibrillation will minimize patient sedation time and discomfort while undergoing defibrillator threshold testing. [source] Washing Machine Associated 50 Hz Detected As Ventricular Fibrillation by An Implanted Cardioverter DefibrillatorPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2001XAVIER SABATÉ SABATÉ, X., et al.: Washing Machine Associated 50 Hz Detected As Ventricular Fibrillation by An Implanted Cardioverter Defibrillator. This case report describes a patient with an automatic ICD who suffered a defibrillation shock without warning symptoms. An electrical interference can be observed in the stored EGM of the episode. The patient explained that the moment he felt the shock he was touching a washing machine. After correct grounding of this machine the patient did not suffer more inappropriate shocks. [source] Effect of Underlying Heart Disease on the Frequency Content of Ventricular Fibrillation in the Dog HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2000JASON T. JACOBSON Although prior studies have examined the frequency content of heal electro-gram characteristics during fibrillation, little is know about the effects of underlying heart disease on these parameters. This study was designed to compare the frequency content of local electrograms during VF in canine models of acute ischemia, subacute infarction, and chronic myocardial infarction (MI) to those in control animals to test the hypothesis that underlying heart disease can alter the basic characteristics of VF. VF was induced using burst pacing in three groups of mongrel dogs. Five dogs were evaluated 8 weeks after LAD occlusion MI, five were evaluated 5 days after experimental MI, and 5 had VF induced before (control) and immediately after LAD occlusion (ischemia). During VF, unipolar electrograms were recorded from 112 sites on the anterior LV and electrograms were evaluated 15 and 30 seconds after VF initiation in each group. Electrograms were analyzed by fast Fourier transform. No significant time dependent changes in VF characteristics were noted. The peak frequency was highest in control animals and 8-week MI, intermediate in 5-day MI, and lowest in acute ischemia (P < 0.01 for pairwise comparisons). In contrast, the fractional of energy within a bandwidth of 25% peak amplitude was highest in acute ischemia, (P < 0.001) and similar in the other three groups. Infarction decreased total energy by approximately 50%. In conclusion, the pressure of ischemia or infarction alters the frequency content of VF in a complex fashion. In addition to decreasing the peak frequency, the shape of the power spectral curve is altered in models of structural heart disease. These results suggest that the electrophysiological changes produced by infarction or ischemia alter the structural organization of ventricular fibrillation. [source] Ventricular fibrillation caused by electrocoagulation during thoracic surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2010Q. Fu No abstract is available for this article. [source] Heterogeneity of Ventricular Fibrillation Dominant Frequency During Global Ischemia in Isolated Rabbit HeartsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007Ch.B. , JANE CALDWELL M.B. Introduction: Ventricular fibrillation (VF) studies show that ECG-dominant frequency (DF) decreases as ischemia develops. This study investigates the contribution of the principle ischemic metabolic components to this decline. Methods and Results: Rabbit hearts were Langendorff-perfused at 40 mL/min with Tyrode's solution and loaded with RH237. Epicardial optical action potentials were recorded with a photodiode array (256 sites, 15 × 15 mm). After 60 seconds of VF (induced by burst pacing), global ischemia was produced by low flow (6 mL/min), or the solution changed to impose hypoxia (95% N2/5% CO2), low pHo (6.7, 80% O2/20% CO2), or raised [K+]o (8 mM). DF of the optical signals was determined at each site. Conduction velocity (CV), action potential duration (APD90), effective refractory period (ERP), activation threshold, dV/dtmax, and membrane potential were measured in separate experiments during ventricular pacing. During VF, ischemia decreased DF in the left ventricle (LV) (to [58 ± 6]%, P < 0.001), but not the right (RV) ([93 ± 5]%). Raised [K+]o reproduced this DF pattern (LV: [67 ± 12]%, P < 0.001; RV: [95 ± 9]%). LV DF remained elevated in hypoxia or low pHo. During ventricular pacing, ischemia decreased CV in LV but not RV. Raised [K+]o did not change CV in either ventricle. Ischemia and raised [K+]o shortened APD90 without altering ERP. LV activation threshold increased in both ischemia and raised [K+]o and was associated with diastolic depolarization and decreased dV/dtmax. Conclusions: These results suggest that during VF, decreased ECG DF in global ischemia is largely due to elevated [K+]o affecting the activation thresholds in the LV rather than RV. [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Mechanisms of Ventricular Fibrillation Initiation in MADIT II Patients with Implantable Cardioverter DefibrillatorsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2008RYAN ANTHONY M.D. Background:The availability of stored intracardiac electrograms from implantable defibrillators (ICDs) has facilitated the study of the mechanisms of ventricular tachyarrhythmia onset. This study aimed to determine the patterns of initiation of ventricular fibrillation (VF) in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients along with associated electrocardiogram (ECG) parameters and clinical characteristics. Methods:Examination of stored electrograms enabled us to evaluate the rhythm preceding each episode of VF and to calculate (intracardiac) ECG parameters including QT, QT peak (QTp), coupling interval, and prematurity index. Results:Sixty episodes of VF among 29 patients (mean age 64.4 ± 2.5 years) were identified. A single ventricular premature complex (VPC) initiated 46 (77%) episodes whereas a short-long-short (SLS) sequence accounted for 14 (23%) episodes. Of the 29 patients studied, 23 patients had VF episodes preceded by a VPC only, two patients with SLS only, and four patients with both VPC and SLS-initiated episodes. There were no significant differences between initiation patterns in regards to the measured ECG parameters; a faster heart rate with SLS initiation (mean RR prior to VF of 655 ± 104 ms for SLS and 744 ± 222 ms for VPC) approached significance (P = 0.06). The two patients with SLS only were not on ,-blockers compared to 83% of the VPC patients. Conclusion:Ventricular fibrillation is more commonly initiated by a VPC than by a SLS sequence among the MADIT II population. Current pacing modes designed to prevent bradycardia and pause-dependent arrhythmias are unlikely to decrease the incidence of VPC-initiated episodes of VF. [source] | |||||||||||||||||||||||||||||||