Approach to wide complex tachycardias in patients without structural heart disease.
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Atrial Flutter↗
Biomedical subjects
L Eckardt
Publications and source records attributed to L Eckardt.
Verapamil prevents torsade de pointes by reduction of transmural dispersion of repolarization and suppression of early afterdepolarizations in an intact heart model of LQT3.
BACKGROUND: In long QT syndrome (LQTS), prolongation of the QT-interval is associated with sudden cardiac death resulting from potentially life-threatening polymorphic tachycardia of the torsade de pointes (TdP) type. Experimental as well as clinical reports support the hypothesis that calcium channel blockers such as verapamil may be an appropriate therapeutic approach in LQTS. We investigated the electrophysiologic mechanism by which verapamil suppresses TdP, in a recently developed intact heart model of LQT3. METHODS AND RESULTS: In 8 Langendorff-perfused rabbit hearts, veratridine (0.1 microM), an inhibitor of sodium channel inactivation, led to a marked increase in QT-interval and simultaneously recorded monophasic ventricular action potentials (MAPs) (p < 0.05) thereby mimicking LQT3. In bradycardic (AV-blocked) hearts, simultaneous recording of up to eight epi- and endocardial MAPs demonstrated a significant increase in total dispersion of repolarization (56%, p < 0.05) and reverse frequency-dependence. After lowering potassium concentration, veratridine reproducibly led to early afterdepolarizations (EADs) and TdP in 6 of 8 (75%) hearts. Additional infusion of verapamil (0.75 microM) suppressed EADs and consecutively TdP in all hearts. Verapamil significantly shortened endocardial but not epicardial MAPs which resulted in significant reduction of ventricular transmural dispersion of repolarization. CONCLUSIONS: Verapamil is highly effective in preventing TdP via shortening of endocardial MAPs, reduction of left ventricular transmural dispersion of repolarization and suppression of EADs in an intact heart model of LQT3. These data suggest a possible therapeutic role of verapamil in the treatment of LQT3 patients.
Action Potentials↗
Transvenous ICD implantation after artificial tricuspid valve replacement. A new approach placing a transvenous ICD lead in the mid cardiac vein of the coronary sinus.
Implantation of a transvenous device in patients with a tricuspid valve replacement or a complex congenital heart disease with no access to the right ventricle represents problems. The lack of access to the right ventricle might preclude transvenous placement of a defibrillation lead at ICD implantation. A young patient (21 years) with a history of severe chest trauma with rupture of the tricuspid valve as well as the right coronary artery and consecutive inferior myocardial infarction was initially treated with tricuspid valve replacement (St Jude Medical artificial prosthesis, 33 mm) and a bypass graft to the right coronary artery. Four years later, the patient was admitted with a hemodynamically not tolerated ventricular tachycardia (VT: CL 250 ms, LBBB, left axis). The VT could be reproduced during electrophysiological testing. An ICD was implanted subpectorally in combination with a transvenous active fixation ICD lead. The transvenous ICD lead was placed via a guiding catheter into a coronary sinus branch (middle cardiac vein). Acceptable pacing and sensing values could be obtained. The defibrillation threshold was 25 J. In conclusion transvenous ICD lead implantation into a side branch of the coronary sinus in combination with a pectorally implanted "active can" ICD device seems to be an alternative approach. This approach may avoid implantation of additional subcutaneous defibrillation leads or even thoracotomy for ICD implantation.
Adult↗
[Right ventricular tachyarrhythmias--diagnostics and therapy].
Ventricular tachyarrhythmias originating from the right ventricle frequently occur in young, apparently healthy patients with rare underlying cardiac diseases. Among these are arrhythmogenic right ventricular cardiomyopathy (ARVC), idiopathic right ventricular outflow-tract tachycardia (RVOVT), and Brugada syndrome (BrS). All harbor the risk of sudden cardiac death, whereas they differ substantially as to diagnosis, therapy and prognosis. This is the reason why detailed investigations are an essential prerequisite for further efficient individualized management strategies which are mainly directed to prevent sudden cardiac death and to minimize the risk of arrhythmia recurrences in affected patients, respectively. Both antiarrhythmic drug therapy, catheter ablation, and the implantation of an automatic cardioverter defibrillator may, therefore, be a first-line therapeutic option in tailored treatment regimens. This review is a summary of the available literature on pathogenesis, diagnosis, treatment, and prognosis of such diseases associated with right ventricular tachyarrhythmias.
Anti-Arrhythmia Agents↗
[Right ventricular arrhythmias].
Right ventricular arrhythmias predominantly occur in young patients with rare cardiac diseases. Underlying cardiac conditions include idiopathic right ventricular outflow-tract tachycardia (RVOT-VT), arrhythmogenic right ventricular cardiomyopathy (ARVC), Brugada syndrome, and postoperative congenital heart disease (i.e. tetralogy of Fallot). According to the underlying cardiac disease, there are significant differences in the diagnostic and therapeutic management and prognosis which is mainly determined by life-threatening ventricular arrhythmia recurrences and sudden cardiac death. To provide optimal treatment for affected patients, a detailed diagnostic evaluation and risk stratification is mandatory. Tailored treatment strategies aim at the suppression or effective termination of recurrent ventricular tachyarrhythmias and prevention of sudden death by antiarrhythmic drug therapy, catheter ablation, and the implantation of cardioverter-defibrillators. This review summarizes the current knowledge on pathogenesis, diagnosis, treatment and prognosis of those conditions that are associated with arrhythmias originating from the right ventricle.
Arrhythmias, Cardiac↗
Atrioventricular nodal re-entrant tachycardia in a patient with Ebstein anomaly.
The first case of successful slow pathway modulation is reported in a patient with Ebstein anomaly and recurrent atrioventricular nodal re-entrant tachycardia. Typical signals were recorded during electrophysiological study at the slow pathway region between the His bundle and the coronary sinus where ablation was performed successfully. Thus, slow pathway modulation seems to be a safe procedure even in selected patients with Ebstein anomaly.
Adult↗
Amiodarone and acetazolamide for the treatment of genetically confirmed severe Andersen syndrome.
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Acetazolamide↗
[The autonomic nervous system and cardiac arrhythmias].
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Animals↗
[Clinical aspects and molecular genetics of the Jervell- and Lange-Nielsen Syndrome].
In contrast to the Romano-Ward (R-W) syndrome, the Jervell and Lange-Nielsen (J-LN) syndrome is an autosomal recessive inherited disease characterized by QT-prolongation in the electrocardiogram (ECG) and recurrent syncopal attacks which are also typical for the R-W syndrome, but also by congenital deafness. Recently, defect alleles in the genes for KCNQ1 and KCNE1 have been identified in patients with the J-LN syndrome. These genes may be causative for the R-W syndrome as well but in J-LN patients, they are only present in the homozygote or compound heterozygote form. In the present paper, we review the clinical and genetic similarities and differences of the J-LN and the R-W syndrome as well as the diagnostic and therapeutic management of these patients and their family members.
DNA Mutational Analysis↗
Electrophysiologic investigation in Brugada syndrome; yield of programmed ventricular stimulation at two ventricular sites with up to three premature beats.
INTRODUCTION: Numerous reports on the inducibility of ventricular tachyarrhythmias (VT) in patients with atypical right bundle branch block and right precordial ST-elevation (Brugada syndrome) are based on multicentre studies that have used different stimulation protocols. Therefore, we prospectively investigated the inducibility of VT in these patients using a uniform protocol. METHODS: In 41 consecutive patients (29 males) showing a pattern of right bundle branch block and ST-elevation, programmed ventricular stimulation was performed in the right ventricular apex with up to three premature stimuli at sinus rhythm and at four different paced cycle lengths (500, 430, 370, and 330 ms) until refractoriness was reached or reproducible induction of a sustained (>30s) VT occurred. If a VT was not reproducibly inducible, the same protocol was repeated in the right ventricular outflow tract. RESULTS: A history of life-threatening events defined as syncope (n=17) or aborted sudden cardiac death (n=13) was present in 30 patients (73%); 11 individuals were asymptomatic. Inducibility (68%) was similar between symptomatic (n=21, 70%) and asymptomatic patients (n=7, 64%). In 16 (39%) patients, VT were reproducibly inducible. If patients were only stimulated in the right ventricular apex, inducibility rate decreased to 39%. If only two premature beats at two sites were used it was as low as 32%. The mean coupling intervals of the second and third premature stimuli inducing sustained VT were short: 189+/-21 ms vs 186+/-22 ms, respectively. Forty-four percent of all patients (i.e. 64% of the inducible patients) had inducible VT only with coupling intervals shorter than 200 ms. CONCLUSIONS: The stimulation protocol markedly influences the extent of inducibility of VT in patients with right bundle branch block and ST-segment elevation. These findings question the significance of previous multicentre studies using different stimulation protocols and should have implications for further studies.
Adult↗
Idiopathic left ventricular tachycardia localised at the distal end of the posterior fascicle by non-contact activation mapping.
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Adult↗
Tensor analytical evaluation of the effects of a skeletonized activator in the treatment of Class II, Division 1 patients.
PATIENTS AND METHOD: The study covered 40 patients (21 boys and 19 girls) whose Class II, Division 1 malocclusion was being treated with a Klammt open activator. To illustrate growth changes, tensor analysis was used as a superimposition-free comparative technique. At the beginning of treatment for Class II correction, the boys had a mean age of 11.3 years and the girls a mean age of 10.1 years. Patients were evaluated on admission and on attaining normal occlusion. 58 boys and 63 girls participating in a growth study at Kings College School of Medicine and Dentistry, London, served as controls. RESULTS: Prior to treatment the participants suffering from Class II, Division 1 malocclusion exhibited distinct growth deficits in vertical direction. In the control group, the principal direction of mean growth was found to be anterior-inferior. Under the influence of the activator, growth was found to develop in the same direction as in the controls, so that anterior positioning of the lower jaw and an increase in lower facial height were attained.
Activator Appliances↗
[Syncope of unknown origin in heart failure: which diagnostic possibilities should be considered today?].
In patients with congestive heart failure, unexplained syncope is often due to ventricular arrhythmias and associated with a poor prognosis. Electrophysiological studies should be considered early in the work-up of syncope. Implantation of a defibrillator might become necessary in many patients with syncope and heart failure.
Cardiomyopathy, Dilated↗
Torsade de pointes induced by ajmaline.
Ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.
Ajmaline↗
Load-induced changes in repolarization: evidence from experimental and clinical data.
The high incidence of arrhythmias in patients with heart failure, hypertension, valvular heart disease, or mitral walve prolapse suggests a strong link between wall motion abnormalities and arrhythmias. A potential common mechanism underlying these observations may be that overload leads to electrophysiologic changes and facilitates arrhythmias. This article summarizes the interaction between changes in atrial and ventricular loading conditions and repolarization. Most experimental and clinical studies demonstrated 1) a reduction of action potential duration and refractoriness, 2) development of early afterdepolarizations, and 3) ectopic beats originating from these afterdepolarizations. Discrepancies between studies are related to different study designs, i.e., varying magnitude, velocity, and timing of increased load, the level of repolarization at which action potential duration is measured as well as different animal species. Direct effects of increased load on repolarization are most likely caused by activation of stretch-activated nonselective cation ion channels and changes in calcium handling. Current antiarrhythmic drug therapy is aimed at electrical disorders as the primary cause of arrhythmias. If mechanical disorders play a central role in the genesis of cardiac arrhythmias, future treatment should be directed at restoring a more normal mechanical function of the heart. Additional studies will further clarify the nature and clinical significance of load-related changes in repolarization and arrhythmogenesis.
Animals↗
In vivo recording of monophasic action potentials in awake dogs--new applications for experimental electrophysiology.
INTRODUCTION: Despite enormous developments in the field of clinical and experimental electrophysiology there is still a gap in evaluating repolarization in the awake animal. Numerous previous studies have used monophasic action potentials (MAP) to assess repolarization in vitro and in vivo in anesthetized animal models. However, an approach for recording MAP in awake dogs without interference of anesthesia has not yet been developed. METHODS AND RESULTS: We developed an experimental technique to record MAP in conscious dogs by means of conventional rubber introducers which were implanted into the internal jugular vein. In seven awake dogs, atrial as well as ventricular MAP were simultaneously measured without complications. Pacing thresholds were low and stable over time ranging from 0.2 to 4.0 mA. The MAP amplitudes ranged from 10 to 30 mV for ventricular and from 5 to 15 mV for atrial MAP. Continuous MAP recordings of stable amplitude could be made from the same endocardial site for periods of up to one hour. Antegrade and retrograde AV-nodal conduction properties could be assessed. Programmed stimulation was performed to simultaneously determine local refractory periods and MAP duration at cycle lengths from 500 to 200 ms. CONCLUSION: In awake, unsedated dogs the measurement of MAP via rubber introducers permits safe, long-term recording of MAP. Such recordings may be useful for safety pharmacological studies in evaluating cardiovascular and non-cardiovascular drugs with regard to their effects on repolarization. In various canine in vivo models including in vivo models of long QT syndrome, heart failure or sudden cardiac death, the present technique permits electrophysiological measurements without interference of anesthesia.
Action Potentials↗
Cervical intramedullar schistosomiasis as a rare cause of acute tetraparesis.
INTRODUCTION: The trematode infection schistosomiasis affects at least 200 million people in endemic areas. Granulomas cause the typical manifestations of urogenital, intestinal and hepatolienal schistosomiasis. Involvement of other organs especially the central nervous system (CNS) is uncommon. CASE REPORT: We describe a 40-year old male with a history of repeated contact with schistosome contaminated water. After having suffered from flu-like symptoms with fever and arthralgias, he first presented with a polyradiculopathy of unknown origin. Then 4 weeks later an acute tetraparesis occurred. Spinal magnetic resonance imaging (MRI) revealed a spinal stenosis and query medullary hyperintensities at C6-C8 without contrast-enhancement. Serologic testing was positive for schistosomiasis. The intraoperative appearance at decompressive laminectomy revealed a myelitic form of schistosomiasis. Under therapy with praziquantel, initially high dose cortisone and intensive physiotherapy, symptoms slowly improved over months. On follow-up 1 year later, the patient presented with a spastic distally marked tetraparesis and sensory impairment from C6 downwards. CONCLUSION: Cervical intramedullar schistosomiasis is a rare cause of acute tetra- or para-paresis in patients, who have had contact with schistosomes. Early diagnosis is essential because of the excellent prognosis with specific therapy.
Acute Disease↗
Clinical value of electrocardiographic parameters in genotyped individuals with familial long QT syndrome.
Rate corrected QT interval (QTc) and QT dispersion (QTd) have been suggested as markers of an increased propensity to arrhythmic events and efficacy of therapy in patients with long QT syndrome (LQTS). To evaluate whether QTc and QTd correlate to genetic status and clinical symptoms in LQTS patients and their relatives, ECGs of 116 genotyped individuals were analyzed. JTc and QTc were longest in symptomatic patients (n = 28). Both QTd and JTd were significantly higher in symptomatic patients than in asymptomatic (n = 29) or unaffected family members (n = 59). The product of QTd/JTd and QTc/JTc was significantly different among all three groups. Both dispersion and product put additional and independent power on identification of mutation carriers when adjusted for sex and age in a logistic regression analysis. Thus, symptomatic patients with LQTS show marked inhomogenity of repolarization in the surface ECG. QT dispersion and QT product might be helpful in finding LQTS mutation carriers and might serve as additional ECG tools to identify asymptomatic LQTS patients.
Adult↗