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Electrical Instability (electrical + instability)
Selected AbstractsSignal-Averaged Electrocardiographic Parameter Progression as a Marker of Increased Electrical Instability in Two Cases with an Overt Form of Arrhythmogenic Right Ventricular CardiomyopathyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2002BARBARA BAUCE BAUCE, B., et al.: Signal-Averaged Electrocardiographic Parameter Progression as a Marker of In-creased Electrical Instability in Two Cases with an Overt Form of Arrhythmogenic Right Ventricular Cardiomyopathy. In arrhythmogenic right ventricular cardiomyopathy (ARVC) the fibrofatty substitution of the RV myocardium constitutes the substrate for reentrant circuits, leading to the onset of ventricular arrhythmias. This pathological process also accounts for "delayed ventricular potentials" that could be recorded as late potentials using the signal-averaged ECG technique (SAECG). This study examined two patients affected by overt forms of ARVC who showed a worsening of the electrical instability associated with a fast progression of SAECG parameters, while all the other clinical findings remained unchanged. This suggests a possible role of SAECG parameter progression as a marker of increased electrical instability. [source] Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in ratsEXPERIMENTAL PHYSIOLOGY, Issue 3 2006Donatella Stilli We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source] Arrhythmogenesis of T Wave Alternans Associated with Surface QRS Complex Alternans and the Role of Ventricular Prematurity: Observations from a Canine Model of LQT3 SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2002MASAOMI CHINUSHI M.D. Intramural TWA and Its Arrhythmogenesis.Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome. Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes. [source] Arrhythmogenic Right Ventricular Dyspiasia/Cardiomyopathy:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2000Need for an International Registry. Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy. Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a heart muscle disease characterized by peculiar right ventricular involvement and electrical instability that precipitates ventricular arrhythmias and sudden death. The purpose of the present consensus report of the Study Group of the European Society of Cardiology and the Scientific Council on Cardiomyopathies of the World Heart Federation is to review the considerable progress in our understanding of the etiopathogenesis, morbid anatomy, and clinical presentation of ARVD/C since its first description in 1977. This article will focus on the important hut still unanswered issues, mostly regarding risk stratification, clinical outcome, and management of affected patients. Because ARVD/C is relatively uncommon and any one center may have experience with only a few patients, an international registry is being established to accumulate information and enhance the numbers of patients that can be analyzed to answer the pending questions. The registry also will facilitate pathologic, molecular, and genetics research on the etiology and pathogenesis of the disease. Furthermore, availability of an international database will enhance awareness of this largely unrecognized condition among the medical community. Physicians are encouraged to enroll patients in the International Registry of ARVD/C. [source] Temporal Variability of Ventricular Arrhythmias in Boxer Dogs with Arrhythmogenic Right Ventricular CardiomyopathyJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2009B.A. Scansen Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is prevalent in the Boxer. There is little information on the temporal variability of ventricular arrhythmias within affected dogs. Objective: To evaluate ambulatory electrocardiograms (AECG) from Boxers with ARVC for hourly variation in premature ventricular complexes (PVC) and heart rate (HR). Animals: One hundred and sixty-two Boxer dogs with ARVC. Methods: Retrospective, observational study of 1,181 AECGs collected from Boxer dogs at The Ohio State University from 1997 to 2004 was evaluated. The proportion of depolarizations that were PVCs was compared across each hour of the day, during six 4-hour periods of day, to the time after AECG application, and to the maximum and minimum HR. Results: A lower proportion of PVCs was noted during early morning (midnight to 0400 hours) as compared with the morning (0800,1200 hours) and late (1600,2000 hours) afternoon (P= .012). There was no increase in PVC proportion in the 1st hour after AECG application as compared with all other hours of the day (P= .06). There was poor correlation between maximum (,= 0.19) and minimum (,= 0.12) HR and PVC proportion. Conclusions and Clinical Importance: The likelihood of PVC occurrence in Boxer dogs with ARVC was relatively constant throughout the day, although slightly greater during the hours of 0800,1200 and 1600,2000. A biologically important correlation with HR was not apparent. The role of autonomic activity in the modulation of electrical instability in the Boxer with ARVC requires further study. [source] Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic FeaturesPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2002ANTONIO FRANCO FOLINO FOLINO, A.F., et al.: Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features. The identification of subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC) at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death after myocardial infarction. For these reasons, the aim of the study was to evaluate HRV and its correlations with ventricular arrhythmias, heart function, and prognostic outcome in patients with ARVC. The study included 46 patients with ARVC who were not taking antiarrhythmic medications. The diagnosis was made by ECG, echocardiography, angiography, and endomyocardial biopsy. Exercise stress test and Holter monitoring were obtained in all patients. Time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Thirty healthy subjects represented a control group for HRV analysis. The mean follow-up was 10.8 ± 1.86 years. SDNN was reduced in patients with ARVC in comparison with the control group (151 ± 36 vs 176 ± 34, P = 0.00042). Moreover, there was a significant correlation of this index with the age of the patients (r =,0.59, P < 0.001), with the left (r = 0.44, P = 0.002) and right (r = 0.47, P = 0.001) ventricle ejection fraction, with the right ventricular end diastolic volume (r =,0.62, P < 0.001), and with the ventricular arrhythmias, detected during the same Holter record used for HRV analysis (patients with isolated ventricular ectopic beats < 1,000/24 hours, 184 ± 34; patients with isolated ventricular ectopic beats > 1,000/24 hours and/or couplets, 156 ± 25; patients with repetitive ventricular ectopic beats (,3) and/or ventricular tachycardia, 129 ± 25; P < 0.001). During follow-up two patients showed a transient but significant reduction of SDNN and a concomitant increase of the arrhythmic events. In eight patients an episode of sustained ventricular tachycardia occurred, but the mean SDNN of this subgroup did not differ from the mean value of the remaining patients (152 ± 15 vs 150 ± 39; P = NS). Only one subject died after heart transplantation during follow-up (case censored). Time-domain analysis of HRV seems to be a useful method to assess the autonomic influences in ARVC. A reduction of vagal influences correlates with the extent of the disease. The significant correlation between SDNN and ventricular arrhythmias confirmed the influences of autonomic activity in the modulation of the electrical instability in ARVC patients. However, SDNN was not predictive of spontaneous episodes of sustained ventricular tachycardia. [source] Signal-Averaged Electrocardiographic Parameter Progression as a Marker of Increased Electrical Instability in Two Cases with an Overt Form of Arrhythmogenic Right Ventricular CardiomyopathyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2002BARBARA BAUCE BAUCE, B., et al.: Signal-Averaged Electrocardiographic Parameter Progression as a Marker of In-creased Electrical Instability in Two Cases with an Overt Form of Arrhythmogenic Right Ventricular Cardiomyopathy. In arrhythmogenic right ventricular cardiomyopathy (ARVC) the fibrofatty substitution of the RV myocardium constitutes the substrate for reentrant circuits, leading to the onset of ventricular arrhythmias. This pathological process also accounts for "delayed ventricular potentials" that could be recorded as late potentials using the signal-averaged ECG technique (SAECG). This study examined two patients affected by overt forms of ARVC who showed a worsening of the electrical instability associated with a fast progression of SAECG parameters, while all the other clinical findings remained unchanged. This suggests a possible role of SAECG parameter progression as a marker of increased electrical instability. [source] Alternans in QRS Amplitude During Ventricular TachycardiaPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002PHILIPPE MAURY MAURY, P., et al.: Alternans in QRS Amplitude During Ventricular Tachycardia. Although the value of T wave alternans as an index of electrical instability has been extensively investigated, little is known about QRS alternans during VT. Intracardiac electrograms of 111 episodes of spontaneous monomorphic regular VT retrieved from implantable defibrillators in 25 patients were retrospectively selected. Three beat series, representing the total amplitudes and amplitudes from baseline to summit and from baseline to lower point of 16 or 32 successive QRS complexes before deliverance of electrical therapy were generated for each episode. Spectral analysis was then performed using the fast Fourrier transform. VT was considered as alternans if the magnitude of the spectral power at the 0.5-cycle/beat frequency was greater than the mean ± 3 SD of the noise in at least one of the three spectral curves. QRS alternans was present in 23 (20%) of 111 episodes and in 9 (36%) of 25 patients. Alternans was not related to the VT cycle length, QRS duration, QRS amplitude, signal amplification, nor to clinical variables. Alternans was more frequently detected in unipolar configuration and when a higher number of complexes was included in analysis. Failure of antitachycardia pacing was more frequent in case of alternans VT (50% vs 75% success in non-alternans VT, P = 0.05). Spontaneous termination before deliverance of therapy occurred in 16 nonalternans VT but never in alternans episodes (P = 0.02). Alternans in QRS amplitude is a relatively common finding during VT and could be associated with failure of antitachycardia pacing and lack of spontaneous termination. Lower efficacy of electrical therapies in case of QRS alternans must be confirmed in a way to improve the effectiveness of antitachycardia pacing. [source] Late potentials and QT dispersion after high-dose chemotherapy in patients with non-Hodgkin lymphomaCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 3 2010Taru Kuittinen Summary The most common cardiotoxic effects of high-dose cyclophosphamide (CY) are electrocardiographic changes and transient arrhythmias. Therefore, we prospectively assessed serial electrocardiogram (ECG) and signal-averaged electrocardiogram (SAECG) recordings in 30 adult patients with non-Hodgkin lymphoma (NHL) receiving high-dose CY as part of high-dose chemotherapy (HDT) regimen. All patients were treated with anthracyclines earlier. Heart-rate-corrected QT interval and QT dispersion (QTc and QTc dispersion) were measured from ECG. QRS duration and late potentials (LPs) were analysed from SAECG. Both ECG and SAECG were recorded 1 day (d) prior to HDT (d,7) at baseline, and 1 day (d,2), 7 days (d+7), 12 days (+12) and 3 months (m+3) after HDT. Stem cells were infused on day 0 (d0). Cardiac systolic and diastolic function were assessed on (d,7), (d+12) and (m+3) by radionuclide ventriculography. At baseline, four patients presented with LPs. Cardiac systolic function decreased significantly (53 ± 2; 49 ± 2%, P = 0·009 versus baseline), whilst no patient developed acute heart failure. QRS duration prolonged and RMS40 reduced significantly versus baseline (104 ± 3; 107 ± 3 ms, P = 0·003; 41 ± 4; 38 ± 3 ,V, P = 0·03), and six patients (21%) presented with LPs after CY treatment. Both QTc interval and QTc dispersion increased versus baseline (402 ± 5; 423 ± 5 ms, P<0·001; 32 ± 2; 44 ± 3 ms, P = 0·012), and six patients (20%) developed abnormal QT dispersion. In conclusion, high-dose CY causes subclinical and transient electrical instability reflected by occurrence of LPs as well as increased QTc interval and QT dispersion. Thus, longer follow-up is required to confirm the meaning of these adverse effects on cardiac function and quality of life. [source] | ||||||||||