PURPOSE: Left ventricular (LV) filling pressure affects atrial fibrillation (AF) recurrence. We investigated the relationship between diastolic dysfunction and AF recurrence after cardioversion, and whether LV filling pressure was predictive of AF recurrence. MATERIALS AND METHODS: Sixty-six patients (mean 58+/-12 years) with newly diagnosed persistent AF were retrospectively enrolled. We excluded patients with left atrial (LA) diameters larger than 50 mm, thereby isolating the effect of LV filling pressure. We evaluated the differences between the patients with (group 1) and without AF recurrence (group 2). RESULTS: Group 1 showed increased LA volume index (LAVI) and E/e' compared to group 2 (p<0.05). During a mean follow-up period of 25+/-19 months, AF recurrence after cardioversion was 60.6% (40/66). The area under the receiver operating characteristics curve of E/e' for AF recurrence was 0.780 [95% confidence interval (CI): 0.657-0.903], and the optimal cut-off value of the E/e' was 9.15 with 75.0% of sensitivity and 73.1% of specificity. A Kaplan-Meier survival curve showed that the cumulative recurrence-free survival rate was significantly lower in patients with higher LV filling pressure (E/e'>9.15) compared with patients with lower LV filling pressure (E/e'< or =9.15) (log rank p=0.008). Cox regression analysis revealed that E/e' [hazards ratio (HR): 1.100, 95% CI: 1.017-1.190] and LAVI (HR: 1.042, 95% CI: 1.002-1.084) were independent predictors for AF recurrence after cardioversion. CONCLUSION: LV filling pressure predicts the risk of AF recurrence in persistent AF patients after cardioversion.
Aged ; Atrial Fibrillation/*physiopathology ; Electric Countershock ; Female ; Follow-Up Studies ; Heart Atria/pathology/physiopathology ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Proportional Hazards Models ; ROC Curve ; Recurrence ; Regression Analysis ; Retrospective Studies ; Sensitivity and Specificity ; Survival Rate ; Ventricular Dysfunction, Left/*physiopathology

BACKGROUNDMorbidity and mortality after resuscitation largely depend on the recovery of brain function. Ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are the two most prevalent causes of sudden cardiac death. Up to now, most studies have focused on VFCA. However, results from the two models have been largely variable. So, it is necessary to characterize the features of postresuscitation cerebral metabolism of both models.

METHODSForty-four Wuzhishan miniature inbred pigs were randomly divided into three groups: 18 for VFCA group, ACA group, respectively, and other 8 for sham-operated group (SHAM). VFCA was induced by programmed electric stimulation, and ACA was induced by endotracheal tube clamping. After 8 min without treatment, standard cardiopulmonary resuscitation (CPR) was initiated. Following neurological deficit scores (NDS) were evaluated at 24 h after achievement of spontaneous circulation, cerebral metabolism showed as the maximum standardized uptake value (SUVmax) was measured by 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Levels of serum markers of brain injury, neuron specific enolase (NSE), and S100β were quantified with an enzyme-linked immunosorbent assay.

RESULTSCompared with VFCA group, fewer ACA animals achieved restoration of spontaneous circulation (61.1% vs. 94.4%, P < 0.01) and survived 24-h after resuscitation (38.9% vs. 77.8%, P < 0.01) with worse neurological outcome (NDS: 244.3 ± 15.3 vs. 168.8 ± 9.71, P < 0.01). The CPR duration of ACA group was longer than that of VFCA group (8.1 ± 1.2 min vs. 4.5 ± 1.1 min, P < 0.01). Cerebral energy metabolism showed as SUVmax in ACA was lower than in VFCA (P < 0.05 or P < 0.01). Higher serum biomarkers of brain damage (NSE, S100β) were found in ACA than VFCA after resuscitation (P < 0.01).

CONCLUSIONSCompared with VFCA, ACA causes more severe cerebral metabolism injuries with less successful resuscitation and worse neurological outcome.

Animals ; Asphyxia ; complications ; physiopathology ; Brain ; metabolism ; Cardiopulmonary Resuscitation ; Heart Arrest ; metabolism ; pathology ; therapy ; Positron-Emission Tomography ; Swine ; Ventricular Fibrillation ; metabolism ; pathology ; therapy

We investigated whether the presence of J wave on the surface electrocardiography (sECG) could be a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (AMI). We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the enrolled 296 patients, 22 (13.5%) patients were selected as a VF group. The J wave on the sECG was defined as a J point elevation manifested through QRS notching or slurring at least 1 mm above the baseline in at least two leads. We found that the incidence of J wave on the sECG was significantly higher in the VF group. We also confirmed that several conventional risk factors of VF were significantly related to VF during AMI; time delays from the onset of chest pain, blood concentrations of creatine phosphokinase and incidence of ST-segment elevation. Multiple logistic regression analysis demonstrated that the presence of J wave and the presence of a ST-segment elevation were independent predictors of VF during AMI. This study demonstrated that the presence of J wave on the sECG is significantly related to VF during AMI.
Arrhythmias, Cardiac/*diagnosis ; Creatine Kinase/blood ; *Electrocardiography ; Female ; Heart Conduction System/*abnormalities ; Humans ; Male ; Middle Aged ; Myocardial Infarction/*diagnosis/pathology ; Retrospective Studies ; Risk Factors ; Ventricular Fibrillation/*diagnosis/pathology/physiopathology

OBJECTIVETo study the application of positron emission tomography (PET) in detection of myocardial metabolism in pig ventricular fibrillation and asphyxiation cardiac arrest models after resuscitation.

METHODSThirty-two healthy miniature pigs were randomized into a ventricular fibrillation cardiac arrest (VFCA) group (n=16) and an asphyxiation cardiac arrest (ACA) group (n=16). Cardiac arrest (CA) was induced by programmed electric stimulation or endotracheal tube clamping followed by cardiopulmonary resuscitation (CPR) and defibrillation. At four hours and 24 h after spontaneous circulation was achieved, myocardial metabolism was assessed by PET. 18F-FDG myocardial uptake in PET was analyzed and the maximum standardized uptake value (SUVmax) was measured.

RESULTSSpontaneous circulation was 100% and 62.5% in VFCA group and ACA group, respectively. PET demonstrated that the myocardial metabolism injuries was more severe and widespread after ACA than after VFCA. The SUVmax was higher in VFCA group than in ACA group (P<0.01). In VFCA group, SUVmax at 24 h after spontaneous circulation increased to the level of baseline.

CONCLUSIONACA causes more severe cardiac metabolism injuries than VFCA. Myocardial dysfunction is associated with less successful resuscitation. Myocardial stunning does occur with VFCA but not with ACA.

Animals ; Asphyxia ; physiopathology ; Cardiopulmonary Resuscitation ; Gene Expression Regulation ; Heart Arrest ; etiology ; metabolism ; therapy ; Myocardium ; metabolism ; Positron-Emission Tomography ; methods ; Random Allocation ; Swine ; Ventricular Fibrillation ; metabolism

Child ; Electrocardiography ; Humans ; Male ; Ventricular Fibrillation ; physiopathology

Electrical instability easily induces a unidirectional conduction block, resulting in ventricular tachycardia (VT) or even fibrillation (VF). Cardiac memory affects dynamic electrical characteristics through previous pacing so that it makes the memory important in arrhythmia study. This paper investigates the impact of the rapid pacing duration on cellular excitability and its mechanism. Based on the canine endocardial single cell, a one-dimensional tissue model was developed. Simulations were realized with OpenMP parallel programming method. The results showed that with repetitive pacing, the cellular excitability became low while the conduction velocity decreased. Accumulation of intracellular [Ca2+]i and [Na+]i and depletion of [K+]i led to the shift of membrane current-voltage curves, changing the membrane resistance. Excitability determined by the resistance at the large width of stimulus pulse, therefore, it suggested that [Ca2+]i and [K+]i-induced memory formed the ionic substrates for the alteration of excitability.
Action Potentials ; Animals ; Computer Simulation ; Dogs ; Electric Stimulation ; Electrocardiography ; Heart Conduction System ; physiopathology ; Myocardial Contraction ; physiology ; Myocytes, Cardiac ; physiology ; Refractory Period, Electrophysiological ; physiology ; Tachycardia, Ventricular ; etiology ; physiopathology ; Ventricular Fibrillation ; etiology ; physiopathology

BACKGROUNDIbutilide has been commonly used for pharmacologic cardioversion of atrial fibrillation and flutter in clinical settings. The objective of this study was to investigate the effects of ibutilide on the defibrillation threshold (DFT), restitution properties, dispersion of refractoriness and activation patterns during ventricular fibrillation (VF).

METHODSIbutilide was administrated intravenously in six open-chest beagles. Before and after the drug administration, 20-second episodes of VF were electrically induced and recorded with a 10×10 unipolar electrode plaque sutured on the lateral epicardium of the left ventricle. DFT and VF activation patterns, including type of epicardial activation maps, VF cycle length (VF-CL), conduction velocity, wavelength (WL) and reentry incidence, were measured. Restitution properties and dispersion of refractoriness were estimated from activation recovery intervals (ARI) during pacing.

RESULTSCompared to baseline, ibutilide markedly decreased the DFT by 31% ((491 ± 14) V vs. (337 ± 59) V, P < 0.01). The drug significantly reduced the maximal slope of the restitution curve (1.34 ± 0.08 vs. 0.76 ± 0.06, P < 0.01) and its epicardial dispersion (0.36 ± 0.09 vs. 0.21 ± 0.06, coefficient of variation, P = 0.03). The dispersion of refractoriness was enhanced at the pacing cycle length of 300 ms to 160 ms by ibutilide. The drug significantly increased the VF-CL ((96 ± 19) ms vs. (112 ± 20) ms, P < 0.01) and the WL ((41 ± 9) mm vs. (52 ± 14) mm, P = 0.02) during VF, and reduced the reentry incidence by 25% (0.08 ± 0.02 vs. 0.06 ± 0.02, P < 0.01). In the epicardial activation maps, ibutilide significantly reduced the percentage of more complex activation maps during VF.

CONCLUSIONSIntravenous ibutilide significantly decreased the DFT. It might be due to reduction of activation pattern complexity during VF.

Animals ; Anti-Arrhythmia Agents ; therapeutic use ; Dogs ; Pericardium ; drug effects ; Sulfonamides ; therapeutic use ; Ventricular Fibrillation ; drug therapy ; physiopathology

The purpose of the present study was to examine the effects of oxidative stress on ventricular arrhythmias in rabbits with adriamycin-induced cardiomyopathy and the relationship between oxidative stress and ventricular arrhythmia. Forty Japanese white rabbits were randomly divided into four groups (n=10 in each): control group, metoprolol (a selective β1 receptor blocker) group, carvedilol (a nonselective β blocker/α-1 blocker) group and adriamycin group. Models of adriamycin-induced cardiomyopathy were established by intravenously injecting adriamycin hydrochloride (1 mg/kg) to rabbits via the auri-edge vein twice a week for 8 weeks in the adriamycin, metoprolol and carvedilol groups. Rabbits in the control group were given equal volume of saline through the auri-edge vein. Rabbits in the metoprolol and carvedilol groups were then intragastrically administrated metoprolol (5 mg/kg/d) and carvedilol (5 mg/kg/d) respectively for 2 months, while those in the adriamycin and control groups were treated with equal volume of saline in the same manner as in the metroprolol and carvedilol groups. Left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) were measured by echocardiography. Plasma levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), malondialdehyde (MAD) and superoxide dismutase (SOD) were detected. The left ventricular wedge preparations were perfused with Tyrode's solution. The transmural electrocardiogram, transmural action potentials from epicardium (Epi) and endocardium (Endo), transmural repolarization dispersion (TDR) were recorded, and the incidences of triggered activity and ventricular arrhythmias were obtained at rapid cycle lengths. The results showed that TDR and the serum MDA and NT-proBNP levels were increased, and LVEF and the serum SOD level decreased in the adriamycin group compared with the control group. The incidences of triggered activity and ventricular arrhythmia were significantly higher in the adriamycin group than those in the control group (P<0.05). In the carvedilol group as compared with the adriamycin group, the serum SOD level and the LVEF were substantially increased; the TDR, and the serum MDA and NT-proBNP levels were significantly decreased; the incidences of triggered activity and ventricular arrhythmia were obviously reduced (P<0.05). There were no significant differences in the levels of MDA and SOD, LVEF, TDR and the incidences of triggered activity and ventricular arrhythmia between the adriamycin group and the metoprolol group. It was concluded that carvedilol may inhibit triggered activity and ventricular arrhythmias in rabbit with adriamycin-induced cardiomyopathy, which is related to the decrease in oxygen free radials.
Animals ; Anti-Arrhythmia Agents ; administration & dosage ; Antibiotics, Antineoplastic ; Carbazoles ; administration & dosage ; Cardiomyopathies ; chemically induced ; physiopathology ; prevention & control ; Doxorubicin ; Heart Rate ; drug effects ; Male ; Metoprolol ; administration & dosage ; Oxidative Stress ; drug effects ; Propanolamines ; administration & dosage ; Rabbits ; Treatment Outcome ; Ventricular Fibrillation ; chemically induced ; physiopathology ; prevention & control

Under conditions of Na+ channel hyperactivation with aconitine, the changes in action potential duration (APD) and the restitution characteristics have not been well defined in the context of aconitine-induced arrhythmogenesis. Optical mapping of voltage using RH237 was performed with eight extracted rabbit hearts that were perfused using the Langendorff system. The characteristics of APD restitution were assessed using the steady-state pacing protocol at baseline and 0.1 microM aconitine concentration. In addition, pseudo-ECG was analyzed at baseline, and with 0.1 and 1.0 microM of aconitine infusion respectively. Triggered activity was not shown in dose of 0.1 microM aconitine but overtly presented in 1.0 microM of aconitine. The slopes of the dynamic APD restitution curves were significantly steeper with 0.1 microM of aconitine than at baseline. With aconitine administration, the cycle length of initiation of APD alternans was significantly longer than at baseline (287.5 +/- 9.6 vs 247.5 +/- 15.0 msec, P = 0.016). The functional reentry following regional conduction block appears with the progression of APD alternans. Ventricular fibrillation is induced reproducibly at pacing cycle length showing a 2:1 conduction block. Low-dose aconitine produces arrhythmogenesis at an increasing restitution slope with APD alternans as well as regional conduction block that proceeds to functional reentry.
Aconitine/*pharmacology ; Action Potentials/*drug effects ; Animals ; Arrhythmias, Cardiac/*chemically induced/*physiopathology ; Cardiac Pacing, Artificial ; Electrocardiography ; Heart/physiopathology ; Heart Conduction System/physiology ; Myocardium/*pathology ; Rabbits ; Sodium Channels/drug effects/metabolism ; Ventricular Fibrillation/physiopathology

This is a research with the aim of using joint entropy method to analyze the dynamical complexity information on the electrocardiogram signals recording of normal sinus rhythm (NSR), ventricular tachycardia (VT) and ventricular fibrillation (VF). We included the symbolic dynamical theory and surrogate data concept in it. By calculating the joint entropy between original and surrogate time series, we quantified the dynamical complexity of original series. By computer analysis of actual heartbeat rhythm data, the rationality of joint entropy method was confirmed. The results indicated that the joint entropy values of different signals can be of use in distinguishing the NSR, VT and VF signals.
Diagnosis, Differential ; Electrocardiography ; Entropy ; Humans ; Signal Processing, Computer-Assisted ; Tachycardia, Ventricular ; diagnosis ; physiopathology ; Ventricular Fibrillation ; diagnosis ; physiopathology