Performance of an implantable cardioverter-defibrillator lead family.

BACKGROUND: Lead failure is the major limitation in implantable cardioverter-defibrillator (ICD) therapy. Long-term follow-up data for Biotronik Linox ICD leads are limited. Therefore, we analyzed the performance of all these leads implanted at our institution. MATERIALS AND METHODS: All Linox and Linox Smart ICD leads implanted between 2006 and 2015 were identified. Lead failure was defined as electrical dysfunction (oversensing, abnormal impedance, exit block). Lead survival was described, according to Kaplan-Meier. Associations between lead failure and specific variables were examined. p < .05 was considered significant. RESULTS: We included 417 ICD leads. The median follow-up time for Linox (n = 205) was 81 months and for Linox Smart (n = 212) 75 months. During that follow-up time, 30 Linox (14.6%) and 16 Linox Smart leads (7.6%) showed a malfunction. The 5-year lead survival probability was 97.4% for Linox and 95.2% for Linox Smart (log-rank test, p = .19). The 6- and 8-year lead survival probability for Linox was 93.6% and 84.6%, and for Linox Smart 93% and 91.9%. The only factor significantly associated with lead failure was younger patient age at implantation (hazard ratio/year: 0.97, 95% CI: 0.94-0.99, p = .002). CONCLUSION: This relatively large study with a long follow-up period highlights a relevant failure rate of Biotronik Linox leads. The performance of Linox versus Linox Smart ICD leads was comparable. Although we show an acceptable 5-year lead survival probability, we observed a marked drop after just 1 more year of follow-up. In an era of improving heart failure survival probability, a prolonged follow-up of ICD leads is increasingly clinically relevant.

[Reflex syncope-or more? : Ictal asystole!] / Reflexsynkope ­ oder mehr? : Iktale Asystolie!

A 59-year-old male patient was admitted for possible reflex syncope following loss of consciousness during urination. During the visit, a malaise with unconsciousness occurred. Holter ECG at that time showed increasing sinus bradycardia with transition to a junctional escape rhythm (30/min); in addition, there were several sinus pauses > 2.0 s (the longest almost 10 s). This malaise occurred again during routine EEG, when a focal epileptic seizure on the right fronto-temporal with sinus bradycardia after 15 s was documented. Thus, the diagnosis of ictal asystole was made, anticonvulsant therapy was started, and a cardiac pacemaker was implanted.

[Premature ventricular contractions and tachycardia in a structurally normal heart : Idiopathic PVC and VT]. / Ventrikuläre Extrasystolen und Tachykardien bei strukturell normalem Herz : Idiopathische VES und VT.

Premature ventricular contractions (PVC) are a common, often incidental and mostly benign finding. Treatment is indicated in frequent and symptomatic PVC or in cases of worsening of left ventricular function. Idiopathic ventricular tachycardia (VT) is mostly found in patients with a structurally healthy heart. These PVC/VT usually have a focal origin. The most likely mechanism is delayed post-depolarization. Localization of the origin is based on the creation of an activation map with or without combination of pace mapping. Idiopathic PVC/VT are most frequently located on the outflow tracts of the right and left ventricles, including the aortic root. Other typical locations include the annulus of the tricuspid or mitral valve, papillary muscles and Purkinje fibers. Catheter ablation is an alternative to antiarrhythmic medication in symptomatic monomorphic PVC/VT. The success rate is good whereby mapping and ablation can often represent a challenge. This article is the fifth part of a series dedicated to specific advanced training in the field of special rhythmology and invasive electrophysiology. It describes the pathophysiological principles, types and typical findings that can be obtained during an electrophysiological investigation.

Updated Survey on Interventional Electrophysiology: 5-Year Follow-Up of Infrastructure, Procedures, and Training Positions in Germany.

OBJECTIVES: This study provides an update and comparison to a 2010 nationwide survey on cardiac electrophysiology (EP), types and numbers of interventional electrophysiological procedures, and training opportunities in 2015. BACKGROUND: In 2010, German cardiology centers performing interventional EP were identified and contacted to provide a survey on cardiac EP. METHODS: German cardiology centers performing interventional EP in 2015 were identified from quality reports and contacted to repeat the 2010 questionnaire. RESULTS: A majority of 131 centers (57%) responded. EP (ablation procedures and device therapy) was mainly part of a cardiology department (89%) and only independent (with its own budget) in 11%. The proportion of female physicians in EP training increased from 26% in 2010 to 38% in 2015. In total, 49,356 catheter ablations (i.e., 81% of reported ablations in 2015) were performed by the responding centers, resulting in a 44% increase compared with 2010 (the median number increased from 180 to 297 per center). Atrial fibrillation (AF) was the most common arrhythmia interventionally treated (47%). At 66% of the centers, (at least) 2 physicians were present during most catheter ablations. A minimum of 50 (75) AF ablations were performed at 80% (70%) of the centers. Pulmonary vein isolation with radiofrequency point-by-point ablation (62%) and cryoablation (33%) were the preferred ablation strategies. About one-third of centers reported surgical AF ablations, with 11 centers (8%) performing stand-alone surgical AF ablations. Only one-third of the responding 131 centers fulfilled all requirements for training center accreditation. CONCLUSIONS: Comparing 2010 with 2015, an increasing number of EP centers and procedures in Germany are registered. In 2015, almost every second ablation was for therapy for AF. Thus, an increasing demand for catheter ablation is likely, but training opportunities are still limited, and most centers do not fulfil recommended requirements for ablation centers.

[AV-reentrant tachycardia and Wolff-Parkinson-White syndrome : Diagnosis and treatment]. / AV-Reentry-Tachykardie und Wolff-Parkinson-White-Syndrom : Diagnostik und Therapie.

The AV-reentrant tachycardia (AVRT) is a supraventricular tachycardia with an incidence of 1-3/1000. The pathophysiological basis is an accessory atrioventricular pathway (AP). Patients with AVRT typically present with palpitations, an on-off characteristic, anxiety, dyspnea, and polyuria. This type of tachycardia may often be terminated by vagal maneuvers. Although the clinical presentation of AVRT is quite similar to AV-nodal reentrant tachycardias, the correct diagnosis is often facilitated by analyzing a standard 12-lead ECG at normal heart rate showing ventricular preexcitation. Curative catheter ablation of the AP represents the therapy of choice in symptomatic patients. This article is the fourth part of a series written to improve the professional education of young electrophysiologists. It explains pathophysiology, symptoms, and electrophysiological findings of an invasive EP study. It focusses on mapping and ablation of accessory pathways.

Hyperaldosteronism induces left atrial systolic and diastolic dysfunction.

Patients with hypertension and hyperaldosteronism show an increased risk of stroke compared with patients with essential hypertension. Aim of the study was to assess the effects of aldosterone on left atrial function in rats as a potential contributor to thromboembolism. Osmotic mini-pumps delivering 1.5 µg aldosterone/h were implanted in rats subcutaneously (Aldo, n = 39; controls, n = 38). After 8 wk, left ventricular pressure-volume analysis of isolated working hearts was performed, and left atrial systolic and diastolic function was also assessed by atrial pressure-diameter loops. Moreover, left atrial myocytes were isolated to investigate their global and local Ca2+ handling and contractility. At similar heart rates, pressure-volume analysis of isolated hearts and in vivo hemodynamic measurements revealed neither systolic nor diastolic left ventricular dysfunction in Aldo. In particular, atrial filling pressures and atrial size were not increased in Aldo. Aldo rats showed a significant reduction of atrial late diastolic A wave, atrial active work index, and increased V waves. Consistently, in Aldo rats, sarcomere shortening and the amplitude of electrically evoked global Ca2+ transients were substantially reduced. Sarcoplasmic reticulum-Ca2+ content and fractional Ca2+ release were decreased, substantiated by a reduced sarcoplasmic reticulum calcium ATPase activity, resulting from a reduced CAMKII-evoked phosphorylation of phospholamban. Hyperaldosteronism induced atrial systolic and diastolic dysfunction, while atrial size and left ventricular hemodynamics, including filling pressures, were unaffected in rats. The described model suggests a direct causal link between hyperaldosteronism and decreased atrial contractility and diastolic compliance.

Low-Level But Not High-Level Baroreceptor Stimulation Inhibits Atrial Fibrillation in a Pig Model of Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) increases susceptibility to atrial fibrillation (AF) by a combined sympatho-vagal hyperactivation. The purpose of this study was to investigate the effect of autonomic nervous system modulation by low-level baroreceptor stimulation (LL-BRS) compared to high-level BRS (HL-BRS) on atrial arrhythmogenic changes in a pig model of OSA. METHODS AND RESULTS: Sixteen pigs received tracheotomy under general urethane/chloralose anesthesia. Group 1 pigs (n = 8) received LL-BRS (at 80% of that slowing sinus rate) for 3 hours and group 2 pigs (n = 8) received HL-BRS (slowing sinus rate). Changes in atrial effective refractory period (AERP) and AF-inducibility were determined during applied negative thoracic pressure (NTP) for 2 minutes before and at the end of the 3-hour stimulation protocol. Group 1: LL-BRS prolonged AERP from 150 ± 5 to 172 ± 19 milliseconds (P < 0.001). After 3 hours of LL-BRS, NTP-induced AERP-shortening was diminished from -51 ± 10 milliseconds (-34%) to -22 ± 4 milliseconds (-13%) (P < 0.01). AF-inducibility during NTP maneuvers decreased from 90% at baseline to 15% (P < 0.01). Group 2: HL-BRS shortened AERP from 150 ± 17 to 132 ± 8 milliseconds (P = 0.024). After 3 hours of HL-BRS, NTP-induced AERP-shortening was increased from -55 ± 7 milliseconds (-36%) to -72 ± 11 milliseconds (-54%) (P < 0.05) and AF-inducibility was not affected. NTP-induced changes in blood gases and blood pressure were not different between the groups. CONCLUSION: LL-BRS suppressed NTP-induced AERP-shortening and AF-inducibility. By contrast HL-BRS further perpetuated NTP-induced AERP-shortening and increased AF-inducibility. These findings support only the use of LL-BRS as a novel therapeutic modality to treat AF in OSA.

[Typical atrial flutter: Diagnosis and therapy]. / Typisches Vorhofflattern: Diagnostik und Therapie.

Typical, cavotricuspid-dependent atrial flutter is the most common atrial macroreentry tachycardia. The incidence of atrial flutter (typical and atypical forms) is age-dependent with 5/100,000 in patients less than 50 years and approximately 600/100,000 in subjects > 80 years of age. Concomitant heart failure or pulmonary disease further increases the risk of typical atrial flutter.Patients with atrial flutter may present with symptoms of palpitations, reduced exercise capacity, chest pain, or dyspnea. The risk of thromboembolism is probably similar to atrial fibrillation; therefore, the same antithrombotic prophylaxis is required in atrial flutter patients. Acutely symptomatic cases may be subjected to cardioversion or pharmacologic rate control to relieve symptoms. Catheter ablation of the cavotricuspid isthmus represents the primary choice in long-term therapy, associated with high procedural success (> 97 %) and low complication rates (0.5 %).This article represents the third part of a manuscript series designed to improve professional education in the field of cardiac electrophysiology. Mechanistic and clinical characteristics as well as management of isthmus-dependent atrial flutter are described in detail. Electrophysiological findings and catheter ablation of the arrhythmia are highlighted.

[AV nodal reentrant tachycardia. Diagnosis and therapy]. / AV-Knoten-Reentrytachykardie. Diagnostik und Therapie.

The AV nodal reentrant tachycardia (AVNRT) is one of the most common arrhythmias encountered in clinical practice. It is characterized by a constant heart rate and an on/off phenomenon. The clinical symptoms may include palpitations, anxiety, polyuria, and dyspnea. Typically, tachycardia may be disrupted by vagal maneuvers in many patients. First-line treatment of symptomatic AVNRT is radiofrequency ablation. The present article deals with the characteristics, differential diagnosis and treatment of AVNRT in the EP lab. It is the second part of a series of manuscripts which may facilitate further education in the specific field of electrophysiology.

Obstructive respiratory events and premature atrial contractions after cardioversion.

Recurrence of atrial fibrillation (AF) after electrical cardioversion (ECV) is increased in patients with obstructive sleep apnoea (OSA). In patients with persistent AF, with (n=40) and without (n=32) obstructive respiratory events (OREs) during sedation for ECV, we determined the occurrence of premature atrial contractions (PACs) before and after insertion of a nasopharyngeal tube. The influence of acute obstructive respiratory events on atrial electrophysiology after termination of AF was studied in pigs. Incidence of PACs directly after ECV was higher in patients with OREs compared to those without OREs (7±2 versus 1±1 per 10 s, respectively; p<0.01). Occurrence of PACs could be reduced by 79% by insertion of a nasopharyngeal tube. In a subsequent sleeping study, patients with OREs had higher apnoea-hypopnoea indices and more PACs during night. 16 patient with and four patients without OREs had a relapse of AF during 1 week after ECV (p<0.01). In pigs, acute OREs after 30 min of AF increased occurrence of PACs and vulnerability for reinduction of AF, which could be attenuated by atropine, beta-blockers and renal denervation. OREs are associated with increased occurrence of PACs and more early relapse of AF. OREs increase occurrence of PACs and vulnerability for reinduction of AF by sympathovagal imbalance.

Catheter-based renal denervation reduces atrial nerve sprouting and complexity of atrial fibrillation in goats.

BACKGROUND: Atrial fibrillation (AF) leads to structural and neural remodeling in the atrium, which enhances AF complexity and perpetuation. Renal denervation (RDN) can reduce renal and whole-body sympathetic activity. Aim of this study was to determine the effect of sympathetic nervous system modulation by RDN on atrial arrhythmogenesis. METHODS AND RESULT: Eighteen goats were instrumented with an atrial endocardial pacemaker lead and a burst pacemaker. Percutaneous catheter-based RDN was performed in 8 goats (RDN-AF). Ten goats undergoing a sham procedure served as control (SHAM-AF). AF was induced and maintained by burst pacing for 6 weeks. High-resolution mapping was used to record epicardial conduction patterns of the right and left atrium. RDN reduced tyrosine hydroxylase-positive sympathetic nerve staining and resulted in lower transcardiac norepinephrine levels. This was associated with reduced expression of nerve growth factor-ß, indicating less atrial nerve sprouting. Atrial endomysial fibrosis content was lower and myocyte diameter was smaller in RDN-AF. Median conduction velocity was higher (75 ± 9 versus 65 ± 10 cm/s, P = 0.02), and AF cycle length was shorter in RDN-AF compared with SHAM-AF. Left atrial AF complexity (4.8 ± 0.8 fibrillation waves/AF cycle length versus 8.5 ± 0.8 waves/AF cycle length, P = 0.001) and incidence of breakthroughs (2.0 ± 0.3 versus 4.3 ± 0.5 waves/AF cycle length, P = 0.059) were lower in RDN-AF compared with SHAM-AF. Blood pressure was normal and not significantly different between the groups. CONCLUSIONS: RDN reduces atrial sympathetic nerve sprouting, structural alterations, and AF complexity in goats with persistent AF, independent of changes in blood pressure.

Renal denervation: effects on atrial electrophysiology and arrhythmias.

Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with significant morbidity and mortality. Currently, atrial endocardial catheter ablation, mainly targeting focal discharges in the pulmonary veins, is the most widely used interventional treatment of drug-refractory AF. Despite technical improvements, results are not yet optimal. There is ongoing search for alternative and/or complementary interventional targets. Conditions associated with increased sympathetic activation such as hypertension, heart failure and sleep apnea lead to structural, neural and electrophysiological changes in the atrium thereby contributing to the progression from paroxysmal to persistent AF and increasing recurrence rate of AF after PVI. Until now, interventional modulation of autonomic nervous system was limited by highly invasive techniques. Catheter-based renal denervation (RDN) was introduced as a minimally invasive approach to reduce renal and whole body sympathetic activation with accompanying blood pressure control and left-ventricular morphological and functional changes in resistant hypertension. This review focuses on the potential atrial antiarrhythmic and antiremodeling effects of RDN in AF patients with hypertension, heart failure, and sleep apnea and discusses the possible role of RDN in the treatment of AF.

Atrial autonomic innervation: a target for interventional antiarrhythmic therapy?

Atrial fibrillation is the most common arrhythmia and is associated with significant morbidity and mortality. The autonomic nervous system contributes to the creation of atrial fibrillation substrates. Atrial electrophysiology is influenced differently by sympathetic and parasympathetic activation. Several strategies are available to modulate the complex interaction between the autonomic nervous system and the heart. However, different approaches target the problem differently making the prediction of arrhythmogenic and/or antiarrhythmic effects difficult. We discuss the role of the autonomic nervous system on the development of a substrate for atrial fibrillation and explore the potential antiarrhythmic and/or arrhythmogenic effect of modulation of the autonomic nervous system by renal sympathetic denervation, ganglionated plexi ablation, ganglion stellatum ablation, high thoracic epidural anesthesia, low-level vagal nerve stimulation, and baroreflex stimulation.

Renal denervation suppresses ventricular arrhythmias during acute ventricular ischemia in pigs.

BACKGROUND: Increased sympathetic activation during acute ventricular ischemia is involved in the occurrence of life-threatening arrhythmias. OBJECTIVE: To test the effect of sympathetic inhibition by renal denervation (RDN) on ventricular ischemia/reperfusion arrhythmias. METHODS: Anesthetized pigs, randomized to RDN or SHAM treatment, were subjected to 20 minutes of left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size, hemodynamics, premature ventricular contractions, and spontaneous ventricular tachyarrhythmias were analyzed. Monophasic action potentials were recorded with an epicardial probe at the ischemic area. RESULTS: Ventricular ischemia resulted in an acute reduction of blood pressure (-29%) and peak left ventricular pressure rise (-40%), which were not significantly affected by RDN. However, elevation of left ventricular end-diastolic pressure (LVEDP) during LAD ligation was attenuated by RDN (ΔLVEDP: +1.8 ± 0.6 mm Hg vs +9.7 ± 1 mm Hg in the SHAM group; P = .046). Infarct size was not affected by RDN compared to SHAM. RDN significantly reduced spontaneous ventricular extrabeats (160 ± 15/10 min in the RDN group vs 422 ± 36/10 min in the SHAM group; P = .021) without affecting coupling intervals. In 5 of 6 SHAM-treated animals, ventricular fibrillation (VF) occurred during LAD occlusion. By contrast, only 1 of 7 RDN-treated animals experienced VF (P = .029). Beta-receptor blockade by atenolol showed comparable effects. Neither VF nor transient shortening of monophasic action potential duration during reperfusion was inhibited by RDN. CONCLUSIONS: RDN reduced the occurrence of ventricular arrhythmias/fibrillation and attenuated the rise in LVEDP during left ventricular ischemia without affecting infarct size, changes in ventricular contractility, blood pressure, and reperfusion arrhythmias. Therefore, RDN may protect from ventricular arrhythmias during ischemic events.

Potential role of renal sympathetic denervation for the treatment of cardiac arrhythmias.

The autonomic nervous system (ANS) has a pivotal role in the pathogenesis and maintenance of atrial and ventricular arrhythmias. Catheter-based renal denervation (RDN) is associated with a reduction of central sympathetic activity, muscle sympathetic nerve activity, and blood pressure in resistant hypertension. As renal afferent nerves are regulators of central sympathetic tone, RDN opens the possibility to modulate sympathetic activity, but without affecting peripheral chemoreceptors and mechanoreceptors in the heart and other organs. RDN was shown to reduce heart rate in humans and to reduce inducibility of atrial fibrillation (AF) as well as ventricular rate during AF in experimental studies. First evidence indicates that pulmonary vein isolation in combination with RDN increases the rate of AF freedom in patients with resistant hypertension. Furthermore, RDN may have a beneficial impact on ventricular arrhythmia, in particular in patients with coronary artery disease or heart failure.

A survey of German centres performing invasive electrophysiology: structure, procedures, and training positions.

AIMS: To provide a nationwide survey (and reference for the future) on cardiac electrophysiologists, types and numbers of invasive electrophysiological procedures, and training opportunities in 2010. METHODS AND RESULTS: German cardiology centres performing invasive electrophysiology were identified from quality reports and contacted to fill a questionnaire. A majority of 122 centres (65%) responded. Electrophysiology (ablation procedures and device therapy) was mainly part of a cardiology department (82%), and only in 9% independent (own budget). In only 58% of the centres, (at least) two physicians were present during catheter ablations. Although in 2010, women represented 59.4% of physicians <35 years old, only 26% of physicians in electrophysiology training were female. In total, 33 420 catheter ablations were performed with a median number of 180 per centre. Atrial fibrillation (AF) was the most common arrhythmia invasively treated (35%). At least 50 AF ablations were performed in 53% of the centres. Of the centres performing AF ablations, consecutive left atrial arrhythmias were treated by catheter ablation only in 75%, and only 44% had in-house surgical backup. Only one-fourth of the 122 centres fulfilled all requirements for training centre accreditation according to the European Heart Rhythm Association and the German Cardiac Society. CONCLUSION: The results indicate a high number of electrophysiology centres and procedures in Germany. Atrial fibrillation was the most common arrhythmia invasively treated. An increasing demand for catheter ablation is likely, but training opportunities are limited. Women are clearly underrepresented. A co-operation of higher and lower volume electrophysiology centres may be necessary for training purposes.

Calcium dysregulation in ventricular myocytes from mice expressing constitutively active Rac1.

Increased Rac1 activity and its concomitant elevation of reactive oxygen species (ROS) levels is believed to be involved in the development of cardiac diseases such as hypertrophy and arrhythmia. To study the effects of activated Rac1 on the properties of isolated ventricular myocytes we used a transgenic mouse model (RacET) expressing constitutively active Rac1. Concurrent with dilated cardiomyopathy global Ca(2+) handling as well as single cell contractility was substantially decreased. Cellular ROS levels were assessed with two independent assays and unexpectedly depicted decreased ROS production in RacET that was uncoupled from hormonal stimulation. Western blot analysis illustrated a massive increase in cellular Rac1 activity concomitant with a reduction in NADPH-oxidase activity. Analysis of the Ca(2+) current, the ryanodine receptor and fractional Ca(2+) release uncovered defective excitation-contraction (ec) coupling and a substantial increase in sarcoplasmic reticulum Ca(2+) leak together with a larger Ca(2+) spark amplitude and frequency. We conclude that Rac1 activity plays an important role for cardiac diseases but can be uncoupled from NADPH-oxidase activity. Rac1-mediated partial uncoupling of the ec-coupling machinery results in a ROS-independent disarrayed cellular Ca(2+) handling, contractility and impaired cardiac function.