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Combined implantation of cardiac contractility modulation (CCM) with subcutaneous implantable cardioverter-defibrillator (S-ICD) appears a suitable option to reduce the amount of intracardiac leads and complications for patients. Here we report on a patient with ischemic cardiomyopathy carrying an S-ICD in which a CCM device was implanted. During crosstalk testing post-CCM implantation, the S-ICD misannotated QRS complexes and T waves. The problem was solved through reprogramming the CCM, while preserving S-ICD functionality and improving heart failure symptoms. In conclusion, S-ICD combined with CCM seems to be a good and safe option for patients when device interference is being ruled out.

Aims The early repolarization syndrome (ERS) can cause ventricular fibrillation (VF) and sudden death in young, otherwise healthy individuals. There are limited data suggesting that ERS might be heritable. The aim of this study was to characterize the clinical phenotype and to identify a causal variant in an affected family using an exome-sequencing approach. Methods and results Early repolarization syndrome was diagnosed according to the recently proposed Shanghai ERS Score. After sequencing of known ERS candidate genes, whole-exome sequencing (WES) was performed. The index patient (23 years, female) showed a dynamic inferolateral early repolarization (ER) pattern and electrical storm with intractable VF. Isoproterenol enabled successful termination of electrical storm with no recurrence on hydroquinidine therapy during 33 months of follow-up. The index patient’s brother (25 years) had a persistent inferior ER pattern with malignant features and a history of syncope. Both parents were asymptomatic and showed no ER pattern. While there was no pathogenic variant in candidate genes, WES detected a novel missense variant affecting a highly conserved residue (p. H2245R) in the ANK3 gene encoding Ankyrin-G in the two siblings and the father. Conclusion We identified two siblings with a malignant ERS phenotype sharing a novel ANK3 variant. A potentially pathogenic role of the novel ANK3 variant is suggested by the direct interaction of Ankyrin-G with the cardiac sodium channel, however, more patients with ANK3 variants and ERS would be required to establish ANK3 as novel ERS susceptibility gene. Our study provides additional evidence that ERS might be a heritable condition.

Mapping and ablation of atriofascicular fibers can be highly challenging due to the complex and dynamic anatomy of the tricuspid valve annulus. This case highlights the utility of a multi-electrode catheter three-dimensional mapping approach to localize the Mahaim pathway along the tricuspid annulus in order to guide catheter ablation.

Aim: The present study analyzes in depth the impact of different calcification patterns on disturbances of the conduction system in transcatheter aortic valve replacement (TAVR) patients. Methods and Results: A total of 169 preprocedural TAVR multislice computed tomography scans from consecutive transfemoral (TF) TAVRs performed between 2014 and 2017 using either Edwards SAPIEN or Medtronic Evolut R valves were retrospectively evaluated. The volume, distribution, and orientation of annular and valvular aortic valve calcification were measured and their impact on postoperative conduction disturbances was determined using linear and logistic regression analyses. The total volume of calcification and distribution at the aortic annulus or valve did not influence the conduction system. Oval calcification of the left aortic cusp was independently associated with an elevated risk for an increase in atrioventricular block degree (+0.6, p = 0.03). Moreover, orthogonal calcifications at the level of the aortic annulus were associated with an increased risk for QRS prolongation (+26 ms, p = 0.004) and an increased risk for permanent pacemaker implantation (OR 4.3, p = 0.03) after TF TAVR. This was more pronounced in patients undergoing TF TAVR using a balloon-expandable Edwards SAPIEN 3 valve (QRS +38.195 ms, p < 0.001; OR permanent pacemaker 15.48, p = 0.013). Conclusion: Orthogonal annular calcification confers an increased risk for conduction disturbances after TAVR. This is even more pronounced after implantation of balloon-expandable valves.

Introduction Parasystole refers to an ectopic pacemaker that discharges with a constant rate competing with the primary pacemaker of the heart the sinus node. Parasystolic pacemakers have been described in the atrium, atrioventricular node, His bundle, and in the ventricle. Ventricular parasystole usually carries a benign prognosis, but there are a few reports of ventricular tachyarrhythmia initiated by parasystolic beats. Case presentation We present a case of a 15-year-old otherwise healthy teenager with recurrent most likely arrhythmic syncope who was diagnosed with ventricular parasystole from the left posterior fascicle. After exclusion of structural and primary electrical heart disease, the patient was deemed at increased risk of parasystole-induced tachyarrhythmia, and thus catheter ablation of the ectopic focus was performed. Since catheter ablation the patient continues to be free of any symptoms. Discussion This report highlights the potential risks of parasystole in context of recurrent syncope and reviews the available literature on parasystole and ventricular tachyarrhythmia.

Aims The choice of left ventricular pacing configurations (LVPCs) of quadripolar leads used for cardiac resynchronization therapy (CRT) affects haemodynamic response and thus may be a tool for device optimization. The value of surface electrocardiograms and interventricular time delays (IVDs) for optimization is unknown. Methods and results Sixteen patients implanted with a CRT device with a quadripolar LV lead underwent invasive testing of LV d P /d t . QRS durations at baseline (bl) and during biventricular pacing (biv) were measured using different LVPCs (total of 141 LVPCs; 8.8 per patient). Variations in QRS duration during biv were calculated for each patient (ΔQRS) and, when compared with intrinsic QRS duration, for all LVPCs (ΔQRSLVPC). Interventricular time delays between the poles of the LV lead were obtained from intracardiac electrograms. ΔIVD was calculated as IVDmax − IVDmin. Parameters were correlated with LV d P /d t . ΔQRS and ΔQRSLVPC both significantly correlated with LV d P /d t ( P 168 ms ( P < 0.001), but not

Exercise-induced ventricular tachycardia (EIVT) is typical and quite common in patients with long QT-Syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT). Although patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) or hypertrophic cardiomyopathy (HCM) experience EIVT infrequently, the occurrence of EIVT is of great prognostic value in these patients. The following overview will introduce these cardiomyopathies and highlight the importance of their EIVT.

Objective. Despite the use of anticoagulation during left atrial (LA) ablation procedures, ischemic cerebrovascular accidents (CVAs) are recognized as a serious complication. Heparin is usually given after safe transseptal access has been obtained, resulting in a short unprotected dwell time of catheters within the LA, which may account for CVAs. We investigated the frequency of CVAs and LA thrombus formation as detected by intracardiac ultrasound (ICE) depending on the timing of heparin administration.Methods and Results. Sixty LA ablation procedures with the use of ICE were performed in 55 patients. Patients were grouped by heparin administration after (Group I, ) and before (Group II, ) transseptal access. Group I patients were younger ( versus years, ); other clinical and echocardiographic characteristics did not differ between groups. Early thrombus formation was observed in 2 (15.4%) of group I patients as compared to 0% of group II patients (). One CVA (2.1%) occurred in one group II patient without prior thrombus detection, and none occurred in group I patients ().Conclusion. Early administration of heparin reduces the risk of early intracardiac thrombus formation during LA ablation procedures. This did not result in reduced rate of CVAs.

In carriers of dual chamber pacemakers and implantable cardioverter-defibrillators (ICD), detection of atrial fibrillation (AF) is crucial for adequate mode switch function and to avoid inappropriate shock delivery. Detection algorithms rely on the atrial rate and on the relationship of atrial to ventricular intracardiac electrograms, but the relative portion of misclassified AF episodes remains high. Although myocardial impedance is a reliable indicator of contraction, little is known about atrial impedance as a marker of atrial arrhythmias. Methods During an electrophysiological study, we investigated the effect of induced AF on impedance at the right atrial free wall (RAFW) and right atrial appendage (RAA) in 20 patients. Using biphasic square-wave pulses (128 Hz, 200 microA/15 micros), impedance changes were recorded during sinus rhythm (SR-1), atrial pacing at 120 beats/min, AF induced by rapid atrial burst pacing, and after spontaneous AF termination (SR-2). Results At the RAA, peak-to-peak impedance amplitude during cardiac cycle (DeltaZ) dropped from 51.7 +/- 35.3 Omega (SR-1) or 49.6 +/- 30.6 Omega (pacing) to 24.6 +/- 22.0 Omega (AF, Por =0.0005), and subsequently increased to 37.7 +/- 24.7 Omega (SR-2, Por = 0.0004 v. AF). At the RAFW, DeltaZ changed from 16.2 +/- 15.5 Omega (SR-1) or 13.5 +/- 9.9 Omega (pacing) to 5.9 +/- 4.1 Omega (AF, Por = 0.003), and to 11.4 +/- 10.7 Omega (SR-2, Por = 0.015). Given a discrimination threshold of 65%, the sensitivity and the specificity of DeltaZ to detect AF were 79 +/- 18 and 89 +/- 14%, respectively (95% confidence interval).AF causes DeltaZ drop in pacemaker and ICD recipients. This impedance based algorithm can be used as an alternative method of AF detection.

Present-day ICD systems offer the possibility to reconstruct an intrathoracic 6-lead ECG (IT-ECG), using the defibrillator coils in the right ventricle and superior vena cava and the left-laterally positioned ICD as electrodes according to Einthoven and Goldberger. The aim of this study was to assess the feasibility of (1) automated P wave recognition in the IT-ECG without an additional atrial electrode as the basis of AV synchronous ventricular pacing (VDD) and for improved differentiation between supraventricular tachyarrhythmias and, (2) the automated detection of pacing evoked atrial potentials (EAP) in dual chamber ICDs as the basis for atrial “autocapture”pacing systems. In 27 patients during ICD implanation intraoperatively, the IT-ECG was digitally recorded. A recently established algorithm for automatic P wave and EAP detection correctly identified 1,663/1,672 (99.5%) P waves (oversensing rate 0.6%) and 543/554 (98.0%) EAP (no oversensing). During subthreshold atrial stimulation, 405/412 (98.3%) P waves were correctly identified (oversensing due to pacemaker spikes,n = 421, without subsequent EAP, 1.9%,n = 8). During stimulated ventricular tachycardia in 26/27 patients retrograde P wave or AV dissociation were identified. The 6-lead IT-ECG, easily implementable in ICD systems, is a diagnostic tool providing reliable information about atrial activation, serving as a basis for VDD pacing in single chamber ICD systems, allowing reliable EAP recognition that enables atrial “autocapture”pacing in dual chamber ICDs, and improves the differentiation between supraventricular and ventricular tachycardia. (PACE 2003; 26[Pt. I]:1472–1478)

FABER, T.S., et al.: Beat-to-Beat Assessment of QT/RR Interval Ratio in Severe Heart Failure and Overt Myocardial Ischemia: A Measure of Electrical Integrity in Diseased Hearts.The study was designed to assess the beat-to-beat variation of ventricular repolarization in patients with myocardial ischemia, heart failure, and in normal subjects. Autonomic tone may alter the dynamic QT/RR interval relation and thus may be involved in ventricular arrhythmia development, especially in the diseased heart. The study included 145 patients (age 16–86 years) with CHF (LVEF ≤ 0.30) or unstable angina pectoris(LVEF > 0.60). The control group consisted of healthy volunteers giving physiological baseline measures for the evaluated parameters: cycle length, QT interval, and QT/RR interval ratio during three time periods. In patients with myocardial ischemia(LVEF > 0.60)and healthy subjects the QT/RR interval ratio did not reveal significant differences between both groups (QT/RRCAD= 0.36 ± 0.77 vs QT/RRcontrols= 0.28 ± 0.83; NS). In sharp contrast, in patients with severe heart failure, RR dependent instantaneous variation of the QT interval was almost missing and regression line analysis disclosed a QT/RR interval slope substantially enhanced by 196% (compared to normal subjects) and 131% (compared to CAD patients; P < 0.05) with a complete loss of circadian modulation (QT/RRCHF= 0.83 ± 0.71 vs QT/RRCAD= 0.36 ± 0.77 vs QT/RRcontrols= 0.28 ± 0.83; P < 0.05). Beat-to-beat QT interval assessment provides a dynamic parameter of physiological and altered repolarization in defined study groups. Compared to other groups (preserved LVEF), patients with left ventricular impairment exhibited a significantly increased sensitivity of repolarization to cycle length (enhanced QT/RR interval ratio) and a blunted circadian modulation of the QT interval. This is consistent with concept that increased repolarization disparity may be deleterious being a potential pathophysiological basis for enhanced arrhythmic risk. (PACE 2003; 26[Pt. I]:836–842)

Background: Series of discharges from an implanted defibrillator (ICD) to terminate life-threatening ventricular tachyarrhythmias are one particular aspect of energy use and success of ICD therapy. Little is known about prevalence, characteristics, and risk stratification of so-called “cluster arrhythmias”. Hypothesis: The objective of this study was to examine the frequency of cluster arrhythmias, to characterize the temporal relationship precisely, and to assess the accompanying circumstances of their occurrence, whereby risk stratification was to be made if appropriate. Methods: In all, 63 consecutive patients were followed prospectively over 727 ± 684 days to determine the presence and characteristics of cluster arrhythmias (45,801 patient days). In 30 patients, 374 ICD episodes of ventricular tachyarrhythmias were analyzed for their temporal relationship. After a first successfully terminated ventricular tachyarrhythmia, further ICD discharges within 3 h were observed during 145 of 374 (39%) episodes; mean time interval between these arrhythmias was 25 ± 32 min. Results: Arrhythmia clusters occurred in 19 of 30 (63%) patients. In multivariate analysis, only underlying heart disease was predictive for accumulation of ventricular tachyarrhythmias. Cluster arrhythmias were more frequent among patients with ischemic heart disease than among those with nonischemic heart disease (40.0 vs. 29.2%, p < 0.05). Ejection fraction, age, gender, and other parameters were not predictive for occurrence of arrhythmia clusters. In 4 of 19 patients, accumulation of ICD discharges was predictive for new onset of myocardial ischemia elicited by exercise test. Conclusions: Cluster arrhythmias are most common in patients with ICDs with coronary heart disease and may indicate disease progression and increasing instability, for example, due to new onset of myocardial ischemia.

The safety and efficacy of adding oral carvedilol (25 mg twice daily) to standardized treatment of unstable angina was assessed in a multicenter, randomized, double-blind, placebo- controlled trial on 116 patients with acute unstable angina. Patients were monitored in an intensive care unit and underwent 48-hour Holter monitoring to assess transient ischemia. Carvedilol as adjunctive therapy resulted in a significant reduction of median heart rate (65 vs 75 beats/min, p

Die moderne Schrittmachertherapie gilt als ein sicheres und zuverlassiges Verfahren in der Behandlung symptomatischer und/oder prognostisch bedeutsamer bradykarder Herzrhythmusstorungen. Etwa jeder sechste Patient verstirbt in der Folgezeit nach Schrittmacherimplantation an einem plotzlichen Herztod, welcher ganz uberwiegend, der Progression der vorbestehenden kardialen Grunderkrankung zuzuordnen ist. In den letzten Jahren wurde aber auch deutlich, das eine permanente Elektrostimulation des Herzens die Gefahr der Auslosung und/oder Aggravation lebensbedrohlicher ventrikularer Herzrhythmusstorungen bergen kann. Insbesondere bei fortgeschrittener myokardialer Schadigung konnen u.a. stimulationsbedingte R-auf-T-Phanomene, “Kurz-lang”-Sequenzen und Wahrnehmungsdefekte z.B. wahrend ventrikularer Arrhythmien oder transitorischer Myokardischamie stimulationsbedingte sekundare lebensbedrohliche Tachyarrhythmien auslosen.

Die adaquate Versorgung von Patienten, die bereits einmal einen Herz-Kreislaufstillstand durch tachykarde Arrhythmien uberlebt haben, war lange Zeit auf eine Behandlung mit Antiarrhythmika beschrankt, wenn der Rhythmusstorung keine behebbare orga-nische Ursache zugrunde lag. Trotz optimierter Pharmakotherapie sterben 30% dieser Patienten innerhalb von drei Jahren durch eine erneute maligne Arrhythmie. Deshalb wurde in den letzten Jahren die Implanta-tion von automatischen, implantierbaren Kardioverter-Defibrillatoren (ICD) der Standard bei der Versorgung dieser Patienten. Zunehmend werden ICDs auch bei Patienten mit stark erhohtem Risiko fur einen plotzlichen Herztod ohne uberlebten Kreislaufstillstand implantiert, ins-besondere bei Patienten mit Kardio-myopathie oder angeborenen ar-rhythmogenen Anomalien des Herzens. In neuen klinischen Studien konnte bei selektierten Patienten ein deutlicher Uberlebensvorteil gegen-uber der Behandlung mit Anti-arrhythmika gezeigt werden [7]. Die Implantation von ICDs wird bei den neuen transvenosen Systemen ohne Thorakotomie durchgefuhrt, wodurch das Operationsrisiko wesentlich verringert wurde. Moderne ICDs werden unter den linken M. pectoralis major implantiert, eine mehrpolige Elektrode im rechten Ventrikel dient der Wahrnehmung, der Stimulation und der Schockab-gabe. Die Gerate sind in weiten Bereichen patientenspezifisch programmierbar und erlauben so eine differenzierte Erkennung und mehrstufige Therapie von ventrikularen Tachykardien und Kammerflimmern. Neben der Defibrillation und der synchronisierten Kardioversion stellt die antitachykarde Stimulation eine hocheffektive und fur die Patienten angenehme Methode zur Beendigung von langsamen ventrikularen Tachykardien dar. Der interne Speicher moderner ICDs dokumentiert nicht nur die Anzahl der Arrhythmien und die abgegebene Therapie, auch intrakardiale EKGs vor und nach den Episoden konnen ausgelesen werden. Diese Eigenschaften erlauben heute eine sehr spezifische und individuelle Anpassung der Therapie an die zugrundeliegende Arrhythmie.

Independent of other established risk factors, depressed heart rate variability (HRV) has been shown to be a powerful predictor of cardiac events after MI. Unfortunately, the need of 24-hour ECG recording and subsequent laborious editing of Holter data limits the clinical use of long-term HRV. In order to perform post-MI risk stratification more efficiently, we evaluated the value of short-term HRV estimates for preselection of patients who might benefit from long-term HRV assessment. Two measures were assessed from 24-hour ambulatory ECGs recorded in 729 survivors of acute MI prior to hospital discharge. In addition to a complete 24-hour HRV index, a standard deviation of normal-to-normal RR intervals (SDNN) was obtained from the first stationary and ectopic free 5-minute segment of the Holter recording. Predictive power (relation between positive predictive accuracy and sensitivity) of a complete 24-hour HRV index in identifying patients who suffered from cardiac mortality or arrhythmic events during a 2-year follow-up was compared to the predictive power of assessing the 24-hour HRV index limited to 50%, 40%, or 20% of patients with the lowest values of 5-minute SDNN. The HRV index was significantly lower in patients who died (19 +/- 11 units) or had an arrhythmic event (AE) (18 +/- 11 units) compared to those who survived without an event (28 +/- 10 resp. 27 +/- 11 units; P < 0.001). Similarly, 5-minute SDNN was significantly lower in patients who died (25 +/- 12 ms) or suffered an AE (26 +/- 13 ms) compared to survivors (40 +/- 19 ms resp. 39 +/- 19 ms; P < 0.001). When limited to patients with depressed 5-minute SDNN, assessment of the HRV index performed better than 5-minute SDNN alone in positive prediction of cardiac events. Preselected assessment of the lowest HRV index in 50% to 20% of the total population yielded a 2-year cardiac event prediction rate as high as analysis of the HRV index in all patients. Long-term HRV assessment for risk stratification after MI in patients preselected by depressed short-term SDNN is safe and efficient, and allows a practical identification of patients with the highest likelihood of cardiac events during long-term follow-up.

The authors developed a computer program that detects myocardial infarction (MI) and left ventricular hypertrophy (LVH) in two steps: (1) by extracting parameter values from a 10-second, 12-lead electrocardiogram, and (2) by classifying the extracted parameter values with rule sets. Every disease has its dedicated set of rules. Hence, there are separate rule sets for anterior MI, inferior MI, and LVH. If at least one rule is satisfied, the disease is said to be detected. The computer program automatically develops these rule sets. A database (learning set) of healthy subjects and patients with MI, LVH, and mixed MI+LVH was used. After defining the rule type, initial limits, and expected quality of the rules (positive predictive value, minimum number of patients), the program creates a set of rules by varying the limits. The general rule type is defined as: disease = lim1l < p1 < or = lim1u and lim2l < p2 < or = lim2u and ... limnl < pn < or = limnu. When defining the rule types, only the parameters (p1 ... pn) that are known as clinical electrocardiographic criteria (amplitudes [mV] of Q, R, and T waves and ST-segment; duration [ms] of Q wave; frontal angle [degrees]) were used. This allowed for submitting the learned rule sets to an independent investigator for medical verification. It also allowed the creation of explanatory texts with the rules. These advantages are not offered by the neurons of a neural network. The learned rules were checked against a test set and the following results were obtained: MI: sensitivity 76.2%, positive predictive value 98.6%; LVH: sensitivity 72.3%, positive predictive value 90.9%. The specificity ratings for MI are better than 98%; for LVH, better than 90%.

Hypertensive heart disease is increasingly considered to be a strong and independent risk factor for sudden cardiac death. Ventricular tachyarrhythmias in these patients are common and mainly the result of electrophysiologic abnormalities and increased electrical vulnerability of the hypertrophic myocardium. However, proarrhythmia in the hypertrophic heart often is facilitated and aggravated by electrolyte disturbances, the sympathoadrenergic tone, transient blood pressure crisis, and especially by the occurrence of myocardial ischemia. Myocardial ischemia in the setting of hypertensive heart disease may result from stenotic lesions in large and/or small coronary artery vessels and, in the absence of both, will result from the altered cellular oxygen supply and consumption in the hypertrophic myocardium. Recent studies have shown that acute and transient myocardial ischemia are common in many hypertensives, often fail to be symptomatic, and that the dynamic interaction of left ventricular hypertrophy, transient myocardial ischemia, and ventricular tachyarrhythmias may provide a crucial link for the high incidence of sudden cardiac death in patients with hypertensive heart disease.

Torsade de pointes is a particular form of polymorphic ventricular tachycardia causing few haemodynamic symptoms, but carries a poor prognosis because of recurrence and sudden death in up to 31% of patients. A wide range of agents have been shown to aggravate and even to cause torsade de pointes by prolonging the QT interval or increasing QT dispersion. For the majority of substances the incidence of torsade de pointes remains unclear, but is of the order of 3 to 15% for a wide range of agents. Elicitation of proarrhythmia by drug-induced QT prolongation is mainly based on increased cellular excitability and/or abnormal dispersion of ventricular repolarisation. Torsade de pointes has been shown to be related to bradycardia-dependent early after-depolarisations and/or increased dispersion of repolarisation. Clinically, patients with predisposing factors prior to medication should be considered at risk of drug-mediated proarrhythmia. Typically, torsade de pointes occurs during the first days of antiarrhythmic therapy. During this phase, QT interval measurement and assessment of the QTc time should be performed frequently. Phases of bradycardia or occurrence of ventricular extra beats with a long coupling interval may be of help to identify patients at high risk of proarrhythmic events. As a first attempt in managing this arrhythmia, magnesium sulphate has been shown to be effective in many patients. In case of recurrence of torsade de pointes, the use of a temporary pacemaker with pacing at about 100 to 120 beats/min is the therapy of choice until the causative agent has been completely eliminated.

The present generation of implantable cardioverter defibrillators (ICDs) provides a very effective device for monitoring and treating life-threatening ventricular tachyarrhythmia. Patients at risk of sudden cardiac death who are directed to this form of treatment usually have severe coronary artery disease, previous myocardial infarction, and low ejection fraction. Progression of the underlying heart disease predisposes these patients to subsequent ischemic events, including symptomatic and asymptomatic myocardial ischemia and reinfarction, which carry a substantial risk of fatal ventricular proarrhythmia. Multipolar lead configurations presently available in the ICD appear to be effective in assessing acute myocardial ischemia as induced by exercise testing or transient coronary artery occlusion. Continuous monitoring of myocardial ischemia (COMONI) by a sophisticated, multimodal ICD appears to be feasible, may offer the means to closely supervise progression and various complications of the underlying heart disease, and may help to guide automatic or interactive antiischemic treatment.

A 61-year-old woman presented to our outpatient department because of audible alerts by her implantable cardioverter-defibrillator (ICD) starting about 2 weeks ago. The ICD (Medtronic Maximo VR 7232) was implanted in 2004 after cardiopulmonary resuscitation caused by spontaneous sustained ventricular tachycardia. Her medical history was significant for restrictive cardiomyopathy, with predominant right ventricular dysfunction, high-grade tricuspid valve insufficiency treated with tricuspid prosthetic valve replacement in 2000, mildly impaired left ventricular function, and permanent atrial fibrillation. Because of the prosthetic valve replacement, stimulation electrodes were implanted epimyocardially and 2 single-finger defibrillation leads were positioned subcutaneously (Medtronic 6996/SQ-Finger). All electrodes were connected to the ICD, which was placed beneath the diaphragm. High-voltage B (HVB) lead impedance is measured against the ICD can and superior vena cava (SVC) lead in parallel. The SVC lead impedance is measured between both finger leads. Interrogation of the ICD revealed a decrease in HVB lead impedance below the limit of 20 Ω about 2 weeks before presentation, causing the acoustic alert (Figure 1). At the time of presentation, HVB lead impedance was 21 Ω, SVC lead impedance was 36 Ω, pacing impedance was 544 Ω, pacing threshold was stable at 0.1 ms at 3 V, and ventricular amplitude was >5.6 mV. Since the last interrogation 3 months earlier, 15 episodes of nonsustained ventricular tachycardia were detected without the need for antitachycardia therapy. It is noteworthy that …

A 71-year-old female patient was referred for catheter ablation of drug-refractory, symptomatic atrial fibrillation. Initial intracardiac echocardiography (ICE) incidentally showed a mobile embolus stuck at a bifurcation of the right pulmonary artery. The procedure was suspended and the finding was subsequently confirmed by computed tomography pulmonary angiography. This case illustrates a potential value of real-time imaging by ICE during invasive procedures.

Percutaneous balloon valvuloplasty has been shown to increase the aortic orifice area and to improve clinical symptoms. However, there are only few data concerning long-term results after balloon valvuloplasty. In this study, 36 patients (11 men, 25 women, mean age 75 +/- 8 years) were followed after balloon valvuloplasty for a period of up to 18 months by means of clinical parameters and repeated Doppler echocardiographic measurements after 1, 3, 6, 12 and 18 months. Invasive measurements revealed a decrease of the systolic peak gradient from 78 +/- 24 to 38 +/- 13 mm Hg (p less than 0.001), and an increase in the aortic orifice area from 0.58 +/- 0.23 to 0.93 +/- 0.2 cm2 (p less than 0.001). The Doppler echocardiographic approach revealed that the maximal instantaneous gradient decreased from 96 +/- 26 to 67 +/- 22 mm Hg (p less than 0.001). The aortic orifice area increased from 0.49 +/- 0.16 to 0.73 +/- 0.21 cm2 (p less than 0.001). Three patients (8%) died in the hospital. After hospital discharge, 16 patients (44%) died and 8 patients (22%) underwent successful aortic valve replacement after a mean follow-up of 8 +/- 6 months. Nine patients (25%) were alive after a follow-up period of 18 months. Seven of these (19%) remained clinically improved. During follow-up, the Doppler echocardiographic results revealed a continuous trend toward the preprocedural severity of the aortic valve stenosis. Progression of restenosis assessed by Doppler echocardiographic measurements was accelerated in the group of patients who subsequently died or underwent repeat balloon valvuloplasty or aortic valve replacement.

Aim The impact of atrial fibrillation (AF) on mortality is not fully understood. We therefore sought to investigate long-term effects of AF on mortality in patients with the need for pacemaker (PM) therapy. Methods and results A total of 1627 PM recipients with AF at implantation were followed in a singlecentre, longitudinal study for up to 35 years. Baseline factors affecting survival and long-term followup were analysed. A total of 7362 patient-years of follow-up (PM implanted between 1971 and 2000, followed until 31 December 31 2005) were analysed. Female PM recipients lived significantly longer than male (P ¼ 0.025; mean survival 91.9 vs. 72.1 months) despite older age at time of inclusion. Mean survival times almost doubled for patients implanted in the last decade, with 139.8 months in the nineties vs. 66.8 months in the seventies and 75.7 months in the eighties (P , 0.001). Male gender, age at implantation, non-syncopal bradycardia, and decade of implantation influenced survival. Conclusion Life expectancy in AF patients after PM implantation has doubled within the last three decades, with a mean survival in the overall population of 7.6 years for women and 6.0 years for men. Survival is influenced by several simple baseline characteristics, which may help to identify patients with very long survival times.

Aims Current studies found an incidence of 12–31% ventricular tachyarrhythmias and sudden cardiac death during cardiac pacing months or even years after pacemaker insertion. MADIT[12][1] and MUSTT[13][2] demonstrated that patients with poor LV function after Myocardial infarction (MI) showing non-sustained ventricular tachycardia (nsVT) and inducibility during electrophysiologic testing benefit from an ICD. The present study was dedicated to assess the global incidence of non-sustained ventricular arrhythmias in a general population of pacemaker patients. Special regard was on patients with a potential ICD indication, e.g. those matching the MADIT/MUSTT criteria. Methods and results Two hundred and thirty-one patients (72 ± 11 years; 134 men) with an indication for dual chamber pacing entered the study. In all patients pacemaker systems capable of automatic storing of intracardiac electrocardiograms were implanted (Pulsar®, Discovery®, Guidant). Follow-up time was 15 months after inclusion. In 54 (25.7%) of 210 patients with at least one follow-up, episodes of nsVT were documented by stored electrocardiograms (up to >30 beats, >200 b.p.m.). Multiple—up to nine—episodes of ventricular tachycardia were retrieved in 31 of these patients. Three out of 14 patients with an LVEF

Aim In the presence of coronary artery disease, implantable cardioverter-defibrillators (ICD) are used effectively for treating life-threatening tachyarrhythmias. Continuous monitoring of myocardial ischaemia would provide a new diagnostic option in future ICD generations. Methods and results In 22 selected patients undergoing coronary angioplasty, percutaneous transluminal coronary angioplasty (PTCA), three electrodes, similar to those used in the ICD, were inserted aiming to create six intra-thoracic ECG (IT-ECG) leads according to Einthoven and Goldberger. In total, 27 PTCA were conducted. The diagnostic efficacy for ischaemia assessment was compared with the surface ECG. The IT-ECG proved to be more sensitive than conventional ECG in early and overall ischaemia assessment. At 30 s of coronary artery occlusion, ischaemic ST-segment alterations (� 0.25 mV) were present in the IT-ECG 2.3 times more often (23 vs. 10/27 PTCA attempts, P , 0.01) and at 90 s 1.4 times more often compared with conventional ECG leads (18 vs. 26/27, P , 0.05). Intra-thoracic Einthoven 2 (SVC þ RVA vs. ICD-housing) and Goldberger 3 (SVC þ ICD-housing vs. RVA) had the highest sensitivity (88/85%). Using � 4 IT-ECG, ischaemia monitoring was independent of severity and site of origin. IT-ECG signals showed double ST-T signal amplitude (4.19+ 0.6 vs. 2.15+ 0.3 mV, ratio: 1.95, P , 0.01) at a QRS/ST amplitude ratio similar in the two ECG techniques. Conclusion This study provides strong evidence that the ICD-based IT 6-lead ECG would provide a new and efficient means of assessing a patient’s daily ischaemic burden.

A 56-year-old man with a history of prior myocardial infarction, ischemic cardiomyopathy and nonsustained episodes of ventricular tachycardia had received a subpectorally placed implantable cardioverter-defibrillator (ICD) (Medtronic Micro-Jewel II® 7223 Cx with a single-coil electrode Medtronic Sprint® 6932) for primary prevention of sudden cardiac death three years ago. He was referred to our department after having received twenty-five inappropriate shocks. Interrogation and testing of the device revealed exit-block; incorrect sensing could easily be reproduced and visualized in the ICD’s marker channel by shaking the ICD can. The patient denied tampering with the device, had no history of recent weight loss, psychiatric illness or any other obvious condition with which rotation of the device could be associated. Chest x-ray revealed knotting of the lead just distally of the ICD header (Fig. 1) and multiple twisting of the lead on its way through the anonymous vein. Twiddler’s syndrome with multiple kinks could be confirmed intraoperatively (Fig. 2). The lead was extracted and the whole system replaced. Twiddler’s syndrome, originally described in a pacemaker patient by Bayliss in 1968 [1], denotes a complication in pacemaker and defibrillator patients, in which manipulation with the device leads to twisting of can and electrodes with the consequence of lead displacement. While most of the patients persistently deny manipulation with the device, this is the accepted mechanism leading to lead dislodgement. Previously reported factors that may predispose to device rotation include advanced age, female gender, obesity, small size of the device relative to its pocket and psychiatric disease. Fortunately, Twiddler’s syndrome is a rare complication in ICD patients, however, it may lead to severe complications such as inappropriate shock delivery, which itself may cause ventricular fibrillation, or unrescued sudden cardiac death. Despite the fact that only a small number of Twiddler’s syndromes in subpectorally implanted devices have been published so far [e.g. 2, 3], it cannot be reasoned that ICDs in this position are less predisposed to twiddle.

Onset and termination of atrial fibrillation are often associated with abrupt changes in heart rate. Presence and time-course of delayed adaptation of the QT/QTc interval are unknown, but a temporary "mismatch" between rate and the QT interval may enhance the risk of proarrhythmia.In a prospective two-part study, time-course of adaptation of ventricular repolarization after abrupt changes in heart rate was assessed during termination of Holter ECG-documented atrial fibrillation episodes (Group 1, 32 patients) and subsequently in 20 patients with sick sinus syndrome and cardiac pacing initiating abrupt bi-directional changes in paced heart rate (Group 2).Conversion of atrial fibrillation showed a 32+/-21 bpm fall in heart rate (P0.05). Restoration of the QTc interval afterwards was delayed byor =1 min in 27%, by 1-2 min in 21%, by 2-5 min in 11% and by5 min in 41% of the cases. Atrial pacing simulating a 30 bpm fall/increase in atrial rate demonstrated that a subsequent transient rate-QT mismatch is a physiological phenomenon (fall of 100 to 70 bpm: initially 90% of the proper QTc interval, compared with 94% after conversion of atrial fibrillation). The restoration curve of QTc adaptation showed an initially fast and subsequently slower time component, with interindividual variation. Clinical parameters, baseline heart rate or the direction of rate changes were not predictive.Delayed adaptation of ventricular repolarization following atrial fibrillation onset and termination is common, requiring minutes for restoring the QT/QTc steady state. Clinical parameters fail to predict patients with a long-lasting rate-QT mismatch. It may carry a significant arrhythmogenic risk particularly in patients on QT altering medication.

Our report describes the late migration of an atrial screw-in lead into the right internal jugular vein causing subsequent subclinical thrombus formation at the tip of the electrode. Previously initiated anticoagulation for atrial fibrillation may have prevented complete occlusion of the internal jugular vein. Therefore, prophylactic anticoagulation should be considered for patients in whom permanent pacing leads are dislodged into central veins and cannot be removed.

FABER, T.S., et al.: Impact of Electrocardiogram Recording Format on QT Interval Measurement and QT Dispersion Assessment. The aim of this study was to determine the effect of recording conditions on the operator dependent measures of QT dispersion in patients with known and/or suspected repolarization abnormalities. Among several methods for risk stratification, QT dispersion has been suggested as a simple estimate of repolarization abnormalities. In a cohort of high and low risk patients, different components of the repolarization process were assessed in the 12-lead ECG using three different paper speeds and amplifier gains. To assess measurement error and reproducibility, a straight line was repeatedly measured. The operator error was 0.675 ± 0.02 mm and the repeatability of the measurement error was 31 ± 6%. The QT interval was most frequently measurable in V2–V5. Depending on the lead selected for analysis, the incidence of visible U waves was greatest in the precordial leads with high amplifier gain and low paper speed, strongly affecting QT interval measurement. The timing of the onset of the QRS complex (QRS onset dispersion) or offset of the T wave was strongly dependent on the paper speed. Paper speed, but not amplifier gain, had a significant shortening effect on the measurement of the maximum QT interval. As QT interval measurement in each ECG lead incorporates QRS onset and T wave offset (depending on the number of visible U waves), the dispersion of each of these parameters significantly affected QT dispersion. Thus, QT dispersion appears to reflect merely the presence of more complex repolarization patterns in patients at risk of arrhythmias.

Die chronische Herzinsuffizienz gleich welcher Ursache, stellt ein komplexes klinisches Syndrom dar, welches aufgrund der Einschrankung der Belastungstoleranz nicht nur die Lebensqualitat des Patienten mindert, sondern auch mit einem signifikant erhohten Risiko fur lebensbedrohliche ventrikulare Tachyarrhythmien verbunden ist. Ebenso wie die Ursachen der Herzinsuffizienz sind auch die Form und der Mechanismus ventrikularer Arrhythmien vielfaltig. So modulieren zellulare, myokardiale und extrakardiale Einflussfaktoren entscheidend die Auslosung und die Aggravation ventrikularer Tachyarrhythmien mit z. T. rascher Degeneration in Kammerflimmern.

Objectives. The proarrhythmic risk of class I antiarrhythmic agents in combination with myocardial ischemia is mainly the result of their effects on ventricular repolarization. This study was designed to evaluate the effect of class Ic antiarrhythmic agents on QT dispersion during myocardial ischemia.Background. QT interval dispersion on the 12-lead electrocardiogram (ECG) has been suggested as a noninvasive marker of inhomogeneous ventricular repolarization and susceptibility to ventricular arrhythmias.Methods. In a randomized, double-blind study, 98 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) were pretreated with propafenone or placebo. QT dispersion was defined as a maximal minus minimal QT interval on the 12-lead ECG before and after PTCA. The power of the study to detect clinically meaningful differences in QT dispersion was 0.75, and a twofold increase in QT dispersion in the propafenone group compared with the placebo group was considered clinically relevant.Results. The QT and corrected QT (QTc) intervals increased significantly during occlusion of the left anterior descending coronary artery (LAD) (9% and 11%, respectively, p < 0.05), whereas occlusion of the circumflex and right coronary arteries had no effect. QTc dispersion increased significantly in the propafenone group during ischemia (+52%, p = 0.002, vs. +23%, p = 0.15). The most considerable effect on QT dispersion was observed during LAD occlusion and ischemia of the anterior wall (+74%, p = 0.025). Corrected JT dispersion (+57%, p = 0.017, vs. +24%, p = 0.23) and the QT dispersion ratio (+1.6%, p = 0.031, vs. 0.9%, p = 0.34) showed similar effects. Plasma levels of propafenone (522 ± 165 μg/liter) did not influence the results.Conclusions. During myocardial ischemia, particularly during LAD occlusion, propafenone results in a significant increase in QT dispersion. The results indicate that QT interval prolongation and enhanced QT dispersion reflect inhomogeneous ventricular repolarization generated by the ischemic anterior wall of the myocardium. These observations may demonstrate a clinically important interaction between myocardial ischemia, repolarization variables and propafenone.(J Am Coll Cardiol 1997;29:561–7)

1. Adenosine is an endogenous nucleoside which causes a brief blockade of the AV nodal conduction pathway following intravenous administration. 2. Such a brief AV block can be used therapeutically for reliable termination of AV nodal re-entry tachycardia and WPW re-entry tachycardia. It can also be used for demasking atrial activity in rapid suspected supraventricular tachycardia with a broad QRS complex or a Delta wave, not present during sinus rhythm with normal AV node conduction, indicating the presence of a hidden WPW syndrome. 3. Side effects after adenosine application are frequent, but very transient rarely serious (1-3% of cases, e.g. status asthmaticus, ventricular fibrillation) and therefore require a certain degree of experience with this drug on the part of the treating physician.

Sudden cardiac death due to ventricular tachyarrhythmias is a threatening cause of mortality in patients after acute myocardial infarction [1, 2]. The risk for subsequent arrhythmic events is highest in those patients in whom an arrhythmogenic substrate is modulated by trigger factors [2]. The anatomical substrate usually develops in the border zone of a myocardial scar where bundles of muscle cells are separated by fibrotic barriers producing a fractionation of the activation wave front and slowing of conduction [3, 4]. In those areas an adequate trigger (e.g. VPB, ischemia, etc.) may then initiate re-entrant tachycardia which is considered to be a common complication of remote myocardial infarction [5–7]. Since effective means for termination of sustained ventricular arrhythmias and prevention of sudden arrhythmic death might currently be considered (e.g. implantable cardioverter-defibrillator) noninvasive identification of high risk patients is highly desirable. One challenging method is the non-invasive assessment of the anatomical substrate from which actual electrical derangement may generate.

In patients with malignant ventricular arrhythmias, antiarrhythmic therapy is known to carry a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias, in whom antiarrhythmic therapy was used and resulted in documented ventricular fibrillation or torsade de pointes. In Cases No. 1 and 2, atrial fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-12 h after conversion to sinus rhythm, documented the spontaneous occurrence of torsade de pointes degenerating into ventricular fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient suffering dilative cardiomyopathy. After 6 days of treatment at a heart rate of 54 beats/min, a marked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillation. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of the QTc-time was documented in Cases No. 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyarrhythmias. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when "benign" cardiac arrhythmias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection of antiarrhythmic agents when used in combination.

During recent years, experimental data have collected convincing evidence for the fatal interaction of myocardial ischemia, ventricular tachyarrhythmias, and sudden cardiac death. In the clinical setting, data reporting on the daily relevance of such a fatal interaction lacked until recently. However, there is now increasing evidence from autoptic studies, from the evaluation of patients who survived one episode of sudden cardiac death, from the follow-up of these patients when treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and, most recently, from studies in patients with stable and especially unstable angina pectoris suffering from Holter-documented ischemic proarrhythmia, that acute and transient myocardial ischemia play an important role for the initiation as well as the aggravation of ventricular tachyarrhythmias and out-of-hospital sudden cardiac death. The present work is directed to summarize our clinical knowledge on this topic and to indicate that preventive strategies for myocardial ischemia are the “antiarrhythmic” of choice in patients with severe coronary artery disease and evidence for ischemic proarrhythmia.

With regard to the restrictive and safe use of class I-antiarrhythmics (AA) clinical criteria predicting drug efficacy and safety have become important. In 140 pts (102 men, 63 ± 7 years) with frequent and symptomatic, but not life-threatening arrhythmias (VA; g 30/h) occurrence, reproducibility and therapeutic consequences of a circadian distribution (CD) of single/repetitive VA was studied. Pts underwent 3 24 h-Holter recordings at baseline, after 2 weeks of placebo and after 6 weeks of dose-titrated antiarrhythmic therapy. 67/140 pts (48%) had reproducible day-night CD (daytime VA increase: 50/67 pts, 75%). In Cox's regression analysis CD was characteristic of a lower VA rate (p l 0.05), but more frequent tachycardia episodes (risk: 3.8 times, p l 0.05) and a lower ejection fraction. AA response was better in pts with CD (3.3 times, p l 005). Day-/night CD pattern was also predictive for a superior response of class IA or IC agents (Fig.). Download : Download high-res image (85KB) Download : Download full-size image In conclusion CD of VA is common in half of the pts with symptomatic VA. When class I agents are used. CD provides clinical evidence for selection of the most effective AA and dose and may help to improve overall antiarrhythmic benefit.